POSTGRADUATE DIARYprime.edu.pk/ophthalmology/2015/jan_mar_2015.pdf · 2015-08-06 · bolic pathway...

Ophthalmology Update Vol. 13. No. 1, January-March 2015ii

Contents � EDITORIAL

� Current Concepts in the Management of VKC Sameera Irfan -----------------------------------------------------------------------------------------------------------------------------------------1

� OPHTHALMIC SECTION / ORIGINAL ARTICLES

� Early Probing in Nasolacrimal Duct Obstruction in Infants and Children Abdul Qayyum et al ------------------------------------------------------------------------------------------------------------------------------------ 4

� Causes of Non-Compliance in Patients with Open Angle Glaucoma Imran Ahmad et al ------------------------------------------------------------------------------------------------------------------------------------- 7

� Postoperative Refractive Outcome after Manual Small Incision Cataract Surgery (MSICS) Maooz Ahmad et al ----------------------------------------------------------------------------------------------------------------------------------- 10

� A Study of Pterygium Surgery with Stem Cell Limbo-Conjunctival Graft in Preventing Recurrence

M. Saeed Zafar Khan et al --------------------------------------------------------------------------------------------------------------------------- 15

� Outcome and Complications after Pan-Retinal Laser Photocoagulation for Proliferative Diabetic Retinopathy: An Experience at CMC Hospital Larkana

Muhammad Amin Shaikh et al --------------------------------------------------------------------------------------------------------------------- 19

� General Impact of Ocular Antiangiogenic Therapy Prof. Marianne Shahsuvaryan ---------------------------------------------------------------------------------------------------------------------- 22

� GENERAL SECTION / ORIGINAL ARTICLES

� Incidence of Achilles Tenotomy in Management of Congenital Equino Varus (Ctev) by Ponseti Casting Technique in Neonates

Syed Dil Bagh Ali Shah et al ------------------------------------------------------------------------------------------------------------------------ 26

� Current Concepts: Acute Pancreatitis, Aetiology, Management & Outcome Aurangzeb Khan et al -------------------------------------------------------------------------------------------------------------------------------- 29

� To Evaluate the Diagnostic Efficacy of Provocative tests in Carpal Tunnel Syndrome Syed Dil Bagh Ali Shah et al ------------------------------------------------------------------------------------------------------------------------ 34

� To Evaluate the Elevations of Intraocular Pressure after Nd: Yag Laser Posterior Capsulotomy

Muhammad Amin Shaikh et al --------------------------------------------------------------------------------------------------------------------- 38

� SHORT COMMUNICATION

� Artificial Retina: Physicists develop an interface to the optical nerve Madiha Durrani -------------------------------------------------------------------------------------------------------------------------------------- 42

iiiOphthalmology Update Vol. 13. No. 1, January-March 2015

The Management of

wishes its readers a Happy New Year

� POSTGRADUATE DIARY

� Aetiology of Diplopia Dr. Jahanzeb Durrani ------------------------------------------------------------------------------------------------------------------------ 43

� OPHTHALMOLOGY NOTEBOOK

� Lahore - A City of Noble Laureates ---------------------------------------------------------------------------------------------------- 45

� Development of Super-Resolved Fluorescence Optical Micrscope – Peep Into the Nanoworld ----------- 46

� Inauguration of Breast Cancer Clinic at Holy Family Hospital, Rawalpindi --------------------------------------- 46

� Letter to the Editor --------------------------------------------------------------------------------------------------------------------------- 47

JUST PUBL ISHED

A Comprehensive Guide for Parents and Students joining Medical College for MBBS/BDS degrees

WHY SHOULD I BECOME A DOCTOR?(First Edition)

by

Prof. Dr. M. Yasin Khan DurraniMBBS., DO., MD., FRCOphth (Lond)

Former: Prof. of Ophthalmology and Consultant Eye SurgeonRawalpindi Medical College & Islamic Int’l Medical College, Rawalpindi,Honorary Prof. of Ophthalmology, First National University, Tianjin, China

Recipient of Presidential award, Government of Pakistan & Pride of Karachi University Award

An Experienced Professor, with 40 Years of Teaching Experience

Available at: 267-A, St: 53, F-10/4, Islamabad & Schazoo Pharmaceutical

Cell: 0333 5158885, Email: [email protected]

1Ophthalmology Update Vol. 13. No. 1, January-March 2015

Vernal keratoconjunctivitis1 is an acute-on-chronic inflammatory disease of conjunctiva and cornea, en-countered in children with its onset usually in the first decade of life. Mild cases of VKC tend to remit with nonspecific and supportive therapy. But severe cases are more protracted, with frequent remissions and relapses; if not treated properly, it can result in sight-threatening complications2 over a period of time. It is mainly a Type I (immediate) hypersensitivity reaction-which occurs when a sensitized individual comes in contact with a specific antigen. However recent find-ings implicate more a complex pathogenesis with the involvement of T lymphocytes as well.1,2

These patients already exhibit large amounts of circulating Immunoglobulin E(IgE) which has a strong affinity for mast cells; the cross-linking of 2 adjacent IgE molecules by the antigen triggers mast cell degranula-tion. This releases various preformed mediators of the inflammatory cascade like histamine, tryptase, chy-mase, heparin, chondroitin sulfate, prostaglandins, thromboxanes, and leukotrienes. These mediators re-sult in an increase in vascular permeability and migra-tion of eosinophils, neutrophils, T and B lymphocytes with proliferation of fibroblasts, and laying down exu-berant amounts of collagen fibers in the conjunctival tissue. Hence the following changes are observed:• Hyperplasia of conjunctival epithelium • Adenoid layer shows marked cellular infiltration

by eosinophils, lymphocytes, plasma cells and his-tiocytes. Conjunctival vessels also show prolifera-tion, increased permeability and vasodilation.

• The Tarsal changes are typically seen in the upper tarsus and involve proliferation of fibrous layer of conjunctiva which later undergoes hyalinization resulting in the formation of giant papilla, typically greater than 0.3 mm in diameter, giving the classic ‘cobble-stone’ appearance. In severe cases, these papillae may undergo hypertrophy to produce

cauliflower-like excrescences of ‘giant papillae’ which may cause mechanical ptosis.

• The limbal form comprises of papillae which have a thick gelatinous appearance along with multiple white spots which are collections of degenerated epithelial cells and eosinophils called Horner-Trantas dots. They undergo rapid dissolution and do not last longer than a week from their initial presentation.

• The cornea may be affected in a variety of ways. Punctate epithelial keratopathy (PEK) results from the toxic effect of inflammatory mediators released from the conjunctiva. PEK can coalesce, resulting in frank epithelial erosions which coalesce to form a shield ulcer, which is typically shallow with white irregular epithelial borders. The major contributing factor in its development is chronic mechanical irritation from the giant tarsal papillae. Vernal pseudogerontoxon may be seen which is a degenerative lesion in the peripheral cornea resembling corneal arcus. Keratoconusis a frequent complication in chronic cases, associated with chronic eye rubbing and superimposed corneal thinning by injudicious use of topical steroids. Corneal vascularization may be seen rarely.

• Symptoms of intense burning and itching, accentuated when patient comes in a warm humid atmosphere, are due to histamine and other inflammatory mediators. Associated symptoms include mild photophobia, lacrimation, stringy discharge and heaviness of eyelids due to the tarsal involvement.

Differential Diagnosis VKC has to be differentiated from the seasonal Allergic Conjunctivitis which is an acute Type 1 hy-persensitivity reaction involving only the conjunctiva. There is marked chemosis and injection of the conjunc-

EditorialCurrent Concepts in the Management of VKC

Editorial

2 Ophthalmology Update Vol. 13. No. 1, January-March 2015

tiva along with eyelid edema which is usually not seen in VKC. Edema is the direct result of increased vascular permeability caused by the release of histamine from conjunctival mast cells.Treatment1) Topical antihistamines competitively and revers-

ibly block histamine receptors and relieve itching, constant eye lid rubbing, conjunctival edema and redness. Their affect is temporary and sympto-matic as they do not affect other pro-inflammatory mediators like prostaglandins and leukotrienes.

2) Mast cell stabilizers are used on a prophylactic basis to prevent mast cell degranulation on sub-sequent exposure to the allergen, on a long term basis. They include cromolyn sodium and lodoxa-mide (Alomide). However, drugs with both mast cell stabilizing ability and anti-histaminic property are the mainstay of therapy for mild forms of VKC like Alcaftadine, olopatadine, nedocromil and ke-totifen.

3) Mucolytics: Acetyl cysteine (0.5%) for mucous plaque formation. This is not available as an oph-thalmic preparation but it can be prepared by dis-solving 1mg powder from acetyl cysteine sachets (Mucolyte) in 10 cc distilled water.

4) Artificial tears: They help to dilute various aller-gens and inflammatory mediators that are pre-sent on the ocular surface and help flushing them. They also provide a barrier function and improve the first-line defense at the level of conjunctival mucosa. Hence eye drops during the day and eye ointment during the night is very helpful.

5) NSAIDs: they act on the cyclo-oxygenase meta-bolic pathway to inhibit the production of prosta-glandins and thromboxanes which results in va-soconstriction, decrease in vascular permeability, leukocytosis, and a decrease on intraocular pres-sure e.g. ketorolac tromethamine.

6) Vasoconstrictors: they provide short-term relief of vascular injection and redness and cause rebound conjunctival injection and inflammation. Hence they are of limited use or should not be used at all.They are available either alone or in conjunction with antihistamines; examples are naphazoline, phenylephrine, oxymetazoline, and tetrahydrozo-line.

7) Corticosteroids: They are the most potent and popular pharmacologic agents used in the treat-ment of chronic ocular allergy. They act at the first step of the arachidonic acid pathway and block phospholipase which prevents converting mem-brane phospholipid into arachidonic acid. Hence,

by preventing the formation of arachidonic acid, corticosteroids effectively block both cyclo-oxy-genase and lipoxygenase pathways, in contrast to NSAIDs, which act only on the cyclo-oxygenase pathway. However, their prolonged and injudi-cious use results in a number of ocular adverse effects, such as delayed wound healing and result-ant corneal thinning, secondary infections (viral, fungal), elevated intraocular pressure and forma-tion of cataract. In addition, the anti-inflammatory and immunosuppressive affects are nonspecific. As a rule, topical steroids should be prescribed for severe cases not responding to conventional thera-py and only for a short period of time. Corticoster-oids exist in various forms and potencies. Lotep-rednoletabonate is rapidly metabolized once it enters the anterior chamber of the eye. Therefore, it is extremely useful in treating ocular surface and superficial corneal inflammations. Relatively weak steroids like medrysone and fluorometholo-ne have a less potency in the eye and fewer ocular adverse effects. In contrast, prednisolone acetate is more potent with a higher incidence of adverse ef-fects.

8) Steroid-Sparing Drugs: In view of the numerous adverse affects of steroids,2 newer Immune Modu-latory Drugs, CYCLOSPORIN-A and TACROLI-MUS have been added to the armamentarium of therapeutic options available for severe form of VKC;3,12 they are known to have minimal side-ef-fects even after prolonged usage. Marked subjec-tive and objective improvement is noted within one month of therapy even in severe cases with marked corneal involvement.

(i) Tacrolimus (fujimycin)4-9 This is an immunosuppressive drug, a mac-

rolide, discovered in 1984 from the bacteria Strep-tomyces tsukubaensis. It is similar in action to cyclosporine-A but with a much higher potency (up to 100 times). It suppresses the activation, proliferation of B & T lymphocytes and forma-tion of cytokines, especially interleukin-2. It was first approved by the Food and Drug Administra-tion (FDA) in 1994 for use in liver transplantation. In ophthalmology, Tacrolimus has mainly been used to suppress immune reactions in corneal transplantations, uveitis, and allergic eye disease. Topical Tacrolimus with concentrations of 0.02–0.1% in ointment form has successfully been used for treatment of atopic keratoconjunctivitis (AKC), giant papillary conjunctivitis, and VKC.

It is available as a topical preparation for the treat-

Editorial


ment of atopic dermatitis (eczema), vitiligo as 1.0% and 0.03% skin cream. It suppresses inflam-mation in a similar way to steroids, and is equally as effective as a mid-potency steroid. It has the important advantage over steroids for not cause skin thinning (atrophy) in addition to other steroid related side-effects. The only known side effects are burning or itching sensation on initial appli-cations, with increased sensitivity to sunlight and heat. Patients should minimize or avoid natural or artificial sunlight exposure. Skin infections should be cleared prior to application as there may be an increased risk of their activation.

(ii) Cyclosporin-A eye drops: Cyclosporin10-12 has the same mechanism of action as Tacrolimus. It has been used affectively for the treatment of VKC, Dry Eye Syndrome, Mooran’s Ulcer, Corneal Melting, Scleritis. It is available as an ophthalmic prepara-tion, Reastasis which are preservative free minims. However it can be prepared from Cyclosporin cap-sules which contain a water miscible gel. For VKC, a concentration of 1% is quite effective prepared by taking gel from 2 capsules and mixing it with 4.5 cc distilled water. They only cause a stinging sensation on instillation, apart from this, there are no known side effects upon prolonged usage.

9) Treatment of large papillae: previously, Cryo ap-plication and surgical excision was performed but supratarsal injection of long-acting steroids along with immunomodulatory drugs are very affective.

10) General Measures: Maintenance of an air-condi-tioned environment and control of dust particles at home and work may also be beneficial. Local meas-ures, such as cold compresses, wearingdark gog-gles to prevent photophobia. Desensitization has also been tried without much rewarding results.

CONCLUSION VKC is a chronic, sight-threatening condition in children; if not treated appropriately, the vision is seri-ously and permanently affected either by the disease process itself like corneal opacities, keratoconus, corne-al vascularization or due to injudicious use of steroids resulting in intractable glaucoma and corneal thinning promoting the keratoconus. Unfortunately, topical steroids still remain a pop-ular choice of first line therapy amongst our ophthal-mic fraternity. This article highlights new, safer and as potent drugs (Cyclosporin and Tacrolimus) as steroids

but without any proven side effects after long term usage. This is because of the poor absorption of these drugs through cornea; they concentrate on the ocular surface and their affect is enhanced by prolonged use Hence in mild cases, antihistamine, a mast cell sta-biliser and lubricant drops during the day and ointment at night suffices. In moderate to severe cases, addition of immune-modulatory drug for at least 4-6 months is mandatory.REFERENCES1. Bonini S, Bonini S, Lambiase A, Marchi S, Pasqualetti P, Zuc-

caro O, et al. Vernal keratoconjunctivitis revisited: a case se-ries of 195 patients with long-term follow-up.Ophthalmol-ogy. 2000;107 (6:1157–1163. [PubMed]

2. Tabbara KF. Ocular complications of vernal keratoconjunctivi-tis. Can J Ophthalmol. 1999;34 (2:88–92.[PubMed]

3. Sawada S, Suzuki G, Kawase Y, Takaku F. Novel immunosup-pressive agent, FK506. In vitro effects on the cloned T cell acti-vation. J Immunol. 1987;139 (6:1797–1803. [PubMed]

4. Sloper CM, Powell RJ, Dua HS. Tacrolimus (FK506) in the man-agement of high-risk corneal and limbalgrafts.Ophthalmol-ogy. 2001;108 (10:1838–1844. [PubMed]

5. Virtanen HM, Reitamo S, Kari M, Kari O. Effect of 0.03% tac-rolimus ointment on conjunctival cytology in patients with severe atopic blepharoconjunctivitis: a retrospective study. Ac-taOphthalmol Scand. 2006;84 (5:693–695.[PubMed]

6. Vichyanond P, Tantimongkolsuk C, Dumrongkigchaiporn P, Jirapongsananuruk O, Visitsunthorn N, Kosrirukvongs P. Vernal keratoconjunctivitis: result of a novel therapy with 0.1% topical ophthalmic FK-506 ointment. J Allergy ClinImmu-nol. 2004;113 (2:355–358. [PubMed]

7. Hanifin JM, Paller AS, Eichenfield L, Clark RA, Korman N, Weinstein G, Caro I, Jaracz E, Rico MJ; US Tacrolimus Oint-ment Study Group (2005). “Efficacy and safety of tacrolimus ointment treatment for up to 4 years in patients with atopic dermatitis”. J Am AcadDerm 53 (2 suppl 2): S186–

8. Kymionis GD, Goldman D, Ide T, Yoo SH. Tacrolimus oint-ment 0.03% in the eye for treatment of giant papillary conjunc-tivitis. Cornea. 2008;27 (2:228–229. [PubMed]

9. Miyazaki D, Tominaga T, Kakimaru-Hasegawa A, Nagata Y, Hasegawa J, Inoue Y. Therapeutic effects of tacrolimus oint-ment for refractory ocular surface inflammatory diseases.Oph-thalmology. 2008;115 (6:988–992.e5. [PubMed]

10. BenEzra D, Pe’er J, Brodsky M, Cohen E. Cyclosporine eye drops for the treatment of severe vernal keratoconjunctivitis. Am J Ophthalmol. 1986;101 (3:278–282. [PubMed]

11. Secchi AG, Tognon MS, Leonardi A. Topical use of cyclo-sporine in the treatment of vernal keratoconjunctivitis.Am J Ophthalmol. 1990;110 (6:641–645. [PubMed]

12. Bleik JH, Tabbara KF. Topical cyclosporine in vernal keratocon-junctivitis. Ophthalmology. 1991;98 (11:1679–1684. [PubMed]

Dr. Sameera Irfan, FRCSConsultant Oculoplastic Surgeon & StrabismologistMughal Eye Trust Hospital, Lahore.Website: www.sameerairfan.com E-Mail: [email protected]


ORIGINAL ARTICLE

Abdul Qayyum

INTRODUCTION The epiphora affects approximately 5-20% of neo-nates. The rate of spontaneous regression is estimated to be 90% within first 3 months of life.1 It is perhaps bet-ter termed as delayed canalization of the nasolacrimal duct, since it resolves spontaneously. The lower end of nasolacrimal duct (at valve of Hasner) is last portion of lacrimal drainage system to canalize. The complete canalization usually occur soon after birth.2 The epi-phora is due to congenital obstruction of the nasolacri-mal duct system. The blockage occurs most frequently at the valve of Hasner at the distal end of the duct. The general stenosis of duct, congenital proximal outflow

and proximal out dysgenesis may be contributing fac-tor of obstruction.3 This obstruction requires surgical intervention, probing of the nasolacrimal duct is highly effective in relieving epiphora & discharge in those pa-tients who do not clear spontaneously with massage and medical treatment. The continued tearing and dis-charging is a potential source of ocular infection and also is a constant anxiety for parents. The optimum time to intervene has long been a topic of controversy.4 Therefore, we probe & irrigate those patients which were not cured with medical treatment, massage and their age was above six months.Aims & Objectives: To evaluate the result of manage-ment of nasolacrimal duct impatency in infants and children, to compare results of conservative therapy and surgical probing and irrigation.Patients & Methods: All the patients were enrolled from the out patients department of Pediatric Ophthal-mology, Bolan Medical College Quetta. A Total of 5110

Abdul Qayyum M.S. (Fellowship in Paed. Ophth)1, Manzoor Ahmed MBBS2

Imran Khan Bazai MBBS3

ABSTRACT Purpose: To evaluate the results of management of nasolacrimal duct impatency in infants and children to compare results of conservative therapy and surgical probing and irrigation.Material & Methods: All the patients were enrolled from the out patients department of Pediatric Ophthalmology, Bolan Medical College Quetta. A Total of 5110 patients were examined during the period from January 2013 to June 2014. Out of these, 97 patients (1.9%) were found to be suffering from congenital nasolacrimal duct obstruction, of these 76 patients (78%) had unilateral obstruction, while 21 patients (22%) had bilateral obstruction. On first visit these patients were kept on conservative treatments (topical antibiotics) and their parents were instructed about the hydrostatic massage at the lacrimal sac area. These patients were re-examined after two to three weeks, if there was no improvement, the patient was either treated surgically, when more than six months of age or the medical treatment was continued when the patient was under the age of six months.In infants older than six months who did not respond to conservative treatment, the probing and syringing were performed. This procedure was performed using a halothane general anesthesia. The lower punctum was dilated with punctum dila-tor then the passages were irrigated with saline to wash out any debris, using the 23 gauge lacrimal cannula on a syringe.The lacrimal probe size 0 or 1 was used (depending on the age of patients). The lacrimal probe was lubricated with anti-biotic ointment. The probe was initially passed vertically, then horizontally and finally downwards and slightly posteriorly. The obstruction was usually felt when 3/4th of probe was inside the passage. It was then taken out and syringing repeated. Topical antibiotics were instilled .The patients were advised to continue treatment for another two weeks, then the patient were re-examined to re-evaluate the results of the surgical procedure after two weeks.Results: 63 patients (65%) had spontaneous relief from tearing and discharge with medical treatment and massage. These include 47 patients (75%) among the 0-6 months age group, 13 patients (20%) among the 7-12 months age group and 5 patients (5%) among the above one year age group (Table-1). 34 patients (35%) required probing. No patient was probed before 6 months of age. Probing cured tearing and discharged in 27 patients (79%) while 7 patients (21%) required repeat probing. Second probing relieved 5 patients (14%) of epiphora & discharge. 2 patients who were older than 1 year remained symptomatic even after 3rd repeat probing (Table-2).Conclusion: All the patients with congenital nasolacrimal duct obstruction should be conservatively treated with antibiotics and hydrostatic massage up to the age of six months. If not relieved with above measures, careful probing may be per-formed before the infant is one year of the age to achieve excellent results.

1Associate Professor & Pediatric Ophthalmologist, 2,3Residents in Ophthalmology

Correspondence: Dr. Abdul Qayyum, Associate Professor & Pediat-ric Ophthalmologist, Department of Ophthalmology, Bolan Medical College, Quetta. [email protected] Cell: 0333 7921566

Received: September 2014 Accepted: November 2014

Early Probing in Nasolacrimal Duct Obstruction in Infants and Children

OPHTHALMIC SECTION



patients were examined during the period from Janu-ary 2013 to June 2014. Out of these, 97 patients (1.9%) were found to be suffering from congenital nasolacri-mal duct obstruction, of these 76 patients (78%) had unilateral obstruction, while 21 patients (22%) had bi-lateral obstruction).METHODS On first visit these patients were kept on conserva-tive treatments (topical antibiotics) and their parents were instructed about the hydrostatic massage at the lacrimal sac area. These patients were re-examined af-ter two to three weeks, if there was no improvement, the patient was either treated surgically, when more than six months of age or the medical treatment was continued when the patient was under the age of six months. In infants older than six months who did not re-spond to conservative treatment, the probing and syringing were performed. This procedure was per-formed using a halothane general anesthesia. The low-er punctum was dilated with punctum dilator then the passages were irrigated with saline to wash out any de-bris, using the 23 gauge lacrimal cannula on a syringe. The lacrimal probe size 0 or 1 was used (depending on the age of patients). The lacrimal probe was lubri-cated with antibiotic ointment. The probe was initially passed vertically, then horizontally and finally down-wards and slightly posteriorly. The obstruction was usually felt when 3/4th of probe was inside the passage. It was then taken out and syringing repeated. Topical antibiotics were instilled. The patients were advised to continue treatment for another two weeks, then the pa-tient were re-examined to re-evaluate the results of the surgical procedures after two weeks.RESULTS 63 patients (65%) had spontaneous relief from tear-ing and discharge with medical treatment and massage. These include 47 patients (75%) among the 0-6 months age group, 13 patients (20%) among the 7-12months age group and 5 patients (5%) among the above one year age group (Table-1). 34 patients (35%) required probing. No patient was probed before 6 months of age. These includes 12 patients (35%) among 0-6months age group,19 pa-tients (56%) among the 7-12months age group and 3 patients (9%) among above 1 year age group (Table-2).Probing cured tearing and discharged in 27 patients (79%) while 7 patients (21%) required repeat probing. Second probing relieved 5 patients (14%) of epiphora & discharge. 2 patients who were older than 1 year remained symptomatic even after 3rd repeat probing (Table-2).

Table-1: Age and sex distribution of patients responds to conservative therapy. 63 patients (65%)

Age Male Female Total patients Results

0-6 months 22 25 47 75%

7-12 months 9 4 13 20%

Over 1 years 2 1 3 5%

Table-2: Age and sex distribution of patients require probing. 34 patients (35%)

Age Male Female Total patients Results

0-6 months 7 5 12 All cured

7-12 months 8 11 19 All cured 5 after

probingOver 1 years 1 2 3 One cured, two

Unsuccessful

DISCUSSION The blockage of nasolacrimal duct is a common anomaly and it is due to delay in the normal develop-ment of system where it enters the nose, resulting in a persistent membrane obstruction at the value of Has-ner5. It is present in 2-4% of all infants at birth. The mechanism of congenital obstruction can be explained by various ways. Anomalous canalization or failure of fusion between ocular and nasal cords is very impor-tant explanation. The abnormal folds in the mucosa & the abnormal cartilaginous or bony development is also suggested by various clinicians6. Most of the cases of Congenital Nasolacrimal duct obstruction resolve spontaneously or with conservative treatment and mas-sage. Only 1-2 % of cases requires surgical intervention in the form of probing and syringing. Some times in neonatal period there is lacrimal sac distention resulting in congenital dacrocystitis and con-genital mucocele, it is probably the only indication of immediate duct probing in neonatal period.7 The prob-ing of Nasolacrimal duct is very effective method for relieving congenital dacrocystenosis in those patients who fail to clear spontaneously, but there is controver-sy concerning the age at which initial probing should be performed. Some authors advocate probing as early as 4 months of age after a trial of topical antibiotics and massage have failed.8 Others recommend wait & see if there is spontaneous clearance of obstruction, if the blockage does not clear up to age to 12-14 months prob-ing should be performed. Our therapeutic strategy is to probe and irrigate any time after six months, but preferably before 14 months of age. We adopt this for following reasons. The rate of spontaneous recovery is high before six months of age as evident in our study (Table-1).



The parents are very concerned & it’s a constant source of anxiety. Constant tearing and discharge is unpleasant to the patients along with suitable source of secondary infection. Early probing may reduce the likely hood of secondary cellulitis which also contributes to failure of subsequent probing. In our series of 97 patients, 63 patients (65%) had spontaneous recovery with conservative treatment with antibiotics & massage. The spontaneous recov-ery was very higher among 0-6 months of age groups (75%), while it dropped to 5% in the age group of above 1 year (Table-1). The 34 patients (35%) required prob-ing and irrigation. Initial probing cleared the epiphora and discharge in 27 patients (79%) and 7 patients (21%) required repeated probing. Second probing relieved 5 patients (14%) of epiphora & discharged while two patients out of these (7%) did not respond to even 3rd probing(Table-2). In Philadelplia same study was carried out on 572 eyes at Children Hospital Philadelplia. In 572 eyes the success rate of initial probing was found to be 97% un-der 13 months of age.9 Robb and others co-workers have achieved 90% cure on initial probing, rising to 96% on repeat probing.10 According to Zia et al, initial probing and irrigation cured 75% of patients while cure rate ris-es to 97% on second repeat probing.11 Our findings are thus substantiate the results of above mentioned work-ers. Katowitz JA et al also mention in their study that earlier probing has high success rate.5

Mac Evan & Young studied 4792 children. They revealed 96% success rate was achieved in the first six months and success rate was fallen to 53% after one year. The mean success rate in this study in first twelve months was 69.3%.12

Mittelman achieved success rate of 87%. He rec-ommends probing for Congenital Nasolacrimal duct obstruction before 11 months of age. According to him the success rate is higher in those below 1 year of the age, (95%) as compared to those above one year of age (73%).13

Zia et al also of the opinion that age at time of prob-ing is an important factor in determining the final out-come.11 Our clinical impression is that age of patients at time of probing is a very important factor which deter-mines the final outcome. In our 2 patients who could

not relieved epiphora, their age was 3 years. It seems that the persistent infection in nasolacrimal duct con-sequent to untreated obstruction results in fibrosis that leads to worsening of obstruction. However according to Robb the success rate is not related to age at the time of probing. He attributes fail-ure to anatomical changes in Nasolacrimal duct & be-lieves that first procedure to be tried for the persistent nasolacrimal duct obstruction in the first 5 years of life should be simple probing.CONCLUSION All the patients with congenital nasolacrimal duct obstruction should be conservatively treated with an-tibiotics and hydrostatic massage up to the age of six months. If not relieved with above measures, careful probing may be performed before the infant is one year of the age to achieve excellent results.REFERENCES1. Paul TU, Medical management of congenital nasolacrimal

duct obstruction. J. Pediatric Ophthalmal and strabismus. 1985;22:67-70.

2. Kanski JJ.Lacrimal drainage system in: Kasnki JJ.Editor Clini-cal Ophthalmology 6th edition, Oxford: Butterworth heineman, 2009:158-159.

3. Nelson,LB,Calhun, J H, Menduke, H. Medical Management of congenital nasolacrimal duct obstruction. Ophthalmology 1985; 92:1187-1190.

4. Peterson, RA, ERobb, RM. The natural history of congenital nasolacrimal duct obstruction. J. Pediatric ophthalmal and stra-bismus 1978;15:246-250.

5. David Taylor Greig S. Hoyt The lacrimal system in: David Tay-lor and Creig S Hoyt-editor. Pediatric Ophthalmology & stra-bisman 3rd edition. Oxford. Elsevier Saunders, 2005.287-290.

6. Jones, LT and Wobing, JL: Surgery of the Eyelids and lacrimal system. Birmingham (Alabama), Aesculapius Publishing Com-pany, 1976,pp162-167.

7. Scott, WE, Fabre, JA, Ossoinig, K:Congenital mucocele of the lacrimal sac. Arch Ophthalmol 97:1556-1558.1979.

8. Kushner, BJ: Congenital nasolacrimal system. Arch Ophthal-mol 100:597-600, 1982.

9. Katowitz JA, Welsh MG: Timing of initial probing and irriga-tion in congenital nasolacrimal duct obstruction Opthalmol-ogy, 1987;94(6):698-705.

10. Robb, RM:probing and irrigation for congenital nasolacrimal duct obstruction. Arch Ophthalmol 104:378-379, 1986.

11. Zia Mohammad, M.Daud Khan Timing of probing in nasolacri-mal duct obstruction in infants and children Pakistan journal of ophthalmology volume -10, Number 4. October ,1994.

12. Browse Caglar, Cagatay; Batur, Muhammed; Yasar, Tekin; Cinal, Adnan outcome of lacrimal massage or probing treat-ments at early late ages for congenital nasolacrimal duct ob-struction Turkish Pediatrics Archive (December 1, 2010). (www.thefreelibrary.com).

13. Mittelman, D. Probing and irrigation for congenital nasolac-rimal duct obstruction (letter to the editor) Arch Ophthalmol 104:1125,1986.


ORIGINAL ARTICLE

Imran Ahmad

INTRODUCTION Glaucoma is an optic neuropathy in which there is optic nerve damage along with visual fields loss which may or may not be associated with raised intraocular pressure.1 Glaucoma is a chronic, progressive and most often asymptomatic disease and is the leading cause of irreversible blindness worldwide. According to WHO statistics glaucoma is now the second leading cause of blindness globally after cataract.2 Glaucoma, however, presents an even greater public health challenge than cataract, because the blindness it causes is irrevers-ible. It is responsible for approximately 15% of blind-ness worldwide.3 It has been estimated that 73 million people are affected by glaucoma and 6.7 million are thought to be blind due to this disease.4 The projections for 2020 are that almost 80 million people will be af-fected by glaucoma.4

Compliance is a measure of the degree to which patient follows prescribed instruction during a defined time period.5 Topical treatments have been reported to delay the onset and worsening of glaucoma, but they must be instilled for life or until a curative treatment becomes available.6 When the intraocular pressure is poorly controlled, sufferers may eventually notice a se-vere restriction of visual fields or even a loss of central vision.7 There are many causes of blindness from glau-

coma but non-compliance to medication is the main reason especially in developing country like Pakistan. The leading cause for non-compliance is forgetfulness followed by side effects, lack of proper counseling of the patient by physician, non-awareness about alternate or new available medications and cost of the drug.8 De-spite of the availability of effective pharmacologic ther-apies, non-compliance in patients with glaucoma has been reported to vary from 24 to 59%.9 Non-compliance with topical therapy may result in unnecessary switch-ing to other drugs or surgical procedure, with addition-al risks and costs.10,11

The purpose of the study was to determine the rate and causes of non-compliance in patients with glaucoma presenting to the Out Patient Department of Khyber Teaching Hospital, Peshawar.Study design: Retrospective cohorts studyMATERIAL AND METHODS The study was conducted from 1st September 2011 to 30th November 2011 in the Out Patient Department of Khyber Teaching Hospital, Peshawar. The inclusion criteria were diagnosed cases of glaucoma that were on anti-glaucoma therapy. All patients underwent comprehensive general and ophthalmic evaluation in-cluding medical and ophthalmic history, best corrected visual acuity, slit lamp examination, IOP measurement and Humphrey visual field test. Detailed history was taken about previous consultations, prescribed medica-tions, doses and timing of drugs. Patients were specially inquired about the reasons for not using the prescribed medications. All these information were recorded in a proforma.RESULTS A 3 months survey was conducted in which a to-

Imran Ahmad FCPS1, Dr. Bakht Samar Khan FCPS2, Mubashir Rehman FCPS3

ABSTRACT: Purpose: To document the causes of non-compliance in patients with open angle glaucoma.Material and Methods: The study was conducted in Outpatient Department of Khyber Teaching Hospital, Peshawar from 1st September to 30th November 2011.Results: A total of 200 patients with open angle glaucoma were included in the study and their compliance to medications was checked. Causes of non-compliance were on-off use of medications (24.43%), improper timing of dose (16.03%), pres-sure controlled leading to discontinuation of treatment (15.27%), no improvement in visual acuity with treatment (12.21%), side effects of drugs (9.92%), costly medications (9.8%), confusing glaucoma medications with other drugs (6.87%) and physical disability (6.10%).Conclusion: The main cause for non-compliance to glaucoma medications was poor health education of patients about glaucoma disease.

1Medical Officer, Pakistan Instituate of Community Ophthalmology (PICO), Hayatabad Medical Complex, Peshawar. 2Assistant Professor Department of Ophthalmology, Khyber Teaching Hospital, Peshawar, 3Medical Officer, Lady Reading Hospital, Peshawar.

Correspondence: Dr. Imran Ahmad, House No: 40, Street No: 2, Sector H1, Phase 2, Hayatabad, Peshawar (KPK). Mob No: 0333-9255244, E-mail: [email protected]

Received: October 2014 Accepted: November 2014

Causes of Non-Compliance in Patients with Open Angle Glaucoma



tal of 200 patients were examined as cases of glaucoma and their compliance to drugs was checked. Patients age ranged was from 42-85 years with a mean age of 62.7 + 12.5 years. Surprisingly in about 65.5% (131) pa-tients there was poor compliance to medications. Out of 65.5% patients, 12.2% (16) patients reported no im-provement in vision which resulted in discontinuation of medications. 9.92% (13) patients stopped their medi-cines due to side effects of drugs. 16.03% (21) patients were using medications but not on proper timing as were advised by the doctor. 9 (6.87%) patients confused the drugs with other non-glaucoma medicines due to poly pharmacy. Most of the patients 32 (24.4%) used medicine on and off and not on regular basis. 12 (9.16%) patients stopped medicine due to non-affordability of drugs. 15.26% (20) patients stopped medicine because they were thinking that their intraocular pressure was under control and had not been advised that these medicines have to be used lifelong. 8 (6.10%) patients were non-compliant to medication because of their de-pendency on others for drops instillation due physical disability.

Causes of poor Compliance in patients with open angle glaucoma

S. No Causes of poor compliance Number of patients Percentage

1 No improvement in VA 16 12.21%2 Side effects of drugs 13 9.92%3 Improper timing of dose 21 16.03%4 Confusing with other drugs 9 6.87%5 On and off use of medication 32 24.43%6 Costly medication 12 9.16%7 Pressure controlled 20 15.27%8 Physical disability 8 6.10%

Total 131 99.99%

Causes of poor compliance in patients with open angle glaucoma

DISCUSSION The purpose of our study was to investigate the causes of non-compliance in patients with glaucoma

presenting to Khyber Teaching Hospital. Many studies have shown that the major contributor to loss of vision in glaucoma patients is non-compliance. But the results of our study were astonishing as in 65.5% of patients presenting to our hospital were having poor compli-ance to medications. In a study compiled by Weintraub M also mentioned that approximately 35% of the glau-coma patients comply almost 100% with therapy.12 The main reason for non-compliance was poor education about glaucoma disease and most of the patients were not well aware about the nature and seriousness of glaucoma and the importance of compliance. So most of these patients take this disease lightly, use glauco-ma medicine on and off and strict adherence to drugs was not followed. The major contributor (24.3%) to non-compliance was on and off use of medications (32 patients). Almost similar results to our study were re-ported by Rotchford AP and Murphy KM in their study that about 24% of patients are omitting their glaucoma medications either frequently or occasionally.13

Another factor which was also strongly related to patient education about glaucoma disease was that 15.27% patient stopped their medicine as they were told that their pressure is under control and were not advised that they have to continue with medications for life long, so they themselves stopped medicines, which resulted in further decrease in visual acuity and progression of glaucoma. 16.03% patients were using glaucoma drops but on improper timings. Every drug is having its anti-glaucoma effect for a specific period of time, like 12 hourly drops has its effect for that period of time and after that another drop should be instilled at proper time to prevent increase in IOP as highlighted in a study done by Granstrom PA.14 16 (12.21%) stopped their medications because they did not notice any im-provement in their vision after using these drugs for a period of time as mentioned in a study done by Ash-burn FS15. So it is very important to counsel the patient about the effect of glaucoma drugs that they will not cause a significant improvement in their vision but will prevent further deterioration of vision. In our study out of 131 patients 13 (9.92%) patients discarded the medi-cine because of the adverse effects associated with these medications and 12 patients stopped drugs due to non-affordability. Other causes for discontinuation of these medications were confusion of drugs with other drops (6.87%) and because of physical disability (6.10%). The use of different sizes or shapes of medications and their containers will help patients to discriminate between different treatments. These two factors also contribute to non-compliance as mentioned in study done by Win-field AJ and his colleagues.16



CONCLUSION There are a number of reasons for poor compli-ance with glaucoma medications, including lack of understanding of the disease, no obvious symptoms, complicated or too frequent drug schedules, lack of improvement in visual acuity, side effects, physical difficulty in administering eye drops and cost. All pa-tients diagnosed as glaucoma must be well informed about the nature and seriousness of disease and must be counseled about the proper timing, side effects of drugs and the effects of treatment on the outcome of the disease.REFERENCES1. Foster PJ, Buhrmann R, Quigley HA, Johnson GJ. The defini-

tion and classification of glaucoma in prevalence surveys. Br J Ophthalmol 2002;86:238-42.

2. Resnikoff S, Pascolini D, Etya’ale D, Kocur I. Global data on visual impairment in the year 2002. Bull world Health Organ 2004;82:844-51.

3. Foster PJ, Johnson GJ. Glaucoma in China: how big is the prob-lem? Br J Ophthalmol 2001;85:1277-82.

4. Quigley HA, Broman AT. Number of people with glaucoma worldwide. Br J Ophthalmol 2006;90:262-7.

5. Schwartz GF, Quigley HA. Adherence and persistence with glaucoma therapy. Surv Ophthalmol 2008;53:57-68

6. Nordmann JP, Baudouin C, Renard JP, Denis P, Lafuma A.

Measurements of treatment compliance using a medical de-vice for glaucoma patients associated with intraocular pressure control: a survery. Clinical Ophthalmology 2010;4:731-9.

7. McKinnon SJ, Goldberg LD, Peeples P, et al. Current manage-ment of glaucoma and the need for complete therapy. Am J Manag Care. 2008;14:20-7.

8. Taylor SA, Galbraith SM, Mills RP. Causes of non-compli-ance with drug regimens in glaucoma patients: A qualita-tive study. Journal of ocular pharmacology and therapeutics. 2002;18(5):401-9.

9. Tsai JC. Medication adherence in glaucoma: approaches for optimizing patient compliance. Curr Opin Ophthalmol 2006;17:190-5.

10. Ichhpujani P. Revisiting the issue of compliance in glaucoma. Journal of Current Glaucoma Practice. 2010;4(2):73-6.

11. Sclar DA. Improving medication compliance: a review of se-lected issues. Clin Ther 1991;13:436-40.

12. Weintraub M. Compliance in the elderly. Clin Geriatr Med 1990;6:445-52.

13. Rotchford AP, Murphy KM. Compliance with timolol treat-ment in glaucoma. Eye 1998;12:234-6.

14. Granstrom MA. Glaucoma patients not compliant with their drug therapy: clinical and behavioral aspects. Br J Ophthalmol 1982;66:464-70.

15. Ashburn FS, Goldberg I, Kass MA. Compliance with ocular therapy. Surv Ophthalmol 1980;24:237-48.

16. Winfield AJ, Jessinam D, Williams A, Esakowitz L. A study of the causes on non-compliance by patients prescribed eye drops. Br J Ophthalmol 1990;74:477-80.

A patient with cellulitis, chemosis, proptosis, and an ulcerated cornea, developed after head injury was diagnosed as carotid cavernous fistula confirmed after angiography. Endovascular coiling was undertaken and the patient recovered.

Differential Diagnosis: Acute angle-closure glaucoma, Ocular lymphoma Periorbital cellulitis, Thyroid ophthalmopathy

Newsnet Online


ORIGINAL ARTICLE

Maooz Ahmad

INTRODUCTION Cataract is the leading cause of blindness world-wide. Approximately 17.6 million people, accounting for 39% of all the causes of blindness, are blind as a re-sult of bilateral cataract globally.1 In Pakistan cataract accounts for 51.5% of the avoidable causes of blind-ness.2 Approximately 570,000 adults are estimated to be blind and 3,560,000 have visual impairment as a result of cataract in Pakistan.3 Phacoemulsification, a standard technique for cataract surgery in developed countries as a routine, and it is not routinely practiced in devel-oping countries including Pakistan due to its complex and expensive equipment and the requirement for a more advanced surgical training.4 Manual Small Inci-sion Cataract Surgery (MSICS) is a good alternative to phacoemulcification that is gaining popularity in de-

veloping countries including Pakistan due to its early wound stability, minimally induced astigmatism, low complication rate and cost-effectiveness.5-6

Postoperative refractive error has been identified to be one of the most common risk factors for poor vis-ual and functional outcome of cataract surgery in Paki-stan.7 Prediction of postoperative refraction depends on several factors including axial length, corneal refractive power, corneal diameter and anterior chamber depth.8 Several formulas have been developed for calculating IOL power9-10 and improvements have been made to an accurate measurement of biometric values11 to enhance the accuracy of the postoperative predicted refraction. In the current study we have determined postop-erative refractive error after MSICS in patients having cataract. Patients undergoing cataract surgery for age related cataract have big expectations in terms of good refractive outcome and there was no local study avail-able regarding refractive outcome after MSICS in our local population. The results of this study will be quite useful in allowing ophthalmologists in making crucial modifications in the procedure for MSICS especially considering the exact measurement of preoperative

Maooz Ahmad MBBS1, Mir Zaman FCPS2, Bilal Khan Orakzai FCPS3, Nuzhat Rahil FCPS4

Bilal Bashir FCPS5, Asif Iqbal MBBS6

ABSTRACTObjective: To determine postoperative refractive outcome after manual small incision cataract surgery among patients with cataract.Materials & Methods: It was a descriptive cross sectional study done in Khyber Istitute of Ophthalmic Medical Sciences (KIOMS), Hayatabad Medical Complex (HMC), Peshawar from September, 2011 till April 2012 on 185 patients. All enrolled patients in our study were through Out Patient Department. After informed consent detailed history was recorded on prede-signed proforma. Axial length was measured in millimeters with Optikon Hiscan AB-scan through contact A-scan biometry and corneal power measured in diopters (D) with Topcon OM-4 Ophthalmometer. Intraocular lens (IOL) power and target postoperative refraction aimed for emmetropia were calculated using SRK II formula while the ‘A’ constant used was that provided by IOL manufacturer. All the patients were operated by a single surgeon using standard manual small incision cataract surgery (MSICS) technique and implanting same type of IOL in all patients.All the patients were followed at 2 weeks postoperatively and subjective refraction was done. Spherical Equivalent (SE) refractive error was determined and recorded on predesigned proforma. Data was analyzed using SPSS version 17.Results: One hundred and eighty five eyes of 185 patients above 40 years of age with age related cataract were included in this study. Sixty nine (37.3%) patients presented in the age group of 51-60 years and ninety nine (56.5%) patients enter-ing the study were male. Spherical equivalent postoperative refractive error was within ± 1.00D of the predicted refraction, which in this study was emmetropia, in 146 (78.9%) of eyes and beyond ± 1.00D in 39 (21.1%) eyes. Out of these 39 eyes 27 (14.6%) eyes had hypermetropic (> +1.00D) and 12 (6.5%) eyes had myopic (< - 1.00D) postoperative refractive error.Conclusion: Postoperative refractive outcome in this study is acceptable and is comparable to other international studies. However the results can be improved further with the use of more advanced equipment, newer IOL formulas and personali-zation of surgeon’s “A” constant for determining the predicted postoperative refraction.Key Words: Manual Small Incision Cataract Surgery; Cataract refractive outcome; Spherical Equivalent postoperative refractive error.

1Postgraduate Trainee, 2Associate Professor. 3Vitreo-Retinal Trainee 4Ophthalmologist, Lady Reading Hospital, Preshawar. 5Medical Of-ficer, Lady Reading Hospital, Preshawar, 6Postgraduate Trainee.

Correspondence: Dr. Maooz Ahmad, House 36, Street 1, Sector L-2, Phase 3, Hayatabad, Peshawar. Cell: 0332 9268859Email:[email protected]


Postoperative Refractive Outcome after Manual Small Incision Cataract Surgery (MSICS)



IOL power calculations. Predicted postoperative refrac-tive status, aimed for emmetropia, and the IOL power was calculated using SRK II formula. The results of the study provide a local reference and also acted as an au-dit for the accuracy of the predicted refraction in our settings. Based on this observation further studies may also be carried out to identify and improve sources of error in calculating IOL power or the predicted postop-erative refraction if appropriate.MATERIAL AND METHODS This descriptive cross sectional study was con-ducted at Khyber Institute of Ophthalmic Medical Sci-ences, Postgraduate Medical Institute, Hayatabad Med-ical Complex, Peshawar. The duration of the study was of eight months and was carried out after the approval of synopsis from 1st September 2011 to 30th April 2012. 185eyes were our sample size, keeping 7.7%15 propor-tion of myopic refractive error of more than 1.00D after MSICS, 95% confidence interval and 3.85% margin of error under WHO sample size calculations. The sam-pling technique was non-probability consecutive sam-plingInclusion criteria:• All patients presenting with age related cataract

were included.• Age group above 40 years were included• Either gender was included.Exclusion criteria:• Patients with an axial length of less than 22.00mm

and more than 24.4mm were excluded from the study through biometry.

• Any patient with sublaxated, traumatic or compli-cated cataract was excluded through history and slit lamp examination.

• Patients with co-existing glaucoma, corneal pa-thology, uveitis, pseudoexfoliation, diabetic retin-opathy, age related macular degeneration and retinal detachment were also excluded from the study through slit lamp examination, applana-tion tonometry, dilated fundus examination and B-Scan if required.

• Patients in whom IOL could not be implanted in the capsular bag were also excluded from the study.

The above mentioned conditions act as confound-ers and if included might have introduced error in the study results. Ethical approval was obtained from the hospital ethical committee. All the patients meeting the inclu-sion criteria (i.e.; presenting with cataract diagnosed on slit lamp examination) were admitted in eye ward

through the out-patient department. Informed written consent was taken from all the patients. The patient’s history and visual acuity (VA) were recorded at pres-entation using standard retro illuminated Snellen chart. All patients had thorough preoperative examination by the consultant ophthalmologist including best cor-rected visual acquity (BCVA), slit lamp evaluation of the anterior segment, and dilated fundus examination using 78D lens and intraocular pressure measurement using Goldmann applanation tonometer. A contact method A-scan biometry, Optikon His-can AB-Scan, was used to measure axial length of eye-ball in millimeter (mm) and an average of 5 readings was recorded as final reading by a single trained oph-thalmic technician. The Topcon OM-4 Ophthalmom-eter was used to measure the corneal power in diopters (D) by the same ophthalmic technician. The A constant used was that provided by the manufacturer of the IOL. The IOL power and the target postoperative refraction aimed for emmetropia were calculated using SRK II formula. Routine investigations were performed for all the study patients on the day of admission. The patients were operated on the next OT list. Manual Small Inci-sion Cataract Surgery was performed by a single con-sultant ophthalmologist, and same IOL was implanted in the capsular bag in all patients. After being operated, all the patients were followed at 2 weeks post-opera-tively and the VA was recorded and subjective refrac-tion was done by a single experienced optometrist to detect the refractive outcome (plano, myopia and hy-permetropia). All the follow-up assessments were done under the supervision of same ophthalmologist. All the above mentioned information including the patient’s name, age, sex and address were recorded in a pro-forma. Strict exclusion criteria were followed to con-trol confounders and bias in the study results. The data was analyzed by means of SPSS software (version 17). Mean ± Standard Deviation (SD) was calculated for nu-merical variables like age. Frequency and percentages (% ages) were calculated for categorical variables like gender and refractive outcome (plano, myopia and hy-permetropia). Refractive outcome was stratified among age and gender to see the effect modifications. All the results were presented in the form of tables and graphs. RESULTS One hundred and eighty five eyes of 185 patients above 40 years of age diagnosed as having cataract and fulfilling the inclusion criteria were included in this study. All the study patients were evaluated at 2 week. The minimum age at which the patient presented



was 43 years while the oldest patient was 91 years of age with a mean of 59.64 years and SD ±10.34. Sixty nine (37.3%) patients presented in the age group of 51-60 years, making it the most common decade of presen-tation for patients with age related cataract. Details re-garding age of our study population are given in Table I. Male gender was observed to be slightly dominant as compared to the female gender in the patients included in the study (Figure. 1). The male to female ratio was almost 1.2:1 Out of the total 185 patients, 39 patients (21.1%) had spherical equivalent (SE) refractive error of more than 1.00D as compared to the target refraction, which in our study was emmetropia. Out of these 12 patients (6.5%) had myopic (myopia exceeding 1.00D) postoper-ative refractive error, 27 patients (14.6%) had hyperme-tropic (> +1.00D) postoperative refractive error while rest of the 146 patients (78.9%) had SE postoperative refractive error within ±1.00D of the target refraction (Plano) (Table II). Spherical equivalent refractive error was observed more frequently in the age groups 51-60 years (n=17; 9.2%) as compared to the other age groups (TableIII). Spherical equivalent refractive error of more than 1.00D was observed more frequently in the male gender as compared to the female gender (Table IV). No post-operative complications such as hyphema, corneal de-compensation, endophthalmitis or IOL malpositioning, which might have interfered with the study results, were observed in any of the patients included in the study.

Table-I: Age distribution of the study population

Table II: frequency of SE postoperative refractive error

Table-III: distribution of SE postoperative refractive error in different age groups

Table-IV: distribution of SE postoperative refractive error in both genders

Figure-1: Gender Distribution of study population

DISCUSSION Modern cataract surgery is no longer considered as a simple procedure for removal of physical barrier to vision, the procedure is largely intended to achieve a desired postoperative refractive outcome.12 Postop-erative refractive error, resulting from inaccurate IOL selection and aphakia, has been reported as leading risk factors in several studies.7, 13-14 The refractive out-come of cataract surgery can be monitored by audit-ing data in relation to spherical targeting, correction of astigmatism or maintaining astigmatism neutrality and provision of near vision.15 Biometry performed for cal-culating an appropriate power of IOL targets spherical equivalent refraction.16 Thus determination of spheri-cal equivalent refraction after cataract surgery and its difference with the predicted postoperative refraction

Age (years) Frequency (n) Percent (%)41-5051-6061-7071-8081-90

91-100

5169431921

27.637.323.210.31.10.5

Total 185 100.0% = percentage; n = number

SE Refractive Error Frequency (n) Percent (%)

Plano 146 78.98

Myopia 12 6.5

Hypermetropia 27 14.6

Total 185 100.0SE = spherical equivalent; Plano = refractive error ≥ -1.00D & ≤ +1.00D; Myopia=refractive error < -1.00 D; Hypermetropia = refractive error > +1.00D; n= number; % = percentage

Age group (Years)

SE refractive errorTotal

Plano Myopia Hyperopia

41 - 50 38 3 10 51

51 - 60 52 7 10 69

61 - 70 37 1 5 43

71 - 80 16 1 2 19

81 - 90 2 0 0 2

91 - 100 1 0 0 1

Total 146 12 27 185SE = Spherical Equivalent; Plano = refractive error ≥ -1.00D & ≤+1.00D; Myopia = refractive error <-1.00 D; Hypermetropia =refractive error > +1.00D.

GenderSE refractive error

TotalPlano Myopia Hypermetropia

Male 75 7 17 99

Female 71 5 10 86

Total 146 12 27 185

SE = Spherical Equivalent; Plano = refractive error ≥ -1.00D & ≤ +1.00D; Myopia = refractive error < -1.00 D; Hypermetropia = refractive error > +1.00D.



provides a very useful tool for auditing accuracy of bi-ometry techniques, appropriateness of the formula(s) used for calculating IOL power and the surgeon’s “A” constant if it has been personalized by the surgeon.15

The current study was intended to determine the predictability of the target postoperative refraction af-ter MSICS. The target refraction in our study was aimed for emmetropia. Postoperative spherical equivalent re-fractive error of all the patients included in the study was determined subjectively 2 weeks after surgery. Postoperative refractive error in our study was within ± 1.00D of the target refraction in 78.9% of cases and beyond this range in 21.1% of cases. 14.6% of the cases had SE refractive error of more than +1.00D while it was less than -1.00D in 6.5% of the cases. Complications like corneal decompensating, hyphema, endophthalmi-tis or IOL malpositioning, which might have interfered with the outcome of study, were not seen in any of the study cases. Our results are comparable to other studies. Zhou et al reported SE refractive error of ± 1.00D in 73.2% of patients after MSICS, refractive error was less than -1.00D in 7.7% of cases and more than +1.00D in 19.1% of cases.17 Our results are comparable and better than their study and the possible reason for this may be that they did not follow any strict exclusion criteria and all the patients undergoing cataract surgery with IOL and then were available for follow up during the study pe-riod were included in the study. Nazzi G et al found 77% of cases with SE refrac-tive error within ± 1.00D of the target refraction18. Gou-zousky M et al reported SE refractive error of -1.00D to +1.00D in 74% of cases19 and Murphy C et al in 72.3% of cases.20 Zaidi FH et al observed similar results in 80% of cases in a consecutive series of 1000 patients undergo-ing cataract surgery.21 Rajan MS et al22 and Lundstrom M23 observed similar results in 83.5% and 79.3% of cas-es respectively. RP Gale et al suggested a benchmark standard of 85% of cases within ± 1.00D of the target refraction after cataract surgery.24 Pervical et al report-ed as many as 97% of cases with SE refractive error of -1.00D to +1.00D.25

Based on these studies, the accepted range for the percentage of cases with SE postoperative refractive er-ror of -1.00D to +1.00D as compared to the predicted refractive state after cataract surgery with IOL implan-tation is 72% - 97%, the average being 84.5%. Our re-sults are well within this range. Over the recent decades the difference between the achieved refraction and the target refraction has been improved by several factors including advances in IOL manufacture, instrumenta-tion for biometry measurement, IOL power formula

and personalization of “A” constant.26 Although results of our study are satisfactory but they can further be improved with the use of advanced equipment for bi-ometry measurements such as immersion A-scan ultra-sound biometry and optical biometry which measure the axial length, an important variable in calculating IOL power, with much precision unlike the contact A-scan ultrasound biometry which we have used in the current study.8

CONCLUSION As patient’s expectations for precise refractive out-comes increase, even incremental improvement in pre-dicting postoperative refractions becomes useful. Al-though results of our study are acceptable as compared to other studies but they can further be improved by enhancing IOL biometry accuracy by using immersion or optical biometry rather than the contact biometry, using one of the newer IOL power calculation formu-las, personalizing the lens “A” constant and periodic tracking of postoperative refractive outcomes.REFERENCES1. Foster A, Gilbert C, Johnson G. Changing patterns in global blind-

ness: 1988–2008. Community Eye Health J. 2008;21(67): 37–9.2. Dineen B, Bourne RA, Jadoon Z, Shah SP, Khan MA, Foster A,

et al. Causes of blindness and visual impairment in Pakistan. Br J Ophthalmol 2007; 91: 1005-10.

3. Jadoon Z, Shah SP, Bourne R, Dineen B, Khan MA, Gilbert CE, et al. Cataract prevalence, cataract surgical coverage and bar-riers to uptake of cataract surgical services in Pakistan: the Pa-kistan National Blindness and Visual Impairment Survey. Br J Ophthalmol 2007; 91: 1269-73.

4. Zaman M, Shah AA, Hussain M, Babar TF, Khan MT, Dawar S. Outcome of sutureless manual extra capsular extraction. J Ayub Med Coll Abbotabad 2009; 21(1): 39-42.

5. Khan MT, Jan S, Hussain Z, Karim S, Khalid MK, Mohammad L. Visual outcome and complications of manual sutureless small incision cataract surgery. Pak J Ophthalmol 2010; 26(1): 32-8.

6. Venkatesh R, Colin SH, Sengupta S, Ravilla D, Krishnan T, Da-vid F. Phacoemulcification versus manual small-incision cata-ract surgery for white cataract. J Cataract Refract Surg 2010; 36: 1849-54.

7. Bourne R, Dineen B, Jadoon Z, Lee PS, Khan A, Johnson GJ, et al. Outcomes of cataract surgery in Pakistan: results from the National Blindness and Visual Impairment Survey. Br J Oph-thalmol 2007;91: 420-6.

8. Lee AC, Qazi MA, Pepose JS. Biometry and intraocular lens power calculation. Curr Opin Ophthalmol 2008; 19: 13-7.

9. Narvaez J, Zimmerman G, Stultin RD, Chand DH. Accuracy of intraocular lens power prediction using the Hoffer Q, Hol-laday 1, Holladay 2 and SRK/T formulas. J Cataract Refract Surg 2006; 32(12): 2050-3.

10. Charalampiduo S, Cassidy L, Eugene N, Loughman J, Nolan J, Stack J, et al. Effect on refractive outcomes after cataract sur-gery of intraocular lens constant personalization using the Hai-gis formula. J Cataract Refract Surg 2010; 36: 1081-9.

11. Rabsilber TM, Jepson C, Auffarth GU, Holzer MP. Intraocular lens power calculation: Clinical comparison of two optical bi-ometry devices. J Cataract Refract Surg 2010; 36(2): 230-4.

12. Vogel A, Dick HB, Krummenauer F. Reproducibility of optical biometry using partial coherence interferometry: intraobserv-



er and interobserver reliability. J Cataract Refract Surg 2001; 27:1961–1968.

13. Bourne RRA, Dineen BP, Ali SM, et al. Outcomes of cataract surgery in Bangladesh: results from a population-based nation-wide survey. Br J Ophthalmol 2003; 87:8.

14. Nirmalan PK, Thulasiraj RD, Maneksha V, et al. A population based eye survey of older adults in Tirunelveli district of south India: blindness, cataract surgery, and visual outcomes. Br J Ophthalmol 2002; 86:505–12.

15. Akingbehin T. Improving refractive results of cataract surgery through audit. Cataract & Refract Surg today Eur Feb 2011. p. 24-23.

16. Chell Paul B. Refractive targeting in cataract surgery. RC Ophth Focus winter 2003; 23.

17. Zhou Z, Congdon NG, Zhang M, Chen L, Zheng Z, Zhang L, et al. Distribution and visual impact of postoperative refractive error after cataract surgery in rural China: Study of Cataract Outcomes and Up-Take of Services report 4. J Cataract Refract Surg 2007;33: 2083-90.

18. Nuzzi G, Cantu C, De Giovanni MA. Older age as a risk factor for deviation from emmetropia in pseudophakia. Eur J Oph-thalmol 2001; 11:133–8.

19. Guzowski M, Rochtchina E, Wang JJ, Mitchell P. Refractive

changes following cataract surgery: the Blue Mountains Eye Study. Clin Exp Ophthalmol 2002; 30:159–162.

20. Murphy C, Tuft SJ, Minassian DC. Refractive error and visual outcome after cataract extraction. J Cataract Refract Surg 2002; 28:62–6.

21. Zaidi FH, Corbett MC, Burton BJL, Bloom PA. Raising the benchmark for the 21st centurydthe 1000 cataract operations and survey: outcomes, consultant-supervised training and sourcing NHS choice. Br J Ophthalmol 2007; 91:731–6.

22. Rajan MS, Keilhorn I, Bell JA. Partial coherence laser interfer-ometry vs conventional ultrasound biometry in intraocular lens power calculations. Eye 2002; 16:552–6.

23. Lundstro¨m M, Stenevi U, Thorburn W. The Swedish National Cataract Register: a 9-year review. Acta Ophthalmol Scand 2002; 80:248–57.

24. Gale RP, Saldana M, Johnston RL, Zuberbuhler B, McKibbin M. Benchmark standards for refractive outcomes after NHS cata-ract surgery. Eye 2009;23:149–152.

25. Percival SP, Vyas AV, Setty SS, Manvikar S. The influence of implant design on accuracy of postoperative refraction. Eye 2002; 16(3): 309–15.

26. Mamalis N. Intraocular lens power accuracy: how are we do-ing? J Cataract Refract Surg 2003;29:1-3.

Ebola:Misinformation and speculation in Health Care, intermittent and unpredictable nature of outbreaks

An outbreak of Ebola virus disease (EVD) has jolted West Africa, claiming thousands of lives in West Africa (Guinea, Liberia, Nigeria, and Sierra Leone), since the virus emerged in Guinea in early 2014 in West Africa, it has captivated the world’s attention and concern, health professionals and the general public are struggling to comprehend these unfolding dynamics and to separate misinformation and speculation from truth.EVD, originally identified in 1976 in Yambuku, Zaire (now Congo), and Nzara, South Sudan, is caused by an RNA virus in the filovirus family. “Ebola” (named after a river in Zaire) encompasses five separate spe-cies — Zaire ebolavirus, Bundibugyoebolavirus, Taï Forest ebolavirus, Sudan ebolavirus, and Reston ebolavirus. Reston ebolavirus is not known to cause disease in humans, but the fatality rates in outbreaks of the other four species have ranged from 25 to 90%. The strain currently circulating in West Africa bears 97% homology to Zaire ebolavirus. This strain has historically resulted in the highest mortality (90%), although the estimated case fatality rate in the current outbreak is less than 60%.Outbreaks, most likely reservoir appears to be a fruit bat, although that linkage has not been confirmed. Trans-mission to humans may have occurred through direct contact with tissue or bodily fluids from an infected animal. Notably, Ebola virus is a zoonotic pathogen, and its circulation among humans is uncommon, which explains the intermittent and unpredictable nature of outbreaks. In fact, although the virus has caused more than 20 outbreaks since its identification in 1976. Traditional practices, such as bathing of corpses before burial, have facilitated transmission. Numerous studies indicate that direct contact with infected bodily fluids — usually feces, vomit, or blood — is necessary for transmission and that the virus is not transmitted from person to person through the air or by casual contact. Typical symptoms include fever, profound weakness, and diarrhea. A maculopapular rash has been de-scribed, and laboratory abnormalities including elevated aminotransferase levels, marked lymphocytopenia, and thrombocytopenia. Hemorrhagic complications occur in fewer than half of infected persons, and gross bleeding is relatively rare. Newsnet Online


ORIGINAL ARTICLE

Saeed Zafar

INTRODUCTION A pterygium is a wing shaped sheet of fibro vas-cular structure which arises from conjunctiva and in-vades the cornea. It is usually more prevalent in resi-dents of hot, temperate climate and represents response to chronic dryness and chronic exposure to sun rays1

(Fig 1). Ultraviolet B is thought to be the major risk fac-tor which causes the elastic degenerative damage to the limbal stem cells barrier with resultant conjunctivaliza-tion of the cornea.2 The common indications for the sur-gical intervention include cosmetic appearance, visual deterioration, ocular motility restriction and chronic congestion. The basic histopathological change in primary pterygium is elastotic degeneration of conjunctiva. It is caused by degeneration of sub-epithelial collagen and replacement with abnormal material that stains for elastin. There is dissolution of Bowmann’s memberane of cornea and dyskeratotic change in epithelial cells ly-ing over the tissue3,4 Pterygium is usually classified into different grades according to the extent of corneal in-

volvement. Grade 1 pterygium extends less than 2 mm on to the cornea. Grade 2 the pterygium involves up to 4 mm of the cornea. Grade 3 is the pterygium encroach-ing more than 4 mm on to the cornea and usually in-volve the visual axis4, 5

Different surgical and non surgical treatment modalities were adopted to prevent the recurrence of pterygium after surgery. Initially surgical excision with bare sclera technique was done. It was associated with a recurrence rate ranging from 30 to 70%.6 Later, in addition to surgical excision, different chemical sub-stances were used to prevent the recurrence. These in-cluded alum powder, silver nitrate. Beta radiations has also been used to and it reduces the recurrence rate up to 5-13%; however, due to severe complications like cataract, keratoconjuntivitis sicca, corneal ulcerations, ptosis, scleral necrosis this mode of treatment lost its popularity.7

Thiotepa an alkyl ting agent was thought to inter-fere with mitosis in fibroblasts cells in the pterygium. Due to various complications like allergic reactions, conjunctival pigment depositions and scleral ulcera-tions its use has declined.8

Mitomycin C is an antibiotic anti metabolite prop-erties by inhibiting DNA replication and is commonly used either intra operatively or post operatively. Vari-ous studies have shown recurrence using intra operative Mitomycin C comparable to those using postoperative Mitomycin C drops were less than 10% for the primary cases and less than 20% for the recurrent cases 9, 10

M. Saeed Zafar Khan FCPS1, Waqar Ahmed FCPS2

Prof Zahid Kamal Siddiqui FCPS, FRCS3, Prof Akram Riaz FRCOphth4

ABSTRACTPurpose: The purpose of this study was to evaluate the efficacy, safety and recurrence rate by using superotemporal conjuntivo-limbal auto graft transplantation technique in the surgical management of pterygium in a population in which pterygia are more prevalent with maximum sun exposure.Material & Methods: A total of 74 patients with primary and recurrent pterygium was surgically treated by the technique of excision and covering with free conjunctivo –limbal autograft between June 2010 and May 2013 at Ch Rehmat Me-morial Hospital/Continental Medical College Lahore. All surgeries were performed under local anesthesia by using limbal counjunctival stem cell graft from the ipsilateral eye and stitched by using 10/0 nylon on to the bare area. During follow-up examination, the best corrected visual acuity, slit lamp examination and complication, recurrence rate were recorded. Results: Recurrence was seen in 4(5.4%) cases, graft disinsertion 2(2.70%) cases, pygonic granuloma 1(1.5%) case, these were dealt with minor surgical revision. Uncorrected visual acuity improved after surgery in 62(83.8%) cases.Conclusion: Conjuntivo-limbal autografting is a simple, safe and minimally invasive technique and it is recommended for the management of both primary and recurrent ptergia in Pakistani populationKeywords: Pterygium, Stem Cell Limbo-Conjunctival Graft, Recurrent Pterygium

1Consultant Eye Surgeon, Iqra Medical Complex, Lahore, 2Senior Registrar, Lahore General Hospital, Lahore, 3Professor of Ophthalmology, FJMC/Sir Ganga Ram Hospital, Lahore, 4Professor of Ophthalmology, Avecina Medical College & Hospital, Professor of Ophthalmology, FJMC/Sir Ganga Ram Hospital, Lahore

Correspondence: Dr . M Saeed Zafar Khan, Consultant Ophthalmologist 95 E-2 Johar Town Lahore, cell 03344073664 E-mail: [email protected]


A Study of Pterygium Surgery with Stem Cell Limbo-Conjunctival Graft in Preventing Recurrence



Amniotic membrane transplantation has also been used as it possesses the anti- inflammatory and anti- fi-broblast activity; however, a study by Prabhasawat et el reported a recurrence rate of 10.95% in primary while 37.5% in recurrent cases 11. Other studies have reported the recurrence rate ranging from 3.8 % to 15.4 % for the primary pterygia. The pioneer work of replacing the damaged lim-bal stem cells was done by Kenyon et al in 1985. In his study total no was 57; out of these16 eyes had primary pterygia while 41 eyes had recurrent ones. After a fol-low up of two years he reported recurrence rate of 3 (5.3%) cases.12 However other authors have failed to achieve the same success rate5,13,14 similarly Koch JM and Guler M have described the inclusion of limbal tis-sues in the graft with low recurrence rate.15,16 The im-portance of limbal tissues use has also been suggested by Figueriredo et al.17 We conducted this study to see outcome of pterygium surgery using limbal stem cell graft in our population from Lahore and surrounding cities of Pakistan.MATERIALS & METHODS This prospective study includes 74 patients with primary and recurrent pterygium who were visit-ing the out patient department of Ch Rehmat Memo-rial Hospital/Continental Medical College Lahore from June 2010 to May 2013. All the entries were made in computerized proforma which included complete oc-ular and medical history, grading of pterygium, visual acuity before/after surgery, surgical technique, compli-cations, and finally recurrence. These cases were treated by the excision of pteryg-ium and covering the bare limbo-scleral area with stem cell conjunctivo-limbal autograft. In this study 16 eyes had mild pterygium, 37 moderate, while 19 eyes had marked pterygium. Seventy eyes had primary pterygi-um while only 4 eyes had recurrent pterygium. All pa-tients were followed for at least a period of six months.Surgical Technique: A standard surgical technique was used by all the surgeons in the study. Initially topical anesthetic drops pro-paracaine hydrochloride 0.5% (Alcaine, Alcon, Inc.) eye drop were used to anesthetize the ocular surface. Xylocaine hydrochloride 2% was injected sub-conjunc-tivally with a 27 G needle above the body of pterygi-um. A nick incision was made in the conjuctiva close to the head of pterygium and dissection was continued posteriorly using Wana’s scissors. The pterygium was separated from the underlying scleral tissue by blunt dissection. The head of pterygium remained attached at the cornea. A mosquito artery forceps was placed un-der the body of pterygium near to its scleral attachment and it was fixed for couple of minutes to achieve the

haemostasis. The clamps were released and body along with head of pterygium was separated from cornea by using corneal scissors. It was assured that no damage should be done to medial rectus muscle during the pro-cess of dissection. Partial keratectomy was done at the nasal limbus by using no 15 Bard-Parker knife. The area was cleaned by using ringer lactate solution. The hae-mostasis was secured by pressure application. Bipolar cautery was used when needed.

Fig-1

Fig-1

Graph-1

Graph-2



The length and width of the bare area was meas-ured and a 2 mm strip of stem cell conjunctivo limbal autograft with variable length according to wound gap was taken from the limbus to superior fornix in the supro-temporal quadrant of the conjunctiva of ipsilat-eral eye. Using 27 G needle nearly 0.5 ml of xylocaine 2% was injected to raise the balloon of conjunctiva con-taining the stem cells. The pre marked area of the con-junctiva was incised by using non toothed conjunctival forceps and fine corneal scissors to avoid the button holing of the conjunctiva. By gentle dissection the graft was dissected up to the limbus and is excised up to 2 mm into the cornea to include the limbal stem cells. The excised conjunctival strip containing the stem cell was slide over to the nasal limbus. The Limbus to limbus orientation was ensured. The graft was anchored with 10/0 nylon sutures. The conjunctiva was thoroughly washed with ringer lactate solution. Antibiotic steroid drops were put and eye pad was placed for at least 72 hours to provide anchorage to the episcleral and limbal tissues. After the removal of bandage topical antibiotic and steroid drops with lubricants were used in every case. Regular follow up was done at one week, two week, one month and six month and finally one year. The signs of infection at the wound and graft rejection were thoroughly assessed. The sutures were removed after 15 to 21 days after the surgery (Fig 2).RESULTS A total number of 74 patients with primary and recurrent pterygium were included. There were 50 male and 24 female (graph 1). The range of the age was from 30 years to 70 years. The mean age of the study group was 38.70 ± 7.60. The percentage of the patients in the range of 41-50 years was 43.24%, whereas 18.9% patients belonged to group with an age 20- 40 years, 29.72% patients were in the age group 51-60 years and finally only 8.1% patients were older then 60 years (graph 2). According to the severity of the pterygium majority i.e. 37 patients had moderate disease, while 18 had mild degree of pterygium and 19 patients had se-vere pterygium (Table 1). 70 eyes had primary, while only 4 eyes had recurrent pterygia.

Table-1

Preoperative visual acuity (BCVA) was noted in 6/12-6/18 in 35 eyes and 6/24- 6/36 in 27 eyes. It im-proved to 6/6 to 6/9 in 47 eyes and 6/12 to 6/18 in

12 eyes on post operative follow up visits. At the first follow up visit after one week all the grafts were in-tact with the complaints of watering and foreign sensa-tions which were attributed to the stitches at the area of wound which were reduced with lubricants. At the second follow up after two weeks the stitches were re-moved. It was noted that the sub-conjunctival edema containing yellow colored fluid had resolved and the color of the graft was showing pinkish hue. After one month all the subjective complaints were resolved and the graft had structural uniformity with the surround-ing conjunctiva and no sub conjunctival scarring was seen. At the final visit, six month post operatively, 70 eyes (94.6%) had no signs of recurrence whereas 4 eyes(5.4%) had recurrence of pterygium, graft dis-in-sertion occurred in 2 (2.7%) of cases, pyogenic granulo-ma in 1 (1.5%). All these complications were dealt with minor surgical revisions. Uncorrected visual acuity im-proved after surgery in 62 (83.8%) cases.DISCUSSION In the present study, out of seventy four patients 50 were male, 24 female and mean age group in this study was 38.70 years. Sadiq et al reported similar pat-tern i.e. 51 female, 21 male and the mean age group in their study was 41.42 years.18 At six months follow up 70 (94.6%) eyes had no signs of recurrence whereas only 4 eyes (5.4%) had recurrence of pterygium. In study by Mahdy19 recurrence rate was 4.75% due to modified surgical technique, although they studied the younger age groups living in the windy, sandy with prolonged exposure to ultra violet radiations while working in the Arabian Gulf region. Another study by Narsani et al20 compared the re-currence of pterygium conjunctival autografting with Mitomycin C. Out of total 112, 70 eyes received the con-junctival graft whereas 42 eyes received preoperatively Mitomycin C. They reported a recurrence of 5.7% in conjunctival auto graft group compared to 8 (19%) in Mitomycin C group. Other complications related to the limbal conjunc-tival auto grafting like 2(2.7%)cases had graft disin-sertion and one case (1.5%) had pyogenic granuloma. However more serious complications like graft necro-sis, corneal dellen or iatrogenic conjunctival cysts were not seen. Similarly Sadiq 18and Mahdy 19did not report severe sight threatening complications. Visual acuity improved in our study after surgery in 62 (83.7%) cases due to reduction in post operative astigmatism. Similarly Rao21 reported visual acuity im-provement or stabilization at preoperative level in 51 eyes(96.2%) with a mean follow up of 12 months. We

Degree of Pterygium

Miled 18

Moderate 37

Marked 19



conclude that the recurrence rates for pterygium exci-sion and limbal conjunctival auto graft in our study is 5.4% which is comparable with other studies Kenyon12

(5.3%), Mahdy19 4.75%) and Narsani20 (5.7%).CONCLUSION In our study, we meticulously dissected the stem cell ultra thin graft devoid of any Tenon,s fasica. The technique is easy to craft and conjunctival limbal stem cell graft is very much near to the normal anatomy and morphology of the limbus. So we recommend limbal conjunctival auto grafting as a procedure of first choice for the surgical management of primary and recurrent ptergia in Pakistani population.REFERENCES1. Threlfall TJ, English DR. Sun exposure and pterygium of the

eye: A dose-response curve. Am J Ophthalmol 1999;128:280-7. 2. Taylor HR, West SK, Rosenthal FS, Munoz B, Newland HS,

Emmett EA. Corneal changes associated with chronic UV ir-radiation. Arch Ophthalmol 1989;107:1481-4.

3. Spencer WH. Ophthalmic pathology: An Atlas and Textbook. 3rd edition. Philadelphia: WB saunders; 1985. Vol I. p 174-76.

4. Austin P, Jakobiec FA, Iwamolot. Elastodysplasia and elasto-dystrophy as the pathologic bases of ocular pterygia and pin-guicula. Ophthalmology 1983;90:96-109.

5. Kenyon KR, Wagoner MD, Hettinger ME. Conjunctival auto-graft transplantation for advanced and recurrent pterygium. Ophthalmology 1985;92:1461-70.

6. Hirst LW. The treatment of pterygium. Acta Ophthalmol 2003; 48:145.

7. Mackenzie FD, Hirst LW, Kynaston B, Bain C. Recurrence rate and complications after beta-irradiation for pterygia. Ophthal-mology 1991;98:1776-81.

8. Joelson GA, Muller P. Incidence of pterygium recurrence in patients treated with thiotepa. Am J Ophthalmol 1976;81:891-92.

9. Rubinfield RS. Serious complications of topical Mitomycin C

after pterygium surgery. Ophthalmology 1992; 99:1647.10. Cheng HC, et al. Low dose intra operative application of topi-

cal Mitomycin C for pterygium surgery. Ophthalmology 1996; 103:674.

11. Prabhasawat P, Barton K, Burkett G, Tseng SC. Compari-son of conjunctival autografts, amniotic membrane grafts and primary closure for pterygium excision. Ophthalmology 1997;104:974-85.

12. Kenyon KR, Tseng SC. Limbal autograft transplantation for ocular surface disorders. Ophthalmology 1989;96:709-23.

13. Chen PP, Ariyasu RG, Kaza V, Labree LD, Mc Donnell PJ. A randomized trial comparing mitomycin C and conjunctival au-tograft after excision of primary pterygium. Am J Ophthalmol 1995;120:151-60.

14. Dowlut MS, Laflamme MY. Les pterygions recidivants: fre-quence et correction par autogreffe conjunctivale. Can J Oph-thalmol 1990;196:295-97.

15. Koch JM, Mellin JB, Wauble TN. The pterygium -Autologous conjunctiva - limbus transplantation as treatment. Ophthalmol-ogy 1992;89:143-46.

16. Guler M, Sobaci G, Liker S, Ozturk F, Muthi FM, Yildirim E. Conjunctival autograft transplantation in cases with recurrent pterygium. Acta Ophthalmol 1994;72:721-26.

17. Figueiredo RS, Cohen EJ, Gomes JAP, Rapuano CJ, Laibson PR. Conjunctival autograft for pterygium surgery: how well does it prevent recurrences? Ophthalmic Surg Lasers 1997;28:99-104. 17

18. Sadiq NM, Arif SA,Bhatia J.use of supro-temopral conjunctival autograft in the surgical management of ptergium;our tech-nique and results. J Ayuab Medical Coll. 2009 ;21 (4),121-4.

19. Mahdy MA, Bhatia J. Treatment of primary pterygium: Role of limbal stem cells and conjunctival autograft transplantation. Oman J Ophthalmol 2009: 23-6.

20. Ashok Kumar Narsani, Shafi Jatoi, Mahtab Alam Khanzda. Re-currence of pterygium with conjunctival autograft verses mito-mycin C. Pak J Ophthalmol 2008. Vol.24 no.1.

21. Rao SK, Lekha T, Mukesh BN, Sitalakshmi G, Padmanabhan P, Conjunctival – Limbal Autograft for primary and recurrent Pterygia: Techniques and results. Indian J Ophthalmol 1998: 46:203-9.

A 7 year old girl complained of decreased vision, 20/40 in the right eye and normal in the left eye. Examination revealed Y-shaped lenticular opacities diagnostic of a sutural cataract. The opacities followed the anterior and posterior Y sutures of the lens, with the anterior suture having the shape of an upright Y and the posterior suture having the shape of an inverted Y. Sutural cataracts are congenital lens opacities that affect the Y sutures of the nucleus of the fetal lens. The sutural cataracts do not progress. Since the effects on vision are minimal. Eyeglasses were prescribed for such patients, with marginal improvement of the vision. Newsnet Online


ORIGINAL ARTICLE

Amin Shaikh

INTRODUCTION Diabetes mellitus is a global epidemic and has crisis proportion in Pakistan.1,2 The international diabe-tes federation (IDF) estimated in 2011 that 366 million adults, aged 20-79 years, of the worlds 7 billion popula-tion have diabetes.3 A recent survey shows that about 8.8 million people are suffering from diabetes in Pakistan and this number is estimated to be doubled in the year 2025.4 Studies performed by Afgani5 and Kayani et al.6

suggest the prevalence of diabetes retinopathy between 22.29% and 33.3 % in Pakistani diabetics. According to the us census bureau, international data base 2004 the extrapolated incidence (The number of new cases diag-nosed each year) of diabetic retinopathy in Pakistan in 38,043.7 Proliferative diabetic retinopathy is the leading cause of blindness among diabetic population and in Pakistan ranked sixth position among treatable causes of blindness8 There are different treatment modalities to deal with proliferative diabetic retinopathy. Early treat-ment diabetes retinopathy study group recommends

pan retinal photocoagulation. In this observational study we document the outcomes and complications of pan retinal photocoagulation (PRP) diabetic patients having proliferative diabetic retinopathy (PRP). PATIENTS AND METHODS This observational study was conducted at De-partment of Ophthalmology Chandka Medical College SMBBMU Larkana From March 2011 to February 2013. Three hundred and sixty one eyes of two hundred thirty two patients fulfilled the inclusion and exclusion crite-ria. Which included proliferative diabetic retinopathy, visual acuity 6/12 or better, age over 30 years and be-low 90 years. Clear media without clinically significant macular edema or other posterior segment pathologies and no history of previous photocoagulation or uncon-trolled glaucoma. All the patients signed an informed consent written in local language. Socio-demographic data: It was entered on the prescribed form including age, gender, address, con-tact number, occupation and level of education. Prior to treatment each patient underwent a full ophthalmic as-sessment which included slit-lamp Biomicroscopy and binocular indirect Ophthalmoscopy. Selected patients were subjected to fluorescien angiography and fundus color photography prior to laser treatment. The patients were treated through a maximally dilated pupil with a PRP lens. The Goldmann three

Muhammad Amin Shaikh DOMS, MSc, MS1, Prof. Syed Imtiaz Ali Shah, FCPS2 Altaf Hussain Sheikh DLO, MS3, Khalid Rasul Shaikh MBBS4, Amanullah Shaikh MBBS, DCH5

ABSTRACTObjective: In this observational study we document the outcomes and complications of pan retinal photocoagulation in diabetic patients having proliferative diabetic retinopathy.Material and Methods: This observational study was conducted at Department of Ophthalmology, Chandka Medical Col-lege SMBBMU Larkana from March 2011 to February 2013. Three hundred and sixty one eyes of two hundred thirty two patients were treated in three sessions. Follow up was planned at one week, one month and three months and then yearly for two years and all the complications were documented. Visual acuity and retinal examination was performed at each fol-low up and any complication was documented. Data was entered on SPSS version 16 for windows and analyzed. Results: Three hundred and sixty one eyes of two hundred and thirty two patients under went pan-retinal photocoagulation. There were 126 (54.4%) females and 106 (45.6) males with a mean age of 62.07 years (SD=8.15). Mean laser shots applied were 3200 with a minimum of 2700 to a maximum of 3800 and an average power of 360 mv (SD=55.63) intra-operative complications occurred in 183 patients. Long term complications included, progression of diabetic retinopathy after a period of complete resolution of new vessels, vitreous hemorrhage, Tractional retinal detachment, progression of cataract, macular edema. Pre-macular fibrosis and macular hemorrhage. At last follow up visual acuity improved in 143 eyes, deteriorated in 183 and remained unchanged in 35 eyes.Conclusion: Pan retinal photocoagulation is a safe and effective procedure. A close follow up is needed after this procedure to avoid long term complications and to treat them as soon as possible.Key word: Laser, pan-retinal photocoagulation, diabetic retinopathy.

1Assistant Professor, Department of Ophthalmology, 2Professor of Ophthalmology, Chandka Medical College Hospital Larkana, 3Associ-ate Prof. ENT, 4Department of Anatomy, 5Department of Paediatrics

Correspondence: Dr. Muhammad Amin Shaikh, Assistant Professor Department of Ophthalmology, Chandka Medical College Hospital Larkana. Email: [email protected]

Received: October 2014 Accepted: November2014

Outcome and Complications after Pan-Retinal Laser Photocoagulation for Proliferative Diabetic Retinopathy:

An Experience at CMC Hospital Larkana

Outcome and Complications after Pan-Retinal Laser Photocoagulation for Proliferative Diabetic Retinopathy


mirror lens was also used if only partial treatment was obtained with a PRP lens. The patients were treated in three treatment sessions at an interval on one week with topical anesthesia (proparacaine). Two thousand and five hundred burns were applied to each eye, of spot size 500 micron and duration 0.1 second. The pow-er was adjusted to produce just noticeable immediate blanching of the retinal pigment epithelium. No addi-tional laser treatment was given during the six weeks period. Additional laser burns were considered after six weeks period if the treatment seemed insufficient. After completion of pan-retinal photocoagulation. Fol-low up was planned at one week, one month, three months and then yearly for two years. Visual acuity and retinal examination was performed at each follow up and any complication was documented. Data was entered on SPSS version 16 for windows. All categorical variables were presented as fre-quencies and percentages in the form of frequency tables, mean, standard deviation and range was meas-ured for all continuous variables.RESULT Three hundred and sixty one eyes of two hundred thirty two patients underwent pan retinal photocoagu-lation from March 2011 to February 2013 at Department of Ophthalmology Chandka Medical College SMBBMU Larkana. Three hundred and sixty one eyes of two hundred thirty two patients are present for analysis. These patients had a follow up of at least two years af-ter which they were censored from the study. There were 126 (54.4%) females and 106 (45.6%) males with a mean age of 62.07 years (SD=8.15). Du-ration of diabetes mellitus ranged from 11 years to 35 years. NVD (new vessels on the disc) were found in 245 eyes. NVE (new vessels elsewhere) in 61 eyes and both in 55 eyes. Visual acuity range was 6/12 in 124 patients 6/9 in 86 and 6/12 in 151 patients. Mean laser shots applied were 3200 with a mini-mum of 2700 to a maximum of 3800 and an average power of 360 MV (SD=55.63) intra-operative complica-tions occurred in 183 patients that include server pain requiring retro bulbar anesthesia in 18 patients and vit-reous hemorrhage in 03 patients. Post laser complica-tions with in first four weeks occurred in 179 patients that included in table no. 1 no regression of new blood vessels was observed in 16 cases for which additional burns were applied. Long term complications includ-ed. Progression of diabetic retinopathy after a period of complete resolution of new vessel. Vitreous hem-orrhage, tractional retinal detachment, progression of cataract, macular edema, pre macular fibrosis and mac-ular hemorrhage (Table II) at last follow up visual acu-

ity improved in 147 eyes deteriorated in 183 and was unchanged in 31 eyes.

Table No-1

Complications Frequency Percent

1. Blurred vision 24 6.6

2. Punctate corneal erosion 14 3.9

3. Clinically significant macular edema 57 15.8

4. Defective night vision 84 23.2

Table No-2

Complications Frequency Percent1. Recurrence of proliferative diabetic

retinopathy 43 11.7

2. Vitreous hemorrhage 12 3.2

3. Tractional retinal detachment 08 2.2

4. Progression of cataract 64 17.5

5. Macular edema 38 10.4

6. Pre-macular fibrosi 21 5.7

7. Macular hemorrhage 07 1.9

DISSCUSSION In this 232 patients, complications after PRP are documented. We will discuss only the long term com-plications by Dubey et al9 1380 eyes were treated for proliferative diabetic retinopathy and followed for 4 years long term complications requiring surgical inter-ventions developed in 23% cases. This might be due to the fact that we performed PRP in three sessions and our follow up is shorter. In a recent study by Aimee et al10 Recurrence or persistence of new vessels was observed in 34% cases after a follow up of six months. Macular edema after PRP has an inci-dence of 34% in patients with prior normal macula. When documented by OCT.11 But clinically signifi-cant macular edema in our series was present in only in 15.8 percent eyes. Another study by MC Donald and Schatz reported macular edema in 43 percent eye as ev-idenced by Fluorescein angiography.12 A recent study shows that macular edema did not develop in any eye after pan retinal photocoagulation. In this study author performed pan retinal photocoagulation in four session and patients included in the study were free of macular edema before photocoagulation.13 In our study macular edema, after pan retinal photocoagulation developed only in 15.8 percent eyes. It might be due to the fact that we have performed the procedure in three session and the patients included in the study had no or minimal macular edema before photocoagulation. The incidence of vitreous hemorrhage after PRP as reported by Kaiser et al is in 37 percent eyes14 In our study vitreous hemor-rhage occurred only in 3.2 percent eye after a period

Outcome and Complications after Pan-Retinal Laser Photocoagulation for Proliferative Diabetic Retinopathy


of quiescent stage. This lower incidence was due to the fact that we included in our study only those patients who had no previous vitreous hemorrhage and were in an initial stage of diabetic retinopathy. Additionally, we performed a complete PRP with a larger number of laser shots. Retinal detachment as reported by Kaiser14 is in 4 percent cases while in our study it is 2.2 percent this might be due to the facts already described.CONCLUSION Pan retinal photocoagulation is a safe and effective procedure. A close follow up is needed after this pro-cedure to avoid long term complications and to treat them as soon as possible.REFERENCE 1. Diabetes: a global epidemic. Pakistan observer. Friday, January

04, 20http://pakobserver.net/detailnews.asp?Id=124865 13 Monday, November 14, 2011.

2. LAM DW, LEROITH D. THE WORLWIDE DIABETES EPI-DEMIC. CURR OPIN ENDOCRINOL DIABETES OBES. 2012 Apr; 19(2): 93-6 doi: 10.1097/ med. Ob013e328350583a.

3. IDF Diabetes Atlas. Fifth Edition 2011.4. Zarina M. treating patients in a tertiary care centre in a devel-

oping country diabetes reviews international. 1994; 3(2): 2-4.5. Afghani T, Qureshi N, Chaudhry KS. Screening for diabetic

retinopathy a comparative study between hospital and com-munity based screening and between paying and non-paying patients. J Ayub Med Coll Abbottabad 2007, 19(1): 16-22.

6. Kayani H, REhan N, Ullah N. Frequency of retinopathy among diabetics admitted in a teaching hospital of Lahore. J Ayub Med Coll Abbottabad 2003, 15(4): 53-57.

7. US census Burea. International data base. 2004.8. Dineen B, Bourne RRA, k Jadoon Z, Shah SP, Khan MA, Fos-

ter A, Gilbert CE, Khan MD. Causes of Blindness and visual impairment in Pakistan. The Pakistan national blindness and visual impairment survey. Br J Ophthalmol.

9. Dubey AK, Nagpal P, Chawla S, Dubey B. A proposed new classification for diabetic retinopathy: the concept of primary and secondary vitreopathy. Indian J Ophthalmol. 2008; 56:23-9.

10. ** Aimee V. Chappelow AV, Tan K, Waheed NK, Kaiser PK. Panretinal photocoagulation for proliferative diabetic retinopa-thy: Pattern Scan laser versus Argon Laser. American Journal of Ophthalmology 2012; 153:137-142.

11. Authors: Soman M, Ganekal S, Nair U, Nair KGR. Effect of pan-retinal photocoagulation on macular morphology and thick-ness in eye with proliferative diabetic retinopathy without clin-ically significant macular edema. Clinical ophthalmology 2012; 6:2013-2017. DOI: http://dx.doi.org/10.2147/OPTH.S37340.

12. McDonald HR, Schatz H. Macular edema following panretinal photocoagulation. Retina (Philadelphia, Pa.) [1985, 5(1):5-10.].

13. Takahashi A, Nagaoka T, Sato E, Yoshida A. Effect of panreti-nal photocoagulation on choridal circulation in the foveal re-gion in patients with severe diabetic retinopathy. Br J Ophtha mol 2008; 92:1369-1373 doi: 10.1136/ bjo.2007.136028.

14. Kaiser RS, Maguire MG, Grunwald JE, Lieb D, Jani B, Brucker AJ, Maguire AM, HO AC, Fine SL. One Year Outcomes of pan-retinal photocoagulation in proliferative diabetic retinopathy. Am J Ophthalmol. 2000; 129(2): 178-85.

Tinea CircinataCurtesy: Kimberly A. Rovansek, M.D. Anthony Papadopolous, M.D.A 46-year-old woman with a history of (HIV) infection had a painful rash on the pre-tibial surface of the leg. The patient reported having been scratched by a cat in the same area three weeks earlier. A violaceous plaque that measured 9 cm by 9 cm and consisted of four concentric rings with intervening areas of normal skin with numerous yellow-white pustules at the periphery of the rings and there was fine scaling of the skin. The CD4 cell count was 365 per cmm, the HIV load was undetectable. The patient had not received any antiretroviral therapy and was treated with oral amoxicillin–500 mg twice daily for 14 days with no noticeable improvement. A skin-scraping specimen prepared with potassium hydroxide was evaluated microscopically and found to contain multiple hyphae. A diagnosis of tinea circinata was made. Tinea circinata, is an uncommon morphologic variant of tinea corporis, is caused by the dermatophyte Trichophyton tonsurans.

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ORIGINAL ARTICLE

Prof. Marianne

INTRODUCTION Vascular endothelial growth factor (VEGF) plays an important role in the patho-physiology of several sight-threatening retinal disorders such as age-related macular degeneration, retinal vein occlusion, diabetic macular edema and proliferative diabetic retinopathy. The discovery of anti-VEGF agents has revolutionized the treatment of these conditions. The term anti-angiogenic therapy was born more than 35 years ago by J. Folkman, who hypothesized that cancer may be treated by abolishing the nutrients and oxygen-providing blood vessels1 by agents that could block the angiogenic cascade. Monoclonal antibodies against Vascular Endothelial Growth Factor (VEGF) were first developed as an intravenous treatment for metastatic colorectal cancer.2, 3

Consequently, several antiangiogenics have been developed for the treatment of sight-threatening retinal diseases , including neovascular age-related macular degeneration, retinal vein occlusions and diabetic mac-ular edema in diabetic retinopathy and ophthalmology has witnessed an explosion in the number of intravitre-al injections delivered to patients over the past 10 years, driven in large part by the introduction and rapid in-corporation of therapy with anti-VEGF agents. Taking into consideration that these patients may present with a different spectrum of underlying diseas-es and potentially higher risk profiles, systemic safety data across multiple anti-angiogenic agents should be analyzed critically. The rising popularity of anti-VEGF

drugs came along with concerns about its safety in clin-ical use. Anti-VEGF agents given intraocularly spread into the systemic circulation and have the potential to cause systemic adverse effects. The objective of this re-view is to evaluate the general impact of ocular phar-macotherapy by vascular endothelial growth factor inhibitors in retinal disorders based on currently avail-able data of the clinical trials. There are 4 anti-VEGF agents that are either ap-proved or in common use in ophthalmology, namely Pegaptanib (Macugen, Pfizer), Ranibizumab (Lucentis, Novartis), Aflibercept or VEGF Trap-Eye (EYLEA, Bay-er) and Bevacizumab (Avastin, Roche). Pegaptanib is a selective VEGF inhibitor, targeting only one isoform of the VEGF molecule, leaving other isoforms unaffected.4 In 2004, pegaptanib (Macugen ( Pfizer and OSI/Eyetech Pharmaceuticals, Inc.) was the first anti-VEGF agent to receive FDA approval for the treatment of neovascular age-related macular degener-ation (AMD). The use of pegaptanib has declined with the release of newer anti-VEGF agents, such as ranibi-zumab (Lucentis™, Genentech, Inc., South San Francis-co, CA, and Novartis Pharma AG, Basel, Switzerland), aflibercept (VEGF-trap eye, Eylea™, Regeneron Phar-maceuticals, Inc., and Bayer Pharma AG, Berlin, Ger-many) and bevacizumab (Avastin™, Genentech, Inc., South San Francisco, CA, and Roche, Basel, Switzer-land). Ranibizumab (Lucentis™; Genentech, South San Francisco, CA, USA) is a humanised antigen binding fragment of a murine full length monoclonal antibody directed against human vascular endothelial growth factor - VEGF A. Ranibizumab binds all active isoforms

Prof. Marianne Shahsuvaryan, D.Sc, Ph.DProf. of Ophthalmology, Yerevan State Medical University, 7 Ap,

26 Sayat-Nova Avenu Yerevan, 0001, Republic of Armenia

ABSTRACTBackground: Vascular endothelial growth factor (VEGF) plays an important role in the pathophysiology of several sight-threatening retinal disorders such as age-related macular degeneration, retinal vein occlusion, diabetic macular edema and proliferative diabetic retinopathy. The discovery of anti-VEGF agents has revolutionized the treatment of these conditions. There are 4 antiangiogenics that are either approved or in common use in ophthalmology, namely pegaptanib (Macu-gen, Pfizer), ranibizumab (Lucentis, Novartis), aflibercept or VEGF Trap-Eye (EYLEA, Bayer) and bevacizumab (Avastin, Roche). Ophthalmology has witnessed an explosion in the number of intravitreal injections delivered to patients over the past 10 years, driven in large part by the introduction and rapid incorporation of therapy with anti-VEGF agents. However, there is some evidence that intravitreal antiangiogenics injections may result in systemic absorption, with the potential for injury in organs that are reliant on VEGF. In this review an attempt is made to explain currently available data of the clinical trials based on their general impact and systemic safety concerns.Keywords: antiangiogenic agents, pegaptanib sodium, ranibizumab, aflibercept intravitreal injections, general impact

Correspondence: E-mail: [email protected]


General Impact of Ocular Antiangiogenic Therapy



of VEGF-A and is thus considered a non-selective VEGF-A inhibitor.5

Aflibercept or VEGF Trap-Eye (EYLEA, Bayer) is a fully human fusion protein, consisting of soluble VEGF receptors 1 and 2, that binds all forms of VEGF-A along with the related Placental Growth Factor (PlGF). VEGF Trap-Eye is a specific and highly potent blocker of these growth factors. Aflibercept acts as a decoy receptor binding-free VEGF.6

Bevacizumab (Avastin, Roche), is a full-length, humanized monoclonal antibody directed against all the biologically active isoforms of vascular endothelial growth factor (VEGF)–A. Bevacizumab binds to the receptor-binding domain of all VEGF-A isoforms.7 Bev-acizumab is FDA-approved for the treatment of colo-rectal cancer. However, because the agent costs sub-stantially less per dose than ranibizumab, it has been widely used off-label since 2004 to treat several retinal diseases. Systemic Effects of Antiangiogenic Therapy: In-traocular injections of anti-angiogenic agents could cause the cardiovascular effects (thrombosis, hemor-rhage, hypertension, proteinuria), as well as the less frequent cerebrovascular accidents, myocardial infarc-tion, transient ischemic attacks, deep vein thrombosis, pulmonary embolism, thrombophlebitis.8,9 Singerman et al.4 in two double-masked randomized studies eval-uated the safety of up to 3 years of pegaptanib sodi-um therapy in the treatment of neovascular AMD and concluded that serious adverse events were rare. The authors found no findings in relation to vital signs or electrocardiogram results suggesting a relationship to pegaptanib treatment. Results of other randomized tri-al10 of pegaptanib sodium for macular edema second-ary to branch retinal vein occlusion (BRVO) revealed a trend towards a higher risk of stroke among patients with a history of heart disease. Pegaptanib (Macugen) is associated with a lower risk of stroke than either Lucentis or Avastin.11 The most probable reason for this finding relates to selective binding just one strain of VEGF. Campbell et al.12 assessing the risk of systemic adverse events associated with intravitreal injections of vascu-lar endothelial growth factor inhibiting drugs in the nested case-control study have found that intravitreal injections of bevacizumab and ranibizumab were not associated with significant risks of ischaemic stroke, acute myocardial infarction, congestive heart failure, or venous thrombo-embolism. The International Intravitreal Bevacizumab Safety Survey gathered adverse events from doctors around the world via the internet13 and showed all ocular and systemic side effects to be under 0.21% including dif-

ferent ocular abnormalities and also blood pressure elevation, transient ischaemic attack, cerebrovascular accident and death. Fung. et al.13 concluded that self-reporting of adverse events after intravitreal beva-cizumab injections did not show an increased rate of potential drug-related ocular or systemic events and these short-term results suggest that intravitreal beva-cizumab seems to be safe. The reliance on self reported information on bev-acizumab use represents a potential limitation of this study. On the other hand, findings reviewed in 2006 were insufficient to evaluate the systemic safety of bev-acizumab. More data are becoming available on this agent. It is recognized that the widespread off-label use of bevacizumab, because of its relative inexpensiveness compared to ranibizumab, raises concerns, particularly when systematic reviews of clinical trials comparing the clinical effectiveness of the two drugs14 suggesting increased frequency of systemic serious adverse events (SAE )15,16 and representing a disadvantage of bevaci-zumab. The results from pooled analysis of two large comparative effectiveness trials for neovascular age-related macular degeneration17-20 suggest that systemic serious side effects (SAEs) were more common in the bevacizumab-treated patients, despite the fact that the risk of death or arteriothrombolic events (ATEs) was similar between the drugs. Few studies are focused on safety profiles of ra-nibizumab in retinal vein occlusion. Clinical evaluation of ranibizumab based on two double-blind randomised trials comparing ranibizumab versus placebo in a total of 795 patients revealed that the incidence of heart fail-ure and transient ischaemic attacks was higher during the second year of ranibizumab therapy than during the first year of treatment.21 For central retinal vein oc-clusion – CRUISE study22 it has been demonstrated that death from unknown cause was found in 0.8%, myocar-dial infarction 0.8%, cerebrovascular events in the 2.4% in ranibizumab group. An incidence of non-ocular seri-ous adverse events for patients suffered from branch retinal vein occlusion and treated by ranibizumab –BRAVO study23 was equal to 9.1%, non-ocular hemor-rhage was reported in 2.3%. Pielen et al.24 conducted a systematic review on this matter and concluded that in general, the incidence of systemic adverse events and rates of death (0-3%) were low and did not significant-ly differ between treatment groups in the multicenter trials.22,23,25,26 In authors opinion24 it is likely that infor-mation on ocular and systemic adverse events varied between trials due to very detailed reporting within most multicenter trials (including additional informa-tion available as online supplements) and, on the other hand, the overall notification of “no ocular and system-



ic adverse events” in a single-center trial. Individuals presenting with considerable systemic diseases in their recent past medical history are most often excluded. Certainly, in all trials numbers of participants are still too low to be calculated to detect small differences in rare systemic events. Dubey et al.27 proved that non-ocular adverse event profile of ranibizumab in patients with diabetic macular edema (DME) is similar to that observed in patients with neovascular age-related mac-ular degeneration or retinal vein occlusion. There is some evidence that intraocular anti-VEGF injections due to systemic absorption may result in injury in organs that are reliant on VEGF, such as the kidney. Pellé et al.28 reported the first case of a patient who developed an acute decrease in kidney function, non-immune microangiopathic hemolytic anemia with schistocytes, and thrombocytopenia after 4 intravitreal injections of ranibizumab. Light microscopy of a kid-ney biopsy specimen showed segmental duplications of glomerular basement membranes with endothelial swelling and several recanalized arteriolar thrombi. Early detection is crucial so that intravitreal injections can be stopped before severe kidney disease occurs. In Sorenson and Sheibani29 opinion perhaps baseline and renal function during treatment (serum creatinine and urinary protein levels, blood pressure) should be care-fully monitored to ensure that the improved visual acuity is not at the expense of renal function. A recent meta-analysis asseccing the non-ocular serious adverse events potentially related to anti-VEGF agents in retinal vein occlusion indicated rare the Antiplatelet Trialists’ Collaboration Arterial Thrombo-embolic Events (APTC ATEs) including myocardial infarction, ischemic stroke, vascular deaths.30 Avery31 evidenced that analysis of large populations will be critical to identify if there is a systemic risk to intravitreal agents, as individual trials are not powered to detect differences in uncom-mon events. There may be subsets of patients, such as patients with diabetes, the elderly or those with recent ATEs such as stroke, who may be at increased risk after intraocular anti-VEGF injection. The latest approved agent is aflibercept. Its greater VEGF binding affinity (140 times that of ranibizumab) coupled with larger molecular size (twice that of ranibi-zumab) and a longer duration of action may allow for a less-frequent dosing schedule than with either bevaci-zumab or ranibizumab with good efficacy.27,32 Concerns have also arisen regarding the safety of aflibercept. It could cause non-ocular haemorrhages and arterial thromboembolic events.33,34 Only recently, aflibercept has been investigated in patients with CRVO in the COPERNICUS (Controlled Phase 3 Evaluation of Re-peated Intravitreal Administration of VEGF Trap-Eye

in Central Retinal Vein Occlusion: Utility and Safety) trial [26]. According to the results of this trial no deaths were reported in the aflibercept 2 mg group during the first 12 months. However, 2 deaths (2.7%) occurred in the sham/aflibercept group. Both deaths had a vascular cause (myocardial infarction and cardiac arrhythmia). Non-lethal myocardial infarction was documented in 1 patient of each group (0.9% and 1.7%). The results from the most recent trial on afliber-cept in age-related macular degeneration35 suggest that although adverse events were carefully noted, there is always a possibility that some systemic effect may not have been captured in this retrospective study. Further clinical trials and comparative studies with aflibercep are needed to establish the systemic safety profile of this agent. Dr. Chakravarthy presented her approach for treating patients with a history of stroke, the patients with diabetes at the annual meeting of the American Academy of Ophthalmology.36 In these cases she would treat with ranibizumab, although she has reservations about long-term therapy in this population due to addi-tional potential systemic risk factors and comorbidities. The latest available data still left the unanswered ques-tions is whether or not there is a difference in the safety profile among the drugs, and how a long-term regimen may impact that profile.36

In summary, almost uniformly all trial evaluating systemic safety of anti-angiogenic agents reveal the se-rious side effects including cardiovascular events, de-spite the fact that the incidence is low. The most probable reason for incidence rate relates to the absence of stratified analysis by age myocardial infarction , stroke risk. Sys-temic safety concern in intraocular pharmacotherapy by anti-angiogenic agents has a strong body of clinical evidence, resulting in plenty of peer reviewed clinical articles.CONCLUSION Several anti-angiogenic agents are being widely used for the treatment of eye diseases like neovascu-lar macular degeneration, retinal vein occlusion and diabetic macular edema. Taking into consideration that these patients may present with a different spectrum of underlying diseases and potentially higher risk pro-files, systemic safety data across multiple anti-angio-genic agents have analyzed critically. Currently available findings obviate the need to raise awareness about cardiovascular risk profile in patients with eye diseases treated by anti-VEGF. Early detection is crucial so that intraocular injections can be stopped before severe accident occurs. REFERENCES:1. Stewart MW.The expanding role of vascular endothelial

growth factor inhibitors in ophthalmology. Mayo Clinic Pro-ceedings , January 1, 2012



2. Homsi J, Daud AI. Spectrum of activity and mechanism of action of VEGF/PDGF inhibitors. Cancer Control. 2007;14(3), 285–294 .

3. Los M, Roodhart JM, Voest EE. Target practice: lessons from Phase III trials with bevacizumab and vatalanib in the treatment of advanced colorectal cancer. Oncologist 2007;12(4), 443–450 .

4. Singerman LJ, Masonson H, Patel M, Adamis AP, Buggage R, Cunningham E, et al. Pegaptanib sodium for neovascular age-related macular degeneration: third-year safety results of the VEGF Inhibition Study in Ocular Neovascularisation (VISION) trial. Br J Ophthalmol. 2008 Dec;92(12):1606-11. doi: 10.1136/bjo.2007.132597. Epub 2008 Jul 9.

5. Rosenfeld PJ, Schwartz SD, Blumenkranz MS, Miller JW, Haller JA, Reimann JD. Maximum tolerated dose of a humanized anti-vascular endothelial growth factor antibody fragment for treat-ing neovascular age-related macular degeneration. Ophthalmol-ogy 2005; 112: 1048–62.

6. Pieramici DJ, Rabena MD. Anti-VEGF therapy: comparison of current and future agents. Eye 2008;22;1330–1336

7. Ferrara N, Hillan KJ, Nowotny W. Bevacizumab (Avastin), a humanized anti-VEGF monoclonal antibody for cancer therapy. Biochem Biophys Res Commun. 2005;333:328–35.

8. Semeraro F, Morescalchi F, Parmeggiani F, Arcidiacono B, Cos-tagliola C. Systemic adverse drug reactions secondary to anti-VEGF intravitreal injection in patients with neovascular age-re-lated macular degeneration. Curr Vasc Pharmacol 2011; 9:629-46.

9. Costagliola C, Agnifili L, Arcidiacono B, Duse S, Fasanella V, Mastropasqua R, et al. Systemic thromboembolic adverse events in patients treated with intravitreal anti-VEGF drugs for neovas-cular age-related macular degeneration. Expert Opin Biol Ther. 2012 Oct;12(10):1299-313. doi: 10.1517/14712598.2012.707176. Epub 2012 Aug 7.

10. Wroblewski JJ, Wells JA 3rd, Gonzales CR. Pegaptanib sodium for macular edema secondary to branch retinal vein occlusion. Am J Ophthalmol. 2010;149:147–154.

11. Tolentino M. Systemic and ocular safety of intravitreal anti-VEGF therapies for ocular neovascular disease Surv Ophthalmol. 2011;56(2):95-113.

12. Campbell RJ, Gill SS, E Bronskill SE, Paterson JM, Whitehead M, Bell CM. Adverse events with intravitreal injection of vascular endothelial growth factor inhibitors: nested case-control study. BMJ 2012;345:e4203

13. Fung AE, Rosenfeld PJ, Reichel E. The International Intravitreal Bevacizumab Safety Survey: using the internet to assess drug safety worldwide. Br J Ophthalmol. 2006;90:1344-134.

14 . Chakravarthy U, Rogers C. Systemic Safety Of Intravitreal VEGF Inhibitors.What concerns remain? Retinal Physician, 2014 Jan, Vol. 11, p.41 – 5.

15. Lanzetta P, Mitchell P, Wolf S, Veritti D. Different antivascular endothelial growth factor treatments and regimens and their out-comes in neovascular age-related macular degeneration; a litera-ture review. Br J Ophthalmol. 2013;97:1497-1507.

16. Schmucker C, Ehlken C, Agostini H, Anges G, Ruecker G, Lel-gemann M, et al. A safety review and meta analysis of bevaci-zumab and ranibizumab: off label versus gold standard. PLoS One. 2012;7:e4270

17. Chakravarthy U, Harding SP, Rogers CA, Downes SM, Lotery AJ, Wordsworth S et al. Ranibizumab versus bevacizumab to treat neovascular age-related macular degeneration: one-year findings from the IVAN randomized trial. Ophthalmology. 2012;119:1399-1411.

18. Chakravarthy U, Harding SP, Rogers CA, Downes SM, Lotery AJ, Wordsworth S et al; IVAN study investigators. Alternative treatments to inhibit VEGF in age-related choroidal neovascular-isation: 2-year findings of the IVAN randomised controlled trial. Lancet. 2013;382:1258-67.

19. CATT Research Group; Martin DF, Maguire MG, Ying GS, Grun-wald JE, Fine SL, Jaffe GJ.et al. Ranibizumab and bevacizumab for neovascular age-related macular degeneration. N Engl J Med. 2011;364:1897-1908.

20. Comparison of Age-related Macular Degeneration Treatments Trials (CATT) Research Group; Martin DF, Maguire MG, Fine SL, Ying GS, Jaffe GJ, Grunwald JE, et al. Ranibizumab and bevaci-zumab for treatment of neovascular age-related macular degen-eration: two-year results. Ophthalmology. 2012;119:1388-98.

21. Ranibizumab and retinal vein occlusion. Too many outstanding questions. Prescrire Int. 2012;21(130):207.

22. Campochiaro PA, Brown DM, Awh CC, Lee SY, Gray S , Saroj N, et al. Sustained benefits from ranibizumab for macular ede-ma following central retinal vein occlusion: twelve-month out-comes of a phase III study. Ophthalmology 2011;118: 2041–2049. doi:10.1016/j.ophtha.2011.02.038. PubMed: 21715011.

23. Brown DM, Campochiaro PA, Bhisitkul RB, Ho AC, Gray S, Sa-roj N et al. Sustained benefits from ranibizumab for macular edema following branch retinal vein occlusion: 12-month out-comes of a phase III study. Ophthalmology 2011; 118: 1594–1602. doi:10.1016/j.ophtha.2011.02.022. PubMed: 21684606

24. Pielen A, Feltgen N, Isserstedt C, Callizo J, Junker B, Schmucker C ,et al. Efficacy and Safety of Intravitreal Therapy in Macular Edema Due to Branch and Central Retinal Vein Occlusion: a Sys-tematic Review. 2013 PLoS ONE 8(10): e78538. doi:10.1371/jour-nal.pone.0078538

25. Heier JS, Campochiaro PA, Yau L, Li Z, Saroj N, Rubio RG, et al. Ranibizumab for macular edema due to retinal vein occlusions: long-term follow-up in the HORIZON trial. Ophthalmology 2012;119: 802–809. doi:10.1016/j.ophtha.2011.12.005. PubMed: 22301066

26. Brown DM, Heier JS, Clark WL, Boyer DS, Vitti R , Berliner AJ, et al. Intravitreal Aflibercept Injection for Macular Edema Sec-ondary to Central Retinal Vein Occlusion: 1-Year Results From the Phase 3 COPERNICUS Study. Am J Ophthalmol. 2013; 155: 429–437. e7 doi:10.1016/j.ajo.2012.09.026. PubMed: 23218699.

27 Dubey, Ashok K., N. R. Biswas, G. K. Das. “Vascular Endothe-lial Growth Factors: Pharmacological aspects and applications in ophthalmic practices.” The Official Scientific Journal of Delhi Ophthalmological Society 2013;24 (2): 88-92.

28. Pellé G, Shweke N, Duong Van Huyen JP, Tricot L, Hessaïne S, Frémeaux-Bacchi V, et al. Systemic and kidney toxicity of in-traocular administration of vascular endothelial growth factor inhibitors. Am J Kidney Dis 2011.;57(5):756-9.

29. Sorenson CM, Sheibani N. Anti–Vascular Endothelial Growth Fac-tor Therapy and Renal Thrombotic Microangiopathy . Arch Oph-thalmol 2011.;129(8):1082. doi:10.1001/archophthalmol.2011.199.

30. Huang P, Niu W, Ni Z, Wang R, Sun X . A Meta-Analysis of Anti-Vascular Endothelial Growth Factor Remedy for Macular Edema Secondary to Central Retinal Vein Occlusion. PLoS ONE 2013; 8(12): e82454. doi:10.1371/journal.pone.0082454.

31. Avery RL. What is the evidence for systemic effects of intravit-real anti-VEGF agents, and should we be concerned? Br J Oph-thalmol 2014;98:i7-i10 doi:10.1136/bjophthalmol-2013-303844

32. Moradi A, Sepah YJ, Sadiq MA, Nasir H, Kherani S, Sophie R et al. Vascular endothelial growth factor trap-eye (Aflibercept) for the management of diabetic macular edema. World J Diabetes 2013 Dec. 15; 4(6): 303-9

33. EYLEA (aflibercept solution for injection) Summary of Product Characteristics. Berlin, Germany: Bayer Pharma AG; 2013.

34. Heier JS, Brown DM, Chong V, Korobeinic J, Kaiser PK, Nguen QD, et al. VIEW 1 and VIEW 2 Study Groups. Intravitreal afliber-cept (VEGF Trap-Eye) in wet age-related macular degeneration. Ophthalmology. 2012;119(12):2537-2548, appendices 1-8. http://www.aaojournal.org/article/S0161-6420(12)00865-2. Accessed December 3, 2012

35. Ferrone PJ, Anwar F, Naysan J,Chaudhary K, Fastenberg D, Gra-ham K. Early initial clinical experience with intravitreal afliber-cept for wet age-related macular degeneration. Br J Ophthalmol 2014;98:i17-i21 doi:10.1136/bjophthalmol-2013-304474

36. Chakravarthy U. Long-term safety of anti-VEGF therapy. Pa-per presented at October 20,2014; Chicago, USA.


ORIGINAL ARTICLE

Syed Dil Bagh Ali

INTRODUCTION The club foot or congenital talipes equinovarus (CTEV) is a complex foot deformity comprises of fore-foot adduction, midfoot cavus and hind foot equinus.1 It is one of the complex and most common congenital deformities. Its incidence is about 1 to 2 per 1,000 live births.2 The objective of the treatment is to achieve a pain free, pliable, plantigrade, functionally and cosmet-ically acceptable foot within the minimum time dura-tion with the least interruption of the socioeconomical life of the parent and child.1,3

The initial treatment of the clubfoot should be non-operative regardless of the severity of the deformity. If there is no improvement, then postero-medial release (PMR) of the soft tissues is indicated. However, disad-vantages of PMR are high complication and recurrence (13-50%) rate and the difficulty of treating recurrenc-es.4 But extensive surgery is not the right approach to the management of CTEV.5 Over the last two decades, Ponseti casting technique has become a gold standard worldwide for the correction of CTEV. It includes serial corrective manipulations, serial application of plaster

casts supported by limited operative intervention (per-cutaneous Achilles tenotomy). Success rate of Ponseti method approaches to 90- 96% in short, mid and long-term results.5-10

The Ponseti technique of CTEV management is effective, produces better results and fewer complica-tions than traditional surgical methods.11 Ponseti cast-ing technique has shown promising results and most of the club feet can be treated with it rather than sur-gery.12 This technique is particularly important in coun-tries, where operative facilities are not available or very limited in the remote areas. The physicians and techni-cians trained in this technique can manage the cases effectively with the cast treatment only.13 The purpose of this study was to know the frequency of tenotomies in club feet treated by ponseti technique. MATERIALS AND METHODS This is a prospective observational study, con-ducted at the Khyber Teaching Hospital Peshawar. The study period was from February 2014 to Septem-ber 2014. All the neonates with CTEV presented to the orthopedic department were treated according to the Ponseti casting technique. Neonates with non-idio-pathic clubfeet i.e. CTEV associated with meningocele, meningomyelocele, arthrogryposis multiplex congen-ita and other neuromuscular causes were excluded. An informed consent was taken from all parents. All rel-evant data were collected from each participant using proformas that included patient’s demography, physi-cal examination, management, Pirani severity scoring score11 (for initial assessment of the severity, and for

Syed Dil Bagh Ali Shah MRCS (UK), FCPS Ortho1, Adnan Khan MBBS2

Syeda Umm-e-Habiba Gillani3, Prof. Zaffar Durrani FRCS Ortho4

ABSTRACTObjective: The purpose of this study is to evaluate the incidence of surgery i.e. tenotomy in Ponseti technique in the man-agement of congenital Talipes Equino Varus (CTEV). Methods: It is a prospective observational study, conducted during the period of Feb., 2014 to Sept., 2014 at the Depart-ment of Orthopedic Surgery Khyber Teaching Hospital Peshawar. All the neonates with CTEV were treated with Ponseti casting technique. Neonates with other congenital deformities, arthrogryposis and myelomeningocele were excluded.Results: Total 37 CTEV feet of 17 neonates were treated. Seventeen were males and four female. Seventeen patients had bilateral and 4 had unilateral involvement. Mean number of plaster casts required per CTEV was 6.50 (range: 6-7). 21/37 (60%) feet required percutaneous tenotomy of Achilles tendon.Conclusion: The Ponseti technique is an excellent, simple, effective, minimally invasive, and inexpensive procedure for the treatment of CTEV deformity. Ideally it can be performed as a day case procedure without general anesthesia even in neonatal period. Percutaneous tenotomy of Achilles tendon is usually needed in the patients who need more number of plasters to correct the initial deformity. Keywords: Congenital Talipes Equino-varus, Ponseti technique.

1Senior Registrar, Orthopaedics-A Ward, Khyber Teaching Hospital, Peshawar, 2Trainee Medical Officer, Orthopaedics-A Ward, Khyber Teaching Hospital, Peshawar, 3General Practitioner, 4Head of the Orthopaedic Department, Khyber Teaching Hospital, Peshawar, Khyber Medical College, Peshawar

Correspondence: Dr. Syed Dil Bagh Ali Shah, Senior Registrar Orthopaedics-A Ward, Khyber Teaching Hospital, Peshawar Cell: 0312 6914030, [email protected], [email protected]

Received: September 2014 Accepted: October 2014

Incidence of Achilles Tenotomy in Management of Congenital Equino Varus (Ctev) by Ponseti Casting

Technique in Neonates

GENERAL SECTION

Incidence of Achilles Tenotomy in Management of Congenital Equino Varus (Ctev) by Ponseti Casting Technique in Neonates


evaluation of the feet after each component of the treat-ment and ultimate final outcome), total number of the casts applied before tenotomy, pre and post procedure complications, like plaster sore, skin excoriation, blister formation, excessive bleeding following tenotomy or any other complication.Treatment protocol and follow up: This treatment in-cluded gentle manipulation of the foot and the serial application of above knee plaster casts at weekly inter-val without anesthesia, as described by Ponseti [1]. The foot was markedly abducted up to 70 degrees without pronation in the last cast, which is very important for complete correction and it prevents early recurrence. Indication of a simple percutaneous Achilles tenotomy was when heel had been corrected and residual equi-nus was observed after the abduction of the foot then a simple percutaneous Achilles tenotomy was performed under anesthesia. After the tenotomy, an additional above knee cast with knee flexed in 90 degrees was ap-plied and left in place for three weeks to allow for heal-ing of the tendon. No window was made in the cast because the tenotomy wound was very minimal. After removal of the cast, a Denis-Browne bar and boots (D-B splint) was used to prevent relapse of the deformity. For the first 3 months D-B splint was worn full time (day and night) or at least 23 hours per day and then for 12 hours at night and 2 to 4 hours at day for a total of 14 to 16 hours during each 24 hour period. The protocol continues until the child is 3 to 4 years of age. During the initial stages of treatment the patients were followed up on a weekly basis. After applying D-B splint, on a monthly basis for three months and then once every three months till the patients is three years of age. Then after three years of age, child is reviewed every six months to one year till age of 5 years and then after 1-2 years till skeletal maturity is achieved.Outcome measurement: Measured by Pirani score.11

This is the main variable of the study which can detect the degree of correction. There are 6 clinical signs : 3 for mid foot, 3 for hind foot. Three signs of mid foot score (MS) and hind foot score (HS) grading the amount of deformity between 0 and 3. The Pirani score 0 means normal foot, the Pirani score 3 means moderately ab-normal foot, the Pirani score 6 means severely abnor-mal foot. The collected data was analyzed.RESULTS During the study period a total of 37 feet in 21 chil-dren 16 bilateral and 5 unilateral treated and followed up diligently. Age ranges was from 3 days to 2 ½ years but most of them were 2 to 6 months old. There were 17 boys and 4 girls with a male female ratio of approxi-mately 4:1. 08 to 10 plasters were needed on average ,

though some of the children needed 15 to 16 but major-ity were corrected with 6 or 7 casts. 21 out of 37 feet needed Achilles tenotomy. Most of children were from poor to average socio-economic group. Mean number of plaster casts required per CTEV was higher for the rigid feet in comparison to non-rigid feet. A total of 21 (57%) feet required percutaneous tenotomy while re-maining feet were improved by plaster cast alone. None of the children suffered from any significant complica-tion, in form of skin excoriation or blister formation. DISCUSSION CTEV is a complex deformity which comprises of four components i.e. equinus, varus, adductus and ca-vus, which are quite challenging to correct. It requires meticulous technique and dedicated effort on the part of treating personnel (physician, technician) and par-ents for the correction of the deformity.13 The aim of management is to reduce or eliminate these deformities as much as possible so that patient has a pain free, plan-tigrade and functional foot with good mobility without calluses and does not need to wear special shoes.14

The Ponseti technique for the correction of CTEV deformity comprises of serial corrective casts with long term brace for maintenance of the correction. The treat-ment needs to be started soon after birth of the baby and then should be followed under close supervision [1,15]. The Ponseti CTEV corrective technique yields satis-factory anatomical and functional results with simple, effective, inexpensive, minimally invasive and ideally suited for all cultures and countries.1

The literature favors the fact that the results were better if this method of treatment is started soon after birth.8,13 CTEV results from a number of factors active from the 12th to 20th weeks of fetal life up to 3-5 years of age.15,16 Majority of the CTEV patients in our series presented in the first month of life (neonatal age).This has been the experience of other authors too13 which reflects the growing awareness of this condition in the parents nowadays. The mean number of plaster casts needed per foot in our series was 3.75, much less as compared to the other series13-18 this is probably owing to the fact that we have analyzed only neonates in the present study. Pre-treatment mean Pirani score in our series is similar to those reported previously.19 Other available studies including this study have shown that rigid feet require more casts than non-rigid feet to cor-rect the deformity. In our study, about 60% of the feet required per-cutaneous tenotomy. On the other hand percutaneous tenotomy was needed in 95% of Gupta’s patients17 and 91% of Dobbs’ patients.20 All the studies reveal that tenotomy was required in those patients who initially

Incidence of Achilles Tenotomy in Management of Congenital Equino Varus (Ctev) by Ponseti Casting Technique in Neonates


had severe deformity. Bor et al quotes, “A club foot that requires many casts for the initial correction is more likely to require future additional surgery in the form of tenotomy or other major surgeries.”7 As majority of patients in our study were neonates, and we started treatment early, so our patients needed tenotomy less frequently. Similarly, majority of pediatric orthopedic surgeons also think that success of Ponseti casting tech-nique is dependent on whether casting begins within hours of birth.20

Maintenance of bracing protocol is the most dif-ficult part of Ponseti casting technique.7 According to the parents in our study group, during the initial two or three days patients were restless and tried to remove the splint. But after that the patients were adjusted with splint. As correction of the foot also largely depends on the brace protocol21 which highlights the fact that pa-rental compliance needs to be improved by educating the parents for the proper use of bracing and the haz-ards of insufficient or improper bracing. Follow-up is another difficult part of the study. se-rial casts with or without tenotomy is only a part of the total management. Parents misunderstand the fact that the initial correction of the foot with serial casts is the main and difficult part of the treatment and hence they do not come for follow up. So, we motivated the par-ents and their family members to solve this problem. Risk of further surgical treatment becomes very high in the patients who are dropped from follow up .Simi-lar to other’s experience22 about ponseti’s technique; we found this treatment technique to be very cost-effective. CONCLUSION CTEV deformity can be effectively managed by Ponseti casting technique with excellent results and with-out significant morbidity. Tenotomy is usually required in those patients who initially have severe deformity.REFERENCES1. Ponseti IV. Clubfoot management. J Pediatr Orthop 2000;

20:699– 7002. Arif M, Inam M, Sattar A, Shabir M. Usefulness of Ponseti tech-

nique in management of congenital telipes equino-varusJ Pak Orthop Assoc 2011;23:62–4

3. Bridgens J, Kiely N (2010) Current management of clubfoot (congenital talipes equinovarus): Clinical review. British Medi-cal Journal 340: 308-312

4. Siapkara A & Duncan R (2007) Congenital talipes equinovarus: a review of current management. Journal of Bone and Joint Sur-

gery Br. 89-B (8): 995-10005. Penny, J (2005) The neglected clubfoot. Techniques in Ortho-

paedics 20 (2): 153-1666. Lourenco A, Morcuende J (2007) Correction of neglected idi-

opathic clubfoot by the Ponseti method. Journal of Bone and Joint Surgery (British) 89B (3): 378-381

7. Adegbehingbe OO, Oginni LM, Ogundele OJ, Ariyib Louren-co A, Morcuende J i AL, Abiola PO, Ojo OD. Ponseti clubfoot management: changing surgical trends in Nigeria. Iowa Or-thop J 2010; 30: 7– 14.

8. Lavy C, Mannion S, Mkandawire N, Tindall A, Steinlechner C, Chimangeni S, Chipofya E (2007) Clubfoot treatment in Ma-lawi – a public health approach. Disability and Rehabilitation 29 (11-12): 857-862

9. Lourenco A, Morcuende J (2007) Correction of neglected idi-opathic clubfoot by the Ponseti method. Journal of Bone and Joint Surgery (British) 89B (3): 378-381

10. Bor N, Coplan JA, Herzenberg JE. Ponseti treatment for idi-opathic clubfoot: minimum 5-year follow up.Clin Orthop Relat Res 2009;467:1263–1270.

11. Porecha MM, Parmar DS, Chavda HR. Mid-term r Van Bosse, H (2011) Ponseti treatment for clubfeet: an international per-spective. Current Opinion in Pediatrics 23: 41-45

12. Results of Ponseti method for the treatment of congenital idi-opathic clubfoot--(a study of 67 clubfeet with mean five year follow-up).J Orthop Surg Res 2011;6:3.

13. Agarwal RA, Suresh MS, Agarwal R. Treatment of congenital clubfoot with Ponseti methodIndian J Orthop 2005;39:244–7.

14. Dyer P J, Davis N. The role of the Pirani scoring system in the management of club foot by the Ponseti method.J Bone Joint Surg Br 2006;88:1082–1084.

15. Dietz F (2002) The genetics of idiopathic clubfoot. Clinical Or-thopaedics and Related Research 401: 39-48

16. Kushner A, Cherian M, Noel L, Spiegel D, Groth S & Etienne C (2010) Addressing the Millennium Development Goals from a surgical perspective. Archives of Surgery 145 (2): 154-160

17. Dobbs M, Gurnett C (2009) Update on clubfoot: etiology and treatment. Clinical Orthopaedics and Related Research 467: 1146-1153.

18. Morcuende JA, Dolan LA, Dietz FR, Ponseti IV. Radical reduc-tion in the rate of extensive corrective surgery for clubfoot us-ing the Ponseti method.Pediatrics 2004;113:376–380.

19. Pirani S, Hodges D & Sekeramayi F (2003) A reliable and valid method of assessing the amount of deformity in the congenital clubfoot deformity (The Canadian Orthopaedic Research So-ciety and the Canadian Orthopaedic Association conference proceeding) in The Journal of Bone and Joint Surgery 90 (B) SUPP_1, 53

20. Gupta A, Singh S, Patel P, Patel J, Varshney MK. Evaluation of the utility of the Ponseti method of correction of clubfoot deformity in a developing nation.Int Orthop 2008;32:75–9.

21. Zionts LE, Dietz FR. Bracing following correction of idiopathic clubfoot using the Ponseti method.J Am Acad Orthop Surg 2010;18:486–493.

22. Halanski MA, Davison JE, Huang JC,Walker CG, Walsh SJ Crawford HA. Ponseti method compared with surgical treat-ment of clubfoot -a prospective comparison J Bone Joint Surg Am 2010;92:270–8


ORIGINAL ARTICLE

Aurangzeb Khan

INTRODUCTION Acute pancreatitis is a systemic disease due to re-versible inflammation of the pancreas. It is a serious condition which carries substantial morbidity and mor-tality. The two commonest cause of the acute pancrea-titis are gallstones and alcohol intake.1 Other causes in-clude abdominal trauma, trauma associated with ERCP, certain drugs, viral infections, biliary tract anomalies and different types of hyperlipidaemias; while in some cases no obvious cause is found and they are labelled as ´idiopathic’.2 The annual incidence of acute pancrea-titis varies between 5 and 80 people per 100,000 of the population1, depending on many factors. In USA and western hemisphere, the alcohol induced pancreatitis is more common than gallstone pancreatitis.3

The commonest symptom of acute pancreatitis is pain in epigastrium which radiates to back and im-proves with sitting upright and leaning forward. It may be associated with nausea and vomiting, and some-

times associated with marked systemic involvement.3 Serum amylase is the most important laboratory test in diagnosing the acute pancreatitis. Others investiga-tions include estimation of serum lipase, ultrasound and computed tomography (CT) scan of the abdomen.4 Atypical cases of acute pancreatitis may be misdiag-nosed. The severity of the acute pancreatitis varies from mild oedematous pancreatitis to severe necrotizing form.5 Mild oedematous pancreatitis mostly has un-eventful recovery while severe necrotizing form is as-sociated with significant morbidity and mortality. Vari-ous severity scoring systems are used for assessing the prognosis of acute pancreatitis. These include the clini-cal scoring scales as Ranson criteria, Glasgow scales, simplified acute physiology score (SAP), acute physiol-ogy and chronic health evaluation ɪɪ (APACHEɪɪ) score, and the CT severity index.6 The complications associ-ated with acute pancreatitis may be local or systemic. The commonest local complication is pseudo-pancreat-ic cyst, which may require surgical intervention. On the other hand, ARDS is the systemic complication which significantly increases the morbidity and mortality of the acute pancreatitis.7

Management of the acute pancreatitis is primarily conservative with good nutritional support, and treat-

Aurangzeb Khan MBBS1, Yousaf Jan FCPS2, Ihsan Ulhaq MBBS3

ABSTRACTBackground: Acute pancreatitis is a common surgical emergency. Timely diagnosis and early proper management can reduce both morbidity and mortality.Objective: To study the aetiology, management and outcome of acute pancreatitis at a tertiary care hospital.Material and Methods: This prospective descriptive study was conducted in department of General surgery, Rehman Medical Institute (RMI) Peshawar from August 2012 to August 2013 after taking permission from local ethical and research committee. All adult patients (> 12 years) presenting with acute pancreatitis at the surgical outdoor clinic and emergency department during the study period were included in the study. Patients with pancreatic malignancy and those initially man-aged elsewhere, later referred to RMI were excluded from the study. Results: This study included 50 patients of acute pancreatitis admitted in ICU and Surgical Ward, 23 (46%) were males and 27 (54%) were females. The mean age of patients was 44.2 years. Five patients were initially managed in ICU. The com-monest etiological factor responsible for acute pancreatitis was gall stone (n=26, 52%) followed by idiopathic pancreatitis (n=13, 26%) and alcoholism. The commonest symptom was the pain in the epigastrium followed by nausea and vomiting. Serum amylase and lipase helped in initial diagnosis. CT scan was the most sensitive modality confirming acute pancrea-titis. The commonest complication of acute pancreatitis included paralytic ileus, electrolyte disturbances, acute respiratory distress syndrome(ARD’s), renal failure,cardiovascular insufficiency, pancreatic pseudocysts and pulmonary infections. The average hospital stay for mild, moderate and severe pancreatitis was 5.2, 7.4 and 10.9 days respectively. All patients were put on injection Imipenem and metronidazole empirically. Morbidity in our study was 27 (54%). One patient (2%) died due to multi-organ failure.Conclusion: Acute pancreatitis is a multisystem disease with high degree of mortality. It needs prompt investigations and very aggressive management to prevent the development of the complications.Key words: Acute pancreatitis, Serum Amylase, Ranson’s criteria.

1Registrar Surgical Unit, Rehman Medical Institute, Hayatabad Pe-shawar. 2,3Registrars, Surgical B Unit, HMC Peshawar.

Correspondence: Dr. Aurangzeb Khan, Registrar Surgical Unit, Re-hman Medical Institute, Hayatabad Peshawar. H No 3, Str 1, Lakhkar Abad, Abpara Market, Canal Lane, University Town Peshawar. 0333-9363767 Email: [email protected]

Received: June 2014 Accepted: September 2014

Current Concepts: Acute Pancreatitis, Aetiology, Management & Outcome



ment of complications when they develop.8 Antibiotics have very important role in conservative management and certain antibiotics (carbapenems, fluoroquinolones and cephalosporins) have been found to penetrate into pancreatic tissues.9 Surgery is only reserved for compli-cations such as pancreatic necrosis, pseudo-pancreatic cyst or pancreatic abscess. Despite advances in under-standing the management of acute pancreatitis, the overall mortality of acute pancreatitis is still around 10%.10

The current study was planned and conducted with an objective to have an idea about the aetiology and presentation of acute pancreatitis, trends in the management and evaluate the outcome of this agonis-ing disease.MATERIAL AND METHODS This prospective descriptive study of 50 patients was conducted in department of General surgery, Re-hman Medical Institute (RMI) Peshawar from August 2012 to August 2013 after taking permission from local ethical and research committee. All adult patients (> 12 years) presenting with acute pancreatitis at the surgi-cal outdoor clinic and emergency department over the study period were included in the study. Patients with pancreatic malignancy and those initially managed elsewhere, later referred to RMI were excluded from the study. The patients were collected from surgical outdoor clinic and emergency centre of RMI. All patients with diagnosis of acute pancreatitis above 12 years were ad-mitted in General surgery ward or ICU depending on the severity of the condition. Data were collected on a specifically designed proforma. The Data was obtained from patient’s medical record as well as interviewing the patients. In case the patient was not able to give his-tory, attendants were interviewed for the sake of data collection. It included findings of detailed history of the illness, thorough physical examination and results of relevant investigations. It also included the treatment given to the patients, the hospital stay (including that in general ward and in ICU), results of the treatment and development of any complication. Patients were followed every two weeks for a peri-od of 8 weeks after being discharged from the hospital. On each follow up visit, they were assessed for physical condition and any complications. The data was stored and analysed in SPSS 15. Frequencies and percentages for various parameters were calculated. The results are displayed in tabulated forms. RESULTS The study included 50 patients of acute pancreati-tis. Out of them 23 (46%) were males and remaining 27 (54%) were females. The mean age of the patients in our

study was 44.2 years (range 17 to 70 years). Majority of the patients (n=41, 82%) were in the 20 to 50 years age group (Table1). The gallstone was responsible for 26 (52%) cases of acute pancreatitis. Other causes include alcohol intake, trauma and viral infection (Table 2). In 13 (26%) pa-tients no obvious cause was found, they were labelled as idiopathic pancreatitis (Table 2). Twelve (24%) pa-tients were admitted through surgical outdoor clinic, 3(6%) were shifted from medical wards while 35 (70%) were admitted from emergency centre. Pain in the epigastrium was found in all patients (100%), which radiates to the back in 26 (52%) patients and to the right hypochondrium in 13 (26%) patients. Nausea was present in 32 (64%) and vomiting in 28 (56%) patients (Table 3). Twenty four (48%) patients had fever (highest was 104 F°) and jaundice was pre-sent in 6 (12%) patients on arrival, which was obstruc-tive in nature. About 5 (10%) patients had tachypnea (respiratory rate > 20/min) (Table 3). The common-est sign was epigastric tenderness (45, 90%), while 32 (64%) and 10 (20%) patients had tenderness in right hypochondrium and right iliac fossa respectively (Ta-ble 3). About 5 (10%) patients had tenderness on digital rectal examination. Cullen and Grey Turner sign was present in 3(6%) and 2 (4%) patients respectively (Table 3). Thirty two (64%) patients had pulse rate more than 100/min and five (10%) patients presented with shock (BP < 90/50) (Table 3). Serum amylase was raised in 43 (86%) patients and serum lipase in 43 (86%) cases. Total leukocyte count (TLC) was raised to above 11,000/mm3 in 48 (96%) pa-tients. Ultrasound was performed in all cases, detected pancreatitis in 5 (10%) patients and gallstones in 26 (52%) cases. Computed tomography was also done an all cases to establish the diagnosis and severity of the pancreatitis, confirmed pancreatitis in 47 (94%) cases respectively. According to Ranson’s criteria, 26 (52%) patients had mild acute pancreatitis, 19 (38%) had mod-erate pancreatitis and 5 (10%) patients had severe acute pancreatitis. Forty three (86%) patients did not need any nu-tritional support. Seven (14%) patients required total parental nutrition, five due to delay in recovery from pancreatitis or due to associated complications, while two because of prolong paralytic ileus. All patients were put on prophylactic antibiotics; the regimen in-cluded injection Imipenem and Metronidazole on em-pirical basis. About 47 (94%) patients responded to this regimen. Among other 3 patients, one was put on Tyga-cilin and the other two on the Colistin, based on the culture and sensitivity report (wound discharge).These patients were later on switched to oral ciprofloxacin in



45 (90%) patients and cefixime in 5 (10%) patients. Out of 50 patients, 47 (94%) were managed con-servatively and 3 (6%) underwent laparotomies. Two were operated because they had peritonitis, and pan-creatitis were diagnosed after laparotomy, while one had laparotomy for pancreatic necrosectomy, perito-neal lavage and closed drainage due to extensive pan-creatic necrosis. The most frequent complications of acute pancrea-titis were paralytic ileus (n=24, 48%), electrolyte distur-bance (n=10, 20%), acute respiratory distress syndrome (ARDS) (n=8, 16%), renal failure (n=6, 12%), cardiovas-cular insufficiency (n=5, 10%), pancreatic pseudocyst (n=4, 8%) and pulmonary infection (n=4, 8%)(Table 4). So the overall morbidity in our study was 27 (54%), while one patient (2%) died due to multi-organ failure. The average hospital stay was 7.5 days. The aver-age hospital stay for mild, moderate and severe acute pancreatitis was 5.2 days, 7.4 days and 10.9 days re-spectively. The shortest hospital stay was 4 days and the longest hospital stay was 21 days. Five patients with severe pancreatitis were initially treated in ICU, while remaining 45 cases were managed in general surgical ward. Average stay of patients in ICU was 5.9 days.

Table-1: Patients demographics

Items number Percentage Sex Male Female

23 27

4654

Age 13-20 21-30 31-40 41-50 51-60 61-70

38132042

616264084

Table-2: Frequency of the various causes of acute pancreatitis (n=50)

Causes Number of patients percentage

Gallstone 26 52

Alcohol 4 8

Trauma 3 6

Viral infection 2 4

Drug induced 1 2

Idiopathic 13 26

Total 50 100

Table-3: Frequencies of various symptoms and signs (n=50)

Table-4: Complications of acute pancreatitis

DISCUSSION Acute pancreatitis is a non-bacterial inflammation of pancreas. It is one of the acute abdominal emergen-cies that need protracted hospital stay and intensive care. Pathologically, acute pancreatitis is a protean disease resulting from an auto-digestion of the pancre-atic parenchyma capable of wide clinical variations.11 Therefore, it represents a spectrum of disease ranging from a mild, self-limited course to a rapidly progres-sive, severe illness.12 Severe acute pancreatitis (SAP) is a multi-system disease characterized in the first phase by multiple organ system failure consequent to a systemic inflammatory response, and in the second by local pan-creatic complications such as necrosis, abscess or pseu-docyst formation.11

Acute pancreatitis accounts for more than 220,000 hospital admission in the United States each year, and the epidemiological studies indicate that this incidence is increasing along with documented increase in obe-sity.11 However, acute pancreatitis in our set up shows a lower incidence frequency when compared to the world literature.13 In a study of non-traumatic causes of acute abdomen from Larkana, acute pancreatitis was observed to be a rare cause of acute abdomen in this area (4 out of 586 cases of acute abdomen, representing an incidence of less than 1%).14 However incidence in other parts of countries is higher; and it has been ob-served that due to adaptation of western life style, the

Variables Number percentage

Pain epigastrium 50 100%

Nausea 32 64%

Vomiting 28 56%

Complications Number of patients Percentage

Paralytic ileus 24 48%

Electrolyte Disturbances 10 20%

ARDS 08 16%

Renal failure 06 12%

Cardiac failure 05 10%

Pseudocyst 04 08%

Pulmonary infections 04 08%

Fever 24 48%

Jaundice 06 12%

Tachypnea 05 10%

Epigastrium tenderness 45 90%

Right hypochondrium tenderness 32 64%

Tenderness in RIF 10 20%

Tenderness on DRE 05 10%

Cullen’s sign 03 6%

Grey Turner’s sign 02 04%

Tachycardia (>100) 32 64%

Shock (BP < 90/50) 05 10%



incidence seems to be increasing.13 Therefore the preva-lence has been reported high in urban populations as compared to rural one. Acute pancreatitis is a major surgical challenge and the nature and purpose of this study was to assess the aetiological factors and mode of presentation of acute pancreatitis at a tertiary care hospital with differ-ent options of management and their outcomes. In our study gallstones were the main cause of acute pancreatitis (52%), which is comparable with the findings of a study conducted by Slavin J15. In most other studies, the two major aetiological factors, biliary disease and alcohol abuse account for more than 80% of the acute pancreatitis.16.17 Many authors have reported predominance of gallstone pancreatitis in their studies, including Xin MJ et al.18 This finding is also observed by Javed Qureshiet al13 from Jamshoro, Asifi M et al17 from Lahore and Shaukat Mirza et al19 from Lahore. Many drugs are also responsible for the develop-ment for acute pancreatitis, including steroids, azathio-prine, thiazide diuretics and sodium valproate.20 In our study one patient had thiazide induced pancreatitis and her symptom were relieved after stopping the in-take of drug. No age or gender is immune to acute pancreati-tis.19 As for the gallstone disease itself, gallstone pancre-atitis was more common in females than males, which also compare with the study of Slavin J.15 In our study, the M:F ratio was observed to be 5:6. Similar results were reported by Tonsi et al from Italy.21 Many national studies support female preponderance observed in our study, including Shaukat Mirza et al19 from Lahore and Farooq Afzal et al22 from Lahore. In contrast Asifi M et al17 from Lahore and Nasim Tarar23 from Peshawar failed to observe female predominance and reported an almost equal incidence among the both genders. This observation could be due to strict inclusion criteria. In our study the mean age of patients was 44.2 years; the youngest patient was 17 years and the eldest was aged 70 years. This is in accordance with Faisal Bhopal et al,12 Javed Qureshi et al,13 AsifiM et al17 and Nasim Tarar.23

In our study epigastric pain was the common pre-senting complaint in all the patients, followed by nau-sea and vomiting (Table 2). Mild to moderate fever was present was noted in half of the cases. These findings are in accordance with JavedQureshiet al13 and Shaukat Mirza et al19 respectively. Although gallstone pancrea-titis was the commonest entity in our series, obstructive jaundice was observed in six cases (12%) only. Elevated serum amylase, serum lipase, ultrasound and CT scan were the main tools of diagnosis. Serum amylase level of 4 or 5 times normal serum level is

usually diagnostic.12,22 In our study serum amylase as raised in 43 (86%) of our cases. Ultrasound abdomen for biliary tract was done in all cases and was found to be accurate in detecting gallstone related pancreatitis in almost all cases. CT scanning is the reliable and non-invasive imaging modality to visualizes the gland, the retro peritoneum and complications of acute pancrea-titis.24 Leung TK et al have reported that the sensitivity of CT severity index is higher than Ranson score and APACHE ӏӏ score, although they are also the predictors for complications, mortality and the length of acute pancreatitis course.25 CT scan was done in all of our cases after initial resuscitation where required. The most frequent complications of acute pan-creatitis in our study were adult respiratory distress syndrome, renal failure, cardiovascular insufficiency and pulmonary infection (Table 4). Similar results were shown by many other studies.26 Xin MJ et al18 and Moreau JA et al27 have shown that most frequent com-plications of acute pancreatitis were adult respiratory distress syndrome (ARDS) followed by multi-organ dysfunction syndrome (MODS), electrolyte disturbanc-es, renal failure, pancreatic encephalopathy and shock. The management of patients with acute pancrea-titis is complicated by the ability to distinguish mild from severe disease during the early stages.28 In our setting, Ranson’s criteria is commonly used to predict the severity, and represents a reliable tool to predict severity in majority of the cases. In one study all pa-tients labelled as severe on Ranson’s scoring criteria were dead within one month after diagnosis29. Using Ranson’s criteria we had 26 cases of mild pancreatitis, 19 cases of moderate pancreatitis and 5 cases of severe acute pancreatitis. We managed majority of our pa-tients (n=47, 94%) on conservative basis. Shaukat Mirza et al19 managed 64% of patients with conservative treat-ment. M Wariset al26 have recommended that conserva-tive policy should be adapted for cases of pancreatitis with systemic complications, while local complications require surgical intervention. We had to operate on 3 of our cases. Pancreatic necrosectomy, peritoneal lavage and closed drainage was performed in one case only, while another two cases were operated on the suspi-cion of acute peritonitis and later found to have pan-creatitis during surgery. Four (8%) of our patients developed pseudocyst formation and presented after discharge over a period ranging from 2 to 3 months. One of them was man-aged conservatively, two required open cystogastros-tomy and one was drained under ultrasound guidance with good result. Infectious complications are common problem in severe acute pancreatitis and the use of



prophylactic antibiotics in early management is advo-cated.30 We also used prophylactic antibiotics in all of our cases. All patients with gallstones (26, 52%) sub-sequently underwent cholecystectomy, including 10 patients operated laparoscopically. All of them had an uneventful recovery. The overall morbidity of acute pancreatitis in our study was 27 (54%), while one of our patients died of his disease. He was a 70 years old male with severe acute pancreatitis, died because of multi-organ failure. There-fore, overall mortality of acute pancreatitis in our study was 2%, while that for severe acute pancreatitis it was 20% (one out of 5). Similar figures have been quoted by Rehana Zikri,11 Faisal Bhoalet al,12 Shaukat Mirza et al,19 M Waris et al26 and Azeem Taz et al29 respectively. CONCLUSION Acute pancreatitis is a multisystem disease with high degree of morbidity. It needs early clinical diag-nosis, prompt investigations and very aggressive man-agement to prevent the development of the complica-tions. Due to increasing incidence of acute pancreatitis, guidelines need to be implemented after all patients are classified on Ranson’s scoring and referred to a special-ised unit for managing pancreatitis or other complica-tions requiring intensive care, radiological, endoscop-ic or surgical procedures in order to reduce the high mortality, which has been reduced over the years due to better understanding of pathophysiology of acute pancreatitis and improvement in adopting therapeutic strategies. REFERENCES1. Hines OJ, Donald GW. Endoscopic transgastric necrosec-

tomy for infected necrotizing pancreatitis.JAMA. 2012 Mar 14;307(10):1084-5.

2. Bakker OJ, Van Santvoort HC, Van Brunschot S, Geskus RB, Besselink MG, Bollen TL. Endoscopic transgastric versus surgi-cal necrosectomy for infected necrotizing pancreatitis: a rand-omized trial. JAMA. 2012;307(10):1053-61.

3. Bravo MT, Justo LM, Lasala JP, Moreira Vicente VF, Ruiz AC. Acute pancreatitis secondary to neuroendocrine pancreatic tu-mors: report of 3 cases and literature review. Pancreas. 2012; 41(3):485-9.

4. Hoque R, Malik AF, Gorelick F, Mehal WZ. Sterile inflamma-tory response in acute pancreatitis.Pancreas. 2012; 41(3):353-7.

5. Bordeje Laguna L, Lorencio Cardenas, Acosta Escribano J. [Guidelines for specialized nutritional and metabolic support in the critically ill patient. Update. Consensus of the Spanish society of Intensive Care Medicine and Coronary Units – Span-ish society of Enteral and Parenteral Nutrition: severe acute pancreatitis]. Med Intensive. 2011; 35(1):33-7.

6. Lyegha UP, Asghar JA, Beilman GJ. Total pancreatectomy and islet autotransplantationas treatment for ampullary adenocar-cinoma in the setting of pancreatic ductal disruption second-ary to acute necrotizing pancreatitis.A case report.JOP. 2012; 13(2):239-42.

7. Ramachandran BS, Murugesan M, Ali M, Pdmanabhan P. Pri-mary pancreatic choriocarcinoma presenting as pancreatitis. JOP. 2012; 13(2):217-8.

8. Lippi G, Valentino M, Carvellin G. Laboratory diagnosis of acute pancreatitis: in search of the Holy Grail. Crit Rev Clin Lab Sci. 2012; 49(1):18-31.

9. Mossner J. Update lecture: benign disease of the exocrine pan-creas. Dig Dis. 2012; 29(1):9-16.

10. Rebours V, Levy P, Bretagne JF, Bommelaer G, Hammel P, Ruszniewski P. Do guidelines influence medical practice? Changes in management of acute pancreatitis 7 years after the publication of the French guidelines.Eur J GastroenterolHepa-tol. 2012; 24(2):143-8.

11. Rehana HZ. Acute pancreatitis: recent advances in diagnosis and management. Ann Pak Inst Med Sci 2006; 2(4):215-17.

12. Faisal GB, Shahid M, Faryal A, Iqbal M: Acute pancreatitis; management, morbidity and mortality experience in a surgical. Professional Med J 2011; 18(3):366-72.

13. Qureshi JN, Memon AS, Saeeda M, Adeel HM: Pattern of acute pancreatitis: The Liaquat university Hospital experience. J Lia-quatUni Med Health Sci 2006; 5(1):28-32.

14. Memon AA, Afsar AB, Shaikh GS, Amanullah J, Quratulain S: Spectrum of disease in patients with non-traumatic acute abdo-men. J LiaquatUni Med Health Sci 2008; 7(3):180-3.

15. Slavin J. Acute pancreatitis. Surg Int. 2002; 59:227-30.16. Modlin IM, Kidd M, Hults C, Hinoue T. Surgeery of chronic

pancreatitis: chronicle of confusion and despair. World J Surg. 2002; 26(11):1382-96.

17. Asifi M, Shahbaz M Ch, Abbas G, Aetiological factors of acute pancreatitis. Ann King Edward Med Uni 2003; 9(1):37-9.

18. Xin MJ, Chen H, Luo B, Sun B. Severe acute pancreatitis in the elderly: Etiology and clinical characteristics. World J Gastroen-terol 2008; 14:2517-21.

19. Shaukhat M, Habib Q, Abrar AA, Behzad AN, Ahmed M, MajeedCh: Acute pancreatitis, critical analysis, diagnostic and therapeutic strategies. Ann King Edward Med Uni 1998; 4(4):25-7.

20. Takeyama Y. [Significance of revised version of prognostic scoring system for severity of acute pancreatitis in Japan]. Ni-hon ShokakibyoGakkaiZasshi. 2008; 105(8):1174-7.

21. Tonsi F, Bacchion M, Crippa S, Malleo G, Bassi C. Acute pan-creatitis at the beginning of the 21st century: The state of the art. World J Gastroenterol.2009; 15:2945-59.

22. Farooq MA, Haroon RI, Haroon J, Ayyaz M, Azeem KM, Asaf BM: An experience of management of acute pancreatitis at Mayo Hospital Lahore. Ann King Edward Med Uni. 1998; 4(3):31-3.

23. Nasim AT, Azhar I, Irfan ZH, Maqsood H. Acute pancreatitis. Professional Med J 2010; 17(2):199-202.

24. Bushra S, Humera A. Spectrum of disease in acute pancreatitis- Role of CT scan. Pak J Radiol 2001; 12(4):22-4.

25. Leung TK, Lee CM, Lin SY, Chen HC, Wang HJ, Shen LK, et al. Balthazar computed tomography severity index is superior to Ranson criteria and APACHE ΙΙ scoring system in predicting acute pancraetitis outcome. World J Gastroenterol.2005; 11:649-52.

26. Waris M, Ayaz M, Ghafoor T, Fahim F. Managenment of acute pancreatitis- A hospital based study. Pak J Surg 2001; 17(3):27-30.

27. Moreau JA, Zinsmeister AR, Melton L, Dimagno EP. Gallstone pancreatitis and the effect of cholecystectomy. A population based cohort study. Mayo Clin Proc. 1998; 63:466-73.

28. Khan Z, Vlodov J, Horovitz J, et al. Urinary trypsinogen activa-tion peptide is more accurate than haemocrit in determining se-verity in patients with acute pancreatitis: a prospective study. Am J Gastroenterol. 2001; 97(8):1973-7.

29. Azeem T, Ghafoor MT, Wasim A, Imran M, Zia Ullah, Sumaira R. Mortality in patients with acute pancreatitis. Pak J Gastroen-terol 2002; 16(2):35-8.

30. Khan MN. Antibiotic prophylaxis in severe acute pancreatitis.Fauji Found Health J. 2000; 1(2):2-6.


ORIGINAL ARTICLE

Syed Dil Bagh Ali

INTRODUCTION Among the entrapment neuropathies Carpal tun-nel syndrome (CTS) is the most common. It accounts for 90% of all entrapment neuropathies. The Ameri-can Academy of Orthopedic Surgeons (AAOS) Clini-cal Guidelines on the Diagnosis of CTS defines it as a symptomatic compression neuropathy of the median nerve at the level of the wrist.1,2

Prevalence of the neurophysiologically confirmed carpal tunnel syndrome in the adult general population in the Netherlands is 0.6% in men and 9.2% in wom-en.3 Similarly, this syndrome affects an estimated 3% of adult Americans and is approximately three times more common in women than men.4

Classically carpal tunnel syndrome presents with pain, numbness, and tingling in the distribution of the median nerve. Although numbness in all fingers may be a more common presentation5 and a reduction in the strength of the grip and function of the affected hand These symptoms are usually worse at night and can awake patients from sleep. Patients often describe the special phenomenon termed the “flick sign”, in which

shaking or flicking their wrists relieves symptoms.8 A systematic study conducted by Stevens et al., has con-firmed that many patients present with the symptoms outside the distribution of median nerve.9

Most of the studies published in the past two dec-ades concluded that forceful or repetitive hand use causes a variety of upper limb diseased conditions, such as tendinitis, tenosynovitis, and carpal tunnel syndrome (CTS). From the enormous experience with Carpal Tunnel Syndrome (CTS) Phalen concluded that occupation was seldom more than an aggravating fac-tor. However, a survey conducted in 1989 reported that up to 47% of all cases of Carpal Tunnel Syndrome (CTS) were thought of to be due to workplace factors.10

Likewise, medical conditions such as diabetes mellitus, diseases of the thyroid, osteoarthritis of the wrist, and any form of inflammation which affects the wrist joints or tendon sheaths are said to be associated with CTS.11,12

DIAGNOSIS Two papers by the Quality Standards Subcom-mittee of the American Academy of Neurology13 and American Association of Electrodiagnostic Medicine, American Academy of Neurology and American Acad-emy of Physical Medicine and Rehabilitation define the guidelines for clinical and neurophysiologic diagnosis of CTS.14 These papers stress the importance of a thor-ough case history, which must focus on the nocturnal paraesthesias, hand positions and repeated move-

Syed Dil Bagh Ali Shah MRCS (UK), FCPS Ortho1

Syeda Umm-e-Habiba Gillani MBBS2, Khaliq ur Rehman FRCS3

ABSTRACTObjective: To evaluate effectiveness and validity of the Phalen, Tinnel and Torniquet tests in diagnosing Carpal Tunnel Syndrome. Methodology: This descriptive interventional study was conducted in the department of Orthopaedic Rehman Medical Institute (R.M.I), Peshawar over a period of nine months May, 2009 to January, 2010. All Patients were more than 20 years and less than 70 years with Carpal Tunnel Syndrome who were not responding to non-operative measures, were included in the study. Phalen, tinnel and Tourniquet tests were performed in these patients. Moreover, electrophysiological studies (Nerve Conduction Studies) were also performed in these patients and all observations noted. Results of these tests and observations compared with per-operative findings which were taken as a gold standard. Results: The wrist flexion test (phalen) was found to be the most sensitive followed by the nerve percussion test (Tinnel). The tornique test was quite insensitive and not very specific and should not be used as a routine screening test in diagnosis of Carpal tunnel syndrome. Conclusion: wrist-flexion test (Phalen) is more sensitive among the provocative tests of Carpal tunnel syndrome. How-ever, combination of all the provocative tests can give a better outcome in order to reach the diagnosis of Carpal Tunnel Syndrome. Keywords: Carpal tunnel syndrome, Provocative tests, Median nerve.

1Senior Registrar, Orthopaedics-A Ward, Khyber Teaching Hospital, Peshawar, 2General Practitioner, 3Consultant Orthopaedic Surgeon, Rehman Medical Institute (RMI), Peshawar.

Correspondence: Dr. Syed Dil Bagh Ali Shah, Senior Registrar Orthopaedics-A Ward Khyber Teaching Hospital Peshawar. Cell: 0312 6914030, [email protected], [email protected]

Received: September 2014 Accepted: October 2014

To Evaluate the Diagnostic Efficacy of Provocative tests in Carpal Tunnel Syndrome



ments, instrument use, vibrating tools.15

A systematic review evaluated the effectiveness of observed findings from the history and physical exami-nation in predicting positive nerve conduction studies. The most highly predictive findings were location of the symptoms, hypolgesia and the weak abduction of the thumb. The consensus committees from the Ameri-can academy of neurology, American association of electro diagnostic medicine, and American academy of physical medicine and rehabilitation, recognize nerve conduction studies as the diagnostic standard for car-pal tunnel syndrome.14

Different conservative measures used in the treat-ment of Carpal tunnel syndrome include wrist splint-ing, oral corticosteroid therapy and local corticosteroid injections.15 Nearly eighty per cent of patients with car-pal tunnel syndrome respond to conservative treatment initially. However, in about eighty per cent of these pa-tients symptoms recur after one year. Indications of car-pal tunnel release surgery are:(a) Patients with symptoms that do not respond to

conservative measures,(b) Patients with severe nerve entrapment as evi-

denced by nerve conduction studies(c) Thenar atrophy(d) Motor weakness However, surgery may be effective even if a symp-tomatic patient has normal nerve conduction stud-ies.16,17,18 Sectioning of transverse carpal ligament was recommended for the first time In 1913 in order to re-lieves pressure over median nerve and this cures symp-toms of Carpal tunnel syndrome. A number of tests have been advocated for diag-nosis of carpal tunnel syndrome since that time. Among these a number of special tests so-called provocative tests are the most popular today. These tests are based on the fact that stress on a damaged median nerve in-creases the symptom of pain or paraesthesia, or both. The purpose of this study was to evaluate the effective-ness and validity of the Phalen, Tinnel and Tourniquet tests in the diagnosis of carpal tunnel syndrome.METHODOLOGY Settings: This descriptive interventional study was conducted in the department of orthopaedic Rehman Medical Institute (R.M.I) Peshawar over a period of nine months from May, 2009 to January, 2010. A total of 50 Patients were enrolled in this study through con-venient sampling. Inclusion Criterion: All patients more than 20 Years and less than 70 years of age with carpal tunnel syndrome not responding to non-operative measures (analgesia, anti-inflammatory medications and night wrist splint) were included. Patients with pregnancy

and patients operated in past for carpal tunnel syn-drome were excluded. Data Collection Procedure: All Patients with car-pal tunnel syndrome fulfilling inclusion criteria were examined and investigated after taking a detailed his-tory at orthopaedic outpatient dept., Rehman Medical Institute (R.M.I) Peshawar. Confounding factors were controlled by excluding patients with median nerve compression proximal to carpal tunnel. Pre-operative Evaluation: Detailed patient history regarding demographic status, duration of carpal tun-nel syndrome and medications used were recorded. All Patients under went following provocative diagnostic tests for carpal tunnel syndrome as follows;19,20

(a) Wrist-flexion (Phalen) test: The patient actively placed the wrist of symptomatic hand in com-plete but unforced flexion for one minute (sixty seconds). The test result was labelled positive if numbness and tingling were produced or exag-gerated in the hand in the distribution of median nerve.

(b) Median-nerve percussion test:16 The examiner gen-tly tapped the area over the median nerve of the wrist. The test result was labelled positive if this produced tingling in the fingers over the distribu-tion of the median nerve.

(c) Tourniquet tests:17 A Pneumatic blood pressure cuff, applied proximal to elbow, was inflated to a pressure higher than patient`s systolic blood pres-sure for a duration of one minute (sixty seconds). The result was labelled positive if the patient expe-rienced paraesthesia or numbness in the thumb or in the index or middle finger.

The data of patients collected on proforma. The re-sults of the provocative tests were compared with the results of electro diagnostic (Nerve Conduction Study) tests and per-operative findings. Most of the patients who were included in the study group had definite abnormalities of nerve-conduction velocity on Nerve Conduction Studies (N.C.S). Operative Technique and Per-Operative Findings: carpal tunnel release in all patients performed in minor operation theatre in Rehman Medical Institute (R.M.I), Peshawar under local anaesthesia and strict aseptic technique as follow: After cleaning over the wrist 10ml of xylocaine diluted in 10 ml of N/Saline injected. Then tourniquet applied over the affected arm. Patient put in supine po-sition and concord arm stretched over the side support and properly cleaned and draped. Following this, hand and wrist squeezed by the surgeon and the assistant while elevating the patient arm. Tourniquet inflated by the operation theatre technician to the level about



100 mmHg above systolic blood pressure of the patient. Then hand of patient was put on side support in supine position and skin incision given. Soft tissues dissected away and a small self-retainer applied. Transverse car-pal ligament identified and incised with great care to release underneath median nerve. Skin approximated with non-absorbable interrupted stitches. Tightness of the carpal tunnel, swelling, bruising and contusion of the median nerve noted. Post-Operative Follow up: Patients reviewed in outpatient department after two weeks to remove stitches, evaluate wound for any complications (infec-tion, gapping). Improvement in the symptoms of me-dian nerve compression noted. Data analysis Procedure: Data was entered in soft-ware SPSS version 10.0. Descriptive statistics were used to calculate mean and standard deviation of age, gen-der and socio-economic status. Frequency and percent-ages were calculated for all categorical data.RESULTS Fifty (50) patients with carpal tunnel syndrome between ages 20-70 years were studied. All the patients were female. Majority belonged to average socio-eco-nomic group. Thirty five (70%) of the fifty hands that were tested had a positive wrist flexion test (Phalen). Twenty (40%) of the fifty hands had a positive median nerve percussion test (Tinnel), while only ten (20%) of the fifty hands had a positive tourniquet test. Our re-sults are summarised in Table-1. All the fifty patients with carpal tunnel syndrome underwent a surgical release of the median nerve. Tight-ness of the carpal tunnel, swelling, bruising, and contu-sion of the median nerve were taken as gold standard for carpal tunnel syndrome. All the patients achieved complete relief of symptoms of paraesthesia and numb-ness. When the results of each of the provocative tests were compared with the results (positive or negative) of each of electrodiagnostic test and per-operative find-ings, no statistically significant positive correlation were found within the study group. Therefore, none of the provocative tests would be a useful predictor of a positive or negative result of any of the other tests.

Table-1: Overview of the provocative diagnostic tests in carpal tunnel syndrome.

DISCUSSION A thorough medical history, physical examina-tion, provocative diagnostic tests and electro diagnostic

(nerve conduction studies) studies are needed to con-firm the diagnosis of carpal tunnel syndrome. Provoca-tive diagnostic tests (Phalen, Tinnel and Tourniquet) are simple to perform, less time consuming and free of cost but have good diagnostic outcome. While, electro-diagnostic tests are the most sensitive and specific for the diagnosis of compression of the median nerve in the carpal tunnel. First abnormality to be noted after onset of median nerve compression in carpal tunnel syndrome is the decrease in sensory amplitude.10, 14

However, there are studies which have shown that a small number of patients with carpal tunnel syn-drome have shown negative electrophysiological stud-ies. In a report by Gruenberg has shown an eight per cent false-negative rate with the use of electro-diagnos-tic studies in a group of thirty-two hands.18 It highlights the fact that it is important to evaluate other studies for their usefulness as adjuncts in the confirmation of carpal tunnel syndrome. The provocative tests for the diagnosis of carpal tunnel syndrome (CTS) under study have been advocated by many authors to substantiate the clinical diagnosis of carpal tunnel syndrome, and some have emphasised that these can be the substitute for electrophysiological diagnostic testing.19 The pro-vocative tests, although not as much sensitive but were found to be very useful for diagnosing median nerve compression neuropathy. We found, as did Phalen, that the Phalen test is the most sensitive and useful of the three provocative tests. Our study shows 70 per cent positive phalen test results, compared with 80 per cent in the study by phalen in 1972. The specificity was 80 per cent, with 20 per cent false-positive test results. 20 The Tinnel test was found sensitive in 40 per cent of patients so much less than Phalen test with regards to its sensitivity. However, the tourniquet test is found to be the least reliable among the provocative tests. Both the Phalen and Tinnel tests are the most use-ful adjuncts in diagnosis of carpal tunnel syndrome. Though, a positive test result is a useful clinical indi-cation that a patient has carpal tunnel syndrome but a negative test result cannot rule out the diagnosis. Simi-larly, role of tourniquet test as a screening tool for diag-nosis of carpal tunnel syndrome is very limited. Possible Limitations of this study: The limitations of this study are; the small number of the patients, per-operative findings and surgeon to surgeon variability. Therefore further trials are needed to confirm the au-thenticity of provocative diagnostic tests in the case of carpal tunnel syndrome.CONCLUSION This study shows the diagnostic role of provoca-tive tests of Carpal Tunnel Syndrome. Amongst the well-known tests Phalen (wrist flexion) seems to be

S. No. Test No. of Patients with +ve tests. %age

1. Phalen 35/50 70%

2. Tinnel 20/50 40%

3. Tourniquet 10/50 20%



the most productive. However, combination of all the provocative tests can give a better outcome in order to reach the diagnosis of Carpal tunnel syndrome. REFERENCES 1. Aroori S, Spence RA. Carpal tunnel syndrome. [Review] [135

refs] Ulster Medical J.2008; 77(1):6–17. 2. American Academy of Orthopedic Surgeons Work Group

Panel. Clinical guidelines on diagnosis of carpal tunnel syn-drome. 2007.

3. Bland JD; Carpal tunnel syndrome. BMJ. 2007 Aug 18;335(7615):343-6.

4. Miller TT, Reinus WR. Nerve entrapment syndromes of the el-bow, forearm, and wrist. AJR Am J Roentgenol. 2010;195 (3): 585-94.

5. Padua L, LoMonaco M, Padua R. Neurophysiological classifica-tion of carpal tunnel syndrome assessment of 600 symptomatic hands. Ital J Neurol Sci. 1997;18:145–50

6. INAIL: Italian Worker’s Compensation Authority, Annual Report 2000. Available 600 symptomatic hands. Ital J Neurol Sci. 1997;18:145–50

7. Dorwart BB. Carpal tunnel syndrome a review [Review] [63 refs] Seminars in Arthritis & Rheumatism. 1984;14(2):134–40.

8. De Angelis, M. V., F. Peierfelice, et al. (2009). “Efficacy of a soft hand brace and a wrist splint for carpal tunnel syndrome: a ran-domized controlled study.” Acta Neurol Scand 119: 68-74

9. Stevens JC, Smith BE, Weaver AL, Bosch EP, Deen HG J r, Wilk-ens JA. Symptoms of 100 patients with electromyo-graphically verified carpal tunnel syndrome. Muscle Nerve. 1999;22:1448–56.

10. Barcenilla, A., L. M. March, et al. (2012). “Carpal tunnel syn-drome and its relationship to occupation: a meta-analysis.” Rheumatology (Oxford) 51(2): 250-261.

11. Atroshi I, Flondell M, Hofer M, Ranstam, J. “Methylpredniso-lone Injections for the Carpal Tunnel Syndrome: A randomized,

Placebo-Controlled Trial.” Annals of Internal Medicine, 2013;159:309-317

12. Bland, J. D. P. (2005). “The relationship of obesity, age, and car-pal tunnel syndrome: More complex than was thought? .” Mus-cle and Nerve 32(4): 527-532.

13. Colombini D, Occhipinti E, Cairoli S. Le affezioni musco-loscheletriche degli arti superiori e inferiori come patologie pro-fessionali; quali e a quali condizioni. Documento di consenso di un gruppo di lavoro nazionale. Med Lav. 2003; 94(3) : 312–29.

14. Dong Q, Jacobson JA, Jamadar DA et-al. Entrapment neuropa-thies in the upper and lower limbs: anatomy and MRI features. Radiol Res Pract. 17;2012: 230679

15. Atroshi, I., C. Gummesson, et al. (2007). “Carpal tunnel syn-drome and keyboard use at work.” Arthritis and Rheumatism 56(11): 3620-3625

16. D’Arcy CA, McGee S. The rational clinical examination. Does this patient have carpal tunnel syndrome?. JAMA. 2000;283:3110–7.

17. Jablecki CK, Andary MT, Floeter MK, Miller RG, Quartly CA, Vennix MJ, et al. Practice parameter: electrodiagnostic studies in carpal tunnel syndrome. Report of the American Association of Electrodiagnostic Medicine, American Academy of Neurol-ogy, and the American Academy of Physical Medicine and Re-habilitation. Neurology. 2002;58:1589–92.

18. Kanaan N, Sawaya RA. Carpal tunnel syndrome: modern diag-nostic and management techniques. Br J Gen Pract. 2001;51:311–4.

19. Longstaff L, Milner RH, O’Sullivan S, Fawcett P. Carpal tun-nel syndrome: the correlation between outcome, symptoms and nerve conduction study findings. J Hand Surg [Br]. 2001;26:475–80.

20. Carter T, Jordan R, Cummins C. Electrodiagnostic techniques in the pre-surgical assessment of patients with carpal tunnel syn-drome. A West Midlands Development and Evaluation Service report. Retrieved January 23, 2003.

First Announcement KAROPHTH 20156th, 7th, 8th March 2015

Pearl Continental Hotel KarachiProf. Idress Adhi, President Congress

Dr. Misbahul Aziz, Chairman Organizing CommitteeDr. Tariq Aziz, Co-Chairman Organizing Committee

Dr. M. Saeed Iqbal, Secretary Organizing CommitteeDr. Vasdev Harani, Chairman Registration Committee

For Further Information, Registration, Abstract submission, Quiz competition and video session

Please contact: Mr. Muhammad Usman Tariq 0306-7484544OSP Office, PMA House,Agha Khan III Road Karachi.

E mail: [email protected]

Thanks & Regards

Dr M Saeed Iqbal Secretary Organizing Committee , OSP Karachi.


ORIGINAL ARTICLE

Amin Shaikh

INTRODUCTION Nd:Yag (Neodium: Yttrium-Aluminum Garnet) laser (light amplification by stimulated emission of radiation) was developed by Geusic, Marcos and Van Uitert in 1964 A.D is most widely used and common-est variety of solid state laser. The advent of Nd: Yag laser in ophthalmology has given the surgeon a great-er therapeutic choice. Neodium Nd3+ is the laser ac-tive element hosted either in glass/crystal. Neodium laser is most efficiently incorporated in the Yttrium Aluminum-Garnet crystal (Y3AL5O2) and commonly termed as YAG, which emits at a wave length of 1064 n.m1

The posterior capsular opacification (PCO), contin-ues to be the most frequent postoperative complication

of extracapsular cataract extraction or phacoemulsifica-tion. Posterior capsular opacification stems from con-tinued viability of lens epithelial cells remaining on an-terior and posterior capsule, these cells migrate across the capsule in response to unknown stimuli, producing fibrous contraction leading to wrinkling and opacifi-cation of capsule.2,3 The incidence of opacification has been reported 10% per year. Half of patients under go-ing cataract extraction with intact posterior capsule will require treatment for opacification, and the percentage is high for children and young adults.4

The management of postoperative capsule opaci-fication consists of creating an opening in the opaque capsule in the axial area. There are different methods for this procedure. In the past, surgical posterior cap-sulotomy was considered to be the best.5 Now-a-days this method is being replaced by neodymium yttrium-aluminum garnet (Nd: YAG) laser capsulotomy, which is a non-invasive procedure.6 Although Nd: YAG laser capsulotomy is a safe procedure, it has its own compli-cations. The most common is an acute rise of intraocu-lar pressure following laser procedure. It is usually

Muhammad Amin Shaikh DOMS, MSc, MS1, Prof. Syed Imtiaz Ali Shah, FCPS2

Manzoor Ali Kandhro DOMS3, Khalid Rasul Shaikh MBBS4, Amanullah shaikh MBBS, (DCH)5

ABSTRACTObjective: To evaluate the elevations of intraocular pressure after Nd:YAG laser posterior capsulotomy in 500 cases.Study Design: Prospective observational study: Place and Duration: Department of Ophthalmology Chandka Medical Col-lege & Civil Hospital Larkana from March 2010 to Sep 2010.Patients and Methods: The study comprises 500 patients performed at department of Ophthalmology, Chandka Medical College Hospital Larkana from March 2010 to Sep 2010. The patients who had undergone extracapsular cataract extraction with posterior chamber intraocular lens implantation and had developed posterior capsular opacification were selected from the out patient department.Results: We studied change of intraocular pressure after Nd: YAG laser posterior capsulotomy in 500 eyes of 500 patients. 260 (52%) were males and 240 (48%) females; all were pseudophakic having different age groups ranging from 10 to 80 years. Goldman applanation tonometer was used for IOP measurement before and after Nd: YAG laser application. Q-Switched Nd: YAG laser was used to perform posterior capsulotomy. Three hours after Nd: YAG laser posterior capsu-lotomy. IOP remained unchanged in 181 (36.2%) eyes, and in 274 (54.8%) eyes IOP raised upto 10mmHg. Out of these 243 (48.6%) eyes developed a rise of IOP upto 6mmHg and only 31 (6.2%) eyes had a rise more than 6mmHg but not over 10mmHg. 45(9%) eyes showed a rise of IOP more than 10mmHg. The mean pressure raised after 3 hours was 5.60mmHg and the mean IOP was 14.65mmHg. Antiglaucoma treatment was started in 50 (10%) eyes. Tab. Acetazolamide 250mg 2-Tablets state along with topical beta-blockers two times a day. Topical NSAID was given to all patients for decreasing intraocular inflammation. On following day i.e. 24 hours after laser treatment only 5 (1%) of eyes had significant elevation of IOP of more than 10mmHg, 204 (40.8%) of eyes had insignificant rise of IOP and 291 (58.2%) of eyes had normal base line IOP.Conclusion: This study confirms that IOP elevation is a frequent complication of Nd: YAG laser posterior capsulotomy. The pressure peak occurs within 3 hours post treatment. There was no correlation between the laser energy or the size of capsulotomy and the rise of IOP. Key words: Intraocular pressure, Neodymium-yttrium aluminum garnet (Nd:YAG) laser, Posterior capsular opacification, and Extracapsular cataract extraction.

1Assistant Professor, Department of Ophthalmology, 2Professor of Ophthalmology, Chandka Medical College, Hospital Larkana, 3Oph-thalmologist, 4Department of anatomy, 5Department of Paediatrics

Correspondence: Dr. Aurangzeb Khan, Registrar Surgical Unit, Re-hman Medical Institute, Hayatabad Peshawar. H No 3, Str 1, Lakhkar Abad, Abpara Market, Canal Lane, University Town Peshawar. 0333-9363767 Email: [email protected]

Received: June 2014 Accepted: September 2014

To Evaluate the Elevations of Intraocular Pressure after Nd: Yag Laser Posterior Capsulotomy

(500 Cases Report)



transient but may be vision threatening.7

PATIENTS AND METHODS An observational prospective study conducted at the department of Ophthalmology Chandka Medi-cal College and Civil Hospital Larkana after obtaining informed consent from all the participants between March 2010 to Sep 2010. Patients with visually sig-nificant posterior capsular opacification were selected from the outpatient department of Ophthalmology civil hospital Larkana. Patient were excluded from the study if there was a history of uncontrolled glaucoma, advanced glaucoma, hazy cornea, very dense posterior capsular opacification, any posterior segment pathol-ogy likely to cause decreased vision after treatment. Baseline data was obtained for each patient before ini-tiation of treatment on a prescribed proforma of each patient underwent complete workup which included a full ocular and medical history, best corrected Snellen’s visual acuity, slit lamp biomicroscopy, Goldmann’s applanation tonometry, gonioscopy and fundoscopy. Pupils were dilated with Tropicamide 1% and Phenyle-phrine 10% eye drops. Immediately before the laser procedure. All the capsulotomies were performed by a qualified ophthalmologist. Five hundred eyes of Five hundreds Patients un-derwent the procedure with a pulse duration of 4 na-nosecond, a spot size of 8 micron, and pulse energies ranging from 0.5-2.0 mJ, coupled to a slit lamp delivery system with a 1064 nm Laser beam. With the patient seated at the slit lamp system, Abraham capsulotomy contact lens (Ocular instruments) was placed onto the eye. The aiming beam was focused on the superior cap-sule 1 mm inside the IOL edge. Nd: YAG laser was applied with a 8.0 micron spot size and a power of 0.5 to 2.0 mJ and pulse duration of 4.0 nanosecond, to cre-ate small openings in the capsule from 12 to 7 ‘o’clock position and then from 12 to 5 ‘o’clock position. A stalk was created by applying few laser shots vertically downward from 5 and 7 ‘o’clock position. Patients were examined at 3 hour, 1 day, one week, two weeks, and 4 weeks after Nd; YAG laser poste-rior capsulotomy. Patients were advised to report any visual complaint to the principal investigator after the laser process. At each visit patients were invited to re-port any symptoms of ocular morbidity and an oph-thalmic examination was performed, which included visual acuity measurement, slit lamp biomicroscopy and Goldman applanation tonometry. In addition go-nioscopy and funduscopy were also performed. Short term complications were defined as intraoperative and during first week after treatment. Patients were also censored if a complication like retinal detachment

took place. Statistical analysis was performed on SPSS version IS for windows. Frequency distribution tables were used to present the data. Mean and standard de-viation were used for continuous variables. Categorical variables were presented as proportions and percent-ages.RESULTS We studied change of intraocular pressure after Nd: YAG laser posterior capsulotomy in 500 eyes of 500 patients. 260 (52%) were males and 240 (48%) females; all were pseudophakic having different age groups ranging from 10 to 80 years. Goldman applanation to-nometer was used for IOP measurement before and af-ter Nd: YAG laser application. Q-Switched Nd: YAG laser was used to perform posterior capsulotomy. Three hours after Nd: YAG laser posterior capsu-lotomy. IOP remained unchanged in 181 (36.2%) eyes, and in 274 (54.8%) eyes IOP raised up to 10mmHg. Out of these 243 (48.6%) eyes developed a rise of IOP up to 6mmHg and only 31 (6.2%) eyes had a rise more than 6mmHg but not over 10mmHg. 45 (9%) eyes showed a rise of IOP more than 10mmHg. The mean pressure raised after 3 hours was 5.60mmHg and the mean IOP was 14.65mmHg. Anti-glaucoma treatment was start-ed in 45 (9%). Tab. Acetazolamide 250mg 2-tablets state along with topical beta-blockers two times a day. Topi-cal NSAID was given to all patients for decreasing in-traocular inflammation. On following day 291 (58.2%) eyes had normal baseline IOP while 204 (40.8%) eyes had an IOP eleva-tion of up to 10mmHg. Out of these 189 (37.8%) eyes had an IOP elevation up to 6mmHg, only 15 (3%) had an IOP elevations of more than 6 to 10mmHg. 5 (1%) eye had IOP of more than 10mmHg. So 40.8% eyes had insignificant elevation of IOP, while only 1% eyes had significant elevation of IOP. Mean I.O.P rise was 4.05mmHg and mean IOP was 12.26mmHg. One week after capsulotomy 370 (74%) eyes had normal baseline IOP while 120 (24%) eyes had rise upto 6mmHg, only 5 (1%) eyes had rise upto 10mmHg and 5 (1%) eyes had rise of more than 10mmHg. So practi-cally 370 (74%) eyes were now towards the normal IOP and only 5 (1%) eyes had very significant rise in IOP. Mean IOP was 11.62mmHg, mean pressure rise was 4mmHg. Two weeks after posterior capsulotomy 402 (80.4%) eyes had normal base line IOP. 98 (19.6%) eyes had rise of IOP upto 6mm Hg the mean pressure rise after 2 weeks was 4mmHg and mean IOP was 11.27mmHg. So 2 weeks after capsulotomy 80.4% eyes were with normal base line IOP and 19.6% eyes had insignificant rise of IOP. Four weeks after posterior capsulotomy 446



(89.2%) eyes had. rise of IOP upto 6mmHg and no pa-tient had IOP rise more than 6mmHg. The mean pres-sure after 4 weeks was 11.05mmHg and mean IOP rise was 3.38mmHg. So after 4 weeks of Nd: Yag laser posterior capsu-lotomy, 89.2% eyes had normal base line IOP and 10.8% eyes had insignificant rise of IOP.

Pre Laser

Post Laser

Pre Laser

Post Laser

DISCUSSION The elevation in intraocular pressure generally starts, immediately after Nd: YAG capsulotomy. It reaches to its peak at 1 – 4 hours and return to base line level within a week, mostly within first 24 hours.8 Be-sides elevating IOP other complications such as, dam-age to IOL, rupture of anterior hyaloid face, iris bleed-ing, cystoid macular oedema, corneal damage and retinal detachment etc may occur.9,10

The main objective of our study was to observe the effect of Nd: YAG laser posterior capsulotomy on in-traocular pressure and to prevent the sight threatening complication of raised IOP11 by controlling unintend-ed rise of IOP with the use of medicine.12 The criteria used to administer the drug were either a rise of IOP of 25mmHg or 10mmHg more above the baseline value.13 The drugs used were tab. Acetazolamide 250mg, 2 tab-let stat along with topical beta blocker.14

In our study intraocular pressure was checked pri-

Change in I.O.P After 3 hours % After 24

hours % After 1 weeks % After 2

weeks % After 4 Weeks %

No change 181 36.2 291 58.2 370 74 402 80.4 446 89.2

Rise up to 6mmHg 243 48.6 189 37.8 120 24 98 19.6 54 10.8

Rise 7 to 10mmHg 31 6.2 15 3 5 1 __ __ __ __

Rise10mmHg and more 45 9 5 1 5 1 __ __ __ __

Total 500 100 500 100 500 100 500 100 500 100

Effect of Nd: Yag laser posterior capsulotomy on IOP

IOP MEAN STANDARD DEVIATION

Pre-laser IOP 11.64 2.76

IOP after 3 hours 14.62 6.13

IOP after 24 hours 12.26 3.88

IOP after 1 week 11.60 3.28

IOP after 2 weeks 11.26 2.68

IOP after 4 weeks 11.04 2.61

Comparison of mean and standard deviation of pre and post laser IOP



or to laser application and than three hours, 24 hours 1 week, 2 week and 4 weeks after the procedure. Any significant rise in IOP was treated accordingly. In our study of 500 cases, Three Hundred Nineteen (63.8%) eyes showed an elevation of IOP after 3 hours of capsu-lotomy. Out of these 243 (48.6%) eyes showed an eleva-tion of up to 6mmHg, 31 (6.2%) eyes showed elevation of up to 9mmHg, and 45 (9%) eyes showed elevation of IOP 10mmHg and more. Study by Ejaz Latif Muhamad et al, on IOP chang-es after Nd: Yag laser posterior capsulotomy, noticed a mean IOP elevation of less than 5mmHg from base-line in 7(9.3%) cases in placebo group. 32% eyes of placebo group had in intraocular pressure elevation of 5-10mmHg from base line as compared to 2 (2.6%) of the apraclonidine – treated group. 10.7% patients of placebo group develop a IOP rise of greater than 10 mmHg.14 A study by Sohail Siddiqui Butt in 1998 ob-served a post laser capsulotomy elevation of IOP with-in 3 Hours in 51 (79.7%) eyes with a rise of 10 mmHg or more in 15 (23.5%) eyes.15

Antigluacoma treatment started in 50 (10%) eyes was. Tab. Acetazolamide 250mg, 2 tablets stat, along with topical beta-blockers one drop twice a day. Non-steroidal anti-inflammatory drugs were topically given to all patients for decreasing intraocular inflammation. On the following day i.e. 24 hours after laser treatment. Only 5 (1%) eye had significant elevation of IOP of more than 10mmHg and 15 (3%) eyes had below 10mmHg and 189 (37.8%) eyes had below 6mmHg. Remaining 291 (58.2%) eyes had normal baseline IOP. Oral ac-etazolamide started in 5 (1%) cases and was given for one week that showed IOP of more than 10mmHg re-maining 45 (9%) eyes were maintained on topical beta-blockers for 4 weeks. So after 24 hours 495 (99%) eyes showed either normal or having rise of IOP <10mmHg and only 5 (1%) eyes were still showing of rise of IOP >10mmHg above baseline value.CONCLUSION This study confirms that IOP elevation is a fre-quent complication of Nd: YAG laser posterior capsu-lotomy. The pressure peak occurs within 3 hours post treatment. In most of patients rise in intraocular pres-

sure is insignificant and IOP comes to base line value or near normal within 24 hours. A few cases may develop markedly high IOP during this period and therefore all the cases should be observed very closely during early 24 hours especially within 3 hours. Post-operatively, and immediate measures should be taken to lower the IOP, as to avoid permanent damage to the optic nerve and the vision.REFERENCES1. Bhattacharya B. Chronology of development of YAG Laser,

Clinical Applications: YAG Laser Ophthalmology 2005; 1 (2): 5-9.

2. Shah SIA. Posterior Capsular Opacification (PCO). Diseases of Lens. Clinical Ophthalmology. AZAMS SONS Ltd. 2009; 2 (7): 73-81.

3. Snell RS, Lemp MA. Clinical anatomy of the eye. Blackwell Scientific Publications 1989: 136.

4. Kanski JJ: Post Operative Posterior Capsular Opacification. Clinical Ophthalmology, A systemic approach. Butterworth, Heinemann. 6 th ed. 2007; 6 (12): 358 - 59.

5. Dewey, S. Posterior Capsule Opacification. Current Opinion in Ophthalmology, 2006 :17(1), 45-53.

6. Geusic, J.E., Marcos, H.M, and Van Uitert, L.G.: “Laser oscillations in Nd-doped yttrium aluminum, yttrium gallium and gadolinium garnets”. Applied Physics Letters 4 10, 182-184 (1964).

7. Tufan Evciman MD, Melih Haboğlu MD, Refraction, intraocular pressure and anterior chamber depth changes after Nd:YAG laser treatment for posterior capsular opacification in pseudophakic eyes: Optometrists Association Australia 2009 Volume 92, Issue 5, pages 412– 415.

8. Barnes E, Murdoch I, Subramaniam S, Cahill A, Kehoe B, Behrend M, Neodymium-yutrium–aluminum–garnet, capsulotomy and intraocular pressure in pseudophakic patients with glaucoma1 Ophthalmology, 2009, Volume 111, Issue 7, Pages 1393-1397

9. Olsen G, Olson RJ. Update on a long-term, prospective study of capsulotomy and retinal detachment rates after cataract surgery. J Cataract Refract Surg 2000; 26: 1017– 21.

10. Arya SK, Sonika, Kochhar S, Kumar S, Kang M, Sood S. Malignant glaucoma as a complication of Nd:YAG laser posterior capsulotomy. Ophthalmic Surg Lasers Imaging. Am J Ophthalmol. 2004;35(3):248-50.

11. Yilmaz S, Ozdil MA, Bozkir N, Maden A. The effect of Nd:YAG laser capsulotomy size on refraction and visual acuity. J Refract Surg 2006; 9: 719–721.

12. Latif E, Khalid, Aaqi M, Aasi NA. Use of topical apraclonidine to prevent intraocular pressure elevation following Nd: YAG laser posterior capsulotomy. In Pakistan J Ophthalmol 1999; 15 (3).

13. Billotte C, Berdeaux G. Adverse clinical consequences of neodymium:YAG laser treatment of posterior capsule opacification. J Cataract Refract Surg 2004; 30: 2064–2071.

14. Ladas ID, Pavlopoulos GP, Kokolakis SN, Prophylactic use of acetazolamide to prevent intraocular pressure elevation following Nd-YAG laser posterior capsulotomy. Br J Ophthalmol. 2008 28(1): 19 – 22.


SHORT COMMUNICATION

Physicists are using the special properties of graphene to produce key elements of an artificial retina. With their research program the researchers were admitted to the heavily funded “Graphene” Flagship Program of the EU. Graphene is viewed as a kind of “miracle solution”: It is thin, transparent and has a tensile strength greater than that of steel. In addition, it conducts electricity better than copper. Since it comprises only a single layer of carbon atoms it is considered two-dimensional. In 2010 the scientists Andre Geim and Konstantin Novoselov were awarded the Nobel Prize for their ground-breaking work on this material. In October 2013, the “Graphene” project was selected alongside the “Human Brain Project” as a Flagship Project of the EU FET Initiative (Future and Emerging Technologies). Under the supervision of Chalmers University of Technology in Sweden, it bundles the research activities and will be funded with one billion euro over ten years. In July 2014 the program took on 66 new partners, including TechnischeUniversitätMünchen (TUM).Optical prostheses for blind people: Because of its unusual properties, Graphene holds great potential for applications, especially in the field of medical technology. A team of researchers led by Dr. Jose A. Garrido at the Walter Schottky Institut of the TUM is taking advantage of these properties. In collaboration with partners from the Institut de la Vision of the Université Pierre et Marie Curie in Paris and the French company Pixium Vision, the physicists

are developing key components of an artificial retina made of Graphene. Retina implants can serve as optical prostheses for blind people whose optical nerves are still intact. The implants convert incident light into electrical impulses that are transmitted to the brain via the optical nerve. There, the information is transformed into images. Although various approaches for implants exist today, the devices are often rejected by the body and the signals transmitted to the brain are generally not optimal.Excellent biocompatibility In contrast to the traditionally used materials, graphene has excellent biocompatibility thanks to its great flexibility and chemical durability. With its outstanding electronic properties, graphene provides an efficient interface for communication between the retina prosthesis and nerve tissue.

(Source: http://www.tum.de/en/about-tum/news/...)

Artificial Retina: Physicists develop an interface to the optical nerve

(A peep into Nano-Technology)

Edited: Dr. Madiha Durrani, FRCS Canada

(Photo: Natalia Hutanu / TUM)


POSTGRADUATE DIARY

Double vision, or diplopia, is a symptom to be tak-en seriously. Some causes of diplopia are relatively mi-nor, but others need urgent medical attention. Double vision is not normal and should be reported promptly. Causes: Opening your eyes and seeing a single, clear image is something you probably take for grant-ed. But that seemingly automatic process depends on the orchestration of multiple areas of the vision system. They all need to work together seamlessly:• The cornea is the clear window into the eye. It does

most of the focusing of incoming light.• The lens is behind the pupil. It also helps focus

light onto the retina.• Muscles of the eye -- extraocular muscles -- rotate

the eye.• Nerves carry visual information from the eyes to

the brain.• The brain is where several areas process visual in-

formation from the eyes. Problems with any part of the visual system can lead to double vision. It makes sense to consider the causes of diplopia according to the part of the visual system that has the problem. Corneal. Problems with the cornea often cause double vision in one eye only. Covering the affected eye makes the double vision go away. The abnormal surface of the eye distorts incoming light, causing dou-ble vision. Damage can happen in several ways:• Infections of the cornea, such as herpes zoster, or

shingles, can distort the cornea.• Corneal scars can alter the cornea, creating une-

qual visual images.• Dryness of the cornea can create double vision. Lens. Cataracts are the most common problem with the lens that causes double vision. If cataracts are present in both eyes, images from both eyes will be dis-torted. Cataracts are treated surgically. Ocular Muscles. If a muscle in one eye is weak, that eye can’t move smoothly with the healthy eye. Gazing in directions controlled by the weak muscle causes double vision. Muscle problems can result from several causes:• Myasthenia gravis is an autoimmune illness that

blocks the stimulation of muscles by nerves inside the head. The earliest signs are often double vision and drooping eyelids, or ptosis.

• Graves’ disease is a thyroid condition that affects

the muscles of the eyes. Graves’ disease commonly causes vertical diplopia, one image is on top of the other.

Nerve palsies. Several different conditions can damage the nerves that control eye muscles and lead to double vision:• Multiple sclerosis can affect nerves anywhere in

the brain or spinal cord. If the nerves controlling the eyes are damaged, double vision can result.

• Guillain-Barre syndrome is a nerve condition that causes progressive weakness. Sometimes, the first symptoms occur in the eyes and cause double vi-sion.

• Uncontrolled diabetes can lead to neuropathies in one of the eyes, causing eye weakness and double vision.

CNS. Since visual processing takes place inside the brain. Many different causes for double vision originate in CNS. They include:• Strokes• Aneurysms• Raised pressure of CSF, trauma, bleeding, or in-

fection• Brain tumors• Migraine headachesSymptoms of Double Vision: Diplopia can occur by itself with no other symptoms. Depending on the cause, other symptoms may be present with double vision, such as:• Misalignment of one or both eyes (a “wandering

eye” or “squinting “ appearance)• Pain with eye movements in one or both eyes• Pain around the eyes, such as in the temples or

eyebrows• Headache

Aetiology of Diplopia Edited by: Dr. Jahanzeb Durrani

Aetiology of Diplopia


• Nausea• Refractive errors• PtosisDiagnosed: Double vision that’s new or unexplained needs medical attention right away. With so many po-tentially serious causes for double vision, it’s important to discover the reason without delay. It is important to diagnose the cause for double vision. Blood tests, a physical exam, and possibly imaging studies like com-puted tomography (CT) or magnetic resonance imag-ing (MRI) are frequently used.One of the most effective tools in diagnosing diplopia, though, is the information you can provide. You can make the diagnosis for double vision more accurate by answering several questions beforehand.• When did the double vision start?• Have you hit your head, fallen, or been uncon-

scious?• Were you in a car accident?• Is the double vision worse at the end of the day or

when you’re tired?• Have you had any other symptoms besides double

vision?• Do you tend to tilt your head to one side? Look at

old pictures, or ask family -- you may not even be aware of the habit.

Now, focus on something unmoving in your field of vi-sion -- a window or a tree.• Are the two objects side by side, or is one on top

of the other? or are they slightly diagonal? Which one is higher or lower?

• Are both images clear but simply unaligned with each other? or is one image blurry and the other clear?

• Cover one eye, then uncover it and cover the oth-er. Does covering either eye make the double vi-sion go away?

• Pretend your field of vision is a clock face. Move your eyes around the clock, from noon to six and up to 12 again. Is your double vision worse at any clock position? Does any position make your dou-ble vision improve?

• Tilt your head to the right, then to the left. Do any of these positions improve the double vision, or make it worse?

Treatment: With double vision, the most important step is to identify and treat the underlying cause. In some cases, double vision can be improved by manag-ing or correcting its cause.• If weak eye muscles are the cause, or if a muscle

has been pinched as a result of injury, surgery may help.

• Myasthenia gravis can be treated with medica-tions.

• Graves’ disease is often curable with surgery or medical therapy.

• Blood sugar in diabetes can be controlled with medicines and/or insulin.

If double vision can’t be reversed, treatments can help people live with double vision. Sometimes, this re-quires wearing an eye patch or special prism glasses to minimize the effect of double vision.

IMPORTANT NOTE

Authors of articles and the subscribers are requested to collect the copies of the Ophthalmology Update from representatives of the concerned area according to the following:

SR# Name Area Number

1 Aamir Zaib Peshawar 03337771210

2 Waqas Majeed Rawalpindi 03337771248

3 Waseem Ejaz Lahore 03337771288

4 Syed Arshad Ali Faisalabad 03337771290

5 Niaz Sheikh Multan 03337771303

6 Khalid Mehmood Karachi 03337771343


Lahore – Popularly known as city of colleges it means a cultural, intellectual and artistic hub of the country which has produced most illustrious men of learning. If history and architecture are your passion there’s an evocative mix, from formidable Mughal monuments to faded legacies of the British Raj. Pakistan is crazy about cricket and one way of breaking the ice with Lahorites is to strike up a conver-sation about the game. Lahore – which, incidentally, is the home to the cricket– sometimes serves as the venue for high-profile international matches. It also has some serene architecture and gardens on the subcontinent. Follwing are the Noble Laureates from Lahore.

1. Joseph Rudyard Kipling was an English short-story writer, poet, and novelist. He wrote tales and poems of British soldier in 1907. He edited the civil & Military Gazette News-paper of Lahore and termed it “mis-tress and most true love”. He won his Noble Prize for writing the best

novel ‘Kim’, the cannon on the Mall in front of the La-hore museum.

2. Prof. Dr. Arthur Holly Compton He worked in the Chemistry Department of the University of Punjab. During his stay he has done lot of research in Magneto-Chemistry and won the Noble in 1927

3. Har Gobind Khorana Noble Prize for Genetics 1968Born at Raipur Kabirwala Dr. Kho-rana was responsible for produc-ing the first man-made gene in his laboratory in the early seventies. This historic invention won him the Nobel Prize for Medicine in 1968.

Khorana, born in a poor family, he took his M.Sc from

Punjab University at Lahore in 1945. Khorana’s work, which is an important scientific landmark of the 20th century, has brought closer the day when synthetic DNA may be introduced into the defective human tis-sues to treat mentally retarded people.

4. Dr. Subrahmanyan Chandra Sekhar Physics 1983Born in Lahore, educated in Government College and served as a lecturer there. Won Noble in (Physics) 1983 for discovering a black hole in the universe. There is a telescope named after him in space

“Chandra” His father was Auditor General in Lahore.

5. Prof. Dr. Abdus Salam Chaud-hary Prof. Dr Mohammad Abdus Salam Chaudhary, Physicist and first Paki-stani Nobel Laureate 1979. Born in Jhang, Punjab, was a Pakistani theo-retical physicist, astrophysicist and Nobel laureate in Physics for his

work in United Field Theory 1979. Salam holds the dis-tinction of being the first Muslim Nobel Laureate. Even today, Salam is considered as one of the most influen-tial scientist and physicist in this country. He found-ed the International Institute of Theoretical Physics at Trieste, Italy later named after him as Abdus Salam In-ternational Institute of Theoretical Physics. He was Pro-fessor of Physics at Government College, Lahore

6. Malala YousafzaiNobel peace prize winner 2014Champion of Children has been given Nobel Peace Prize

Ophthalmology Notebook

LAHORE - A CITY OF NOBLE LAUREATES



Development of Super-Resolved Fluorescence Optical Micrscope

– Peep Into the Nanoworld For a long time, the optical microscope were lim-ited by wavelength of light and other factors. Scientists believed that they could never yield a resolution bet-ter than 0.2 micrometer, but the three scientists i.e., Eric Betzig , William Moerner ( both from USA) and Stefan Hell from Germany were able to break that limit by using molecules that blow on command. The advance took opti-cal microscope into new dimension that made it possible to study the interplay between molecules inside cells, in-cluding the aggregation of disease related proteins. The technology offers advantage over an electron microscope , which offers slightly better resolution but can’t be used to examine cells that are alive. It is used to get better understanding of the nerve cells and brain synapses. Mr. Moerner studied proteins related to Huntington’s disease and Mr. Betzig tracked cell di-vision inside the embryo. Since it will be a powerful microscope , it will en-able the scientists to see how disease develop inside the tiniest cell. They used the glowing molecule in dis-eases such as Parkinson’s Disease, and Alzheimer’s and Huntington’s disorder at a molecular level. Two US and one German scientist win Nobels in Physical Chemistry for opening a window into the nano-world with their development of ‘super-resolved fluorescence microscopy’

Dr. Robert Eric Betzig Prof. William Moerner Dr. Stefan W. Hell

Inauguration of Breast Cancer Clinic at

Holy Family Hospital, Rawalpindi Professor Muhammad Umar, Sitara-i-Imtiaz, Principal of Raw-alpindi Medical College and Chief Executive of Allied Hospitals has recently inaugurated the Breast Cancer Clinic at the surgical out-door of Holy Family Hospital, Rawalpindi. According to different studies 40000 women die due to advanced breast cancer in Pakistan which is much higher as compared to other Asian countries. Ac-cording to a recent study conducted in NORI hospi-tal, Islamabad, the number of new cases of cancer has swelled from 2000 in 1998 to over 4000 in 2013. The incidence has increased by 20% and mortality rate has also increased by 20%. There is one out every 8 women who is likely to suffer from this dreaded disease. It is estimated that the breast cancer is 35% of all the fe-male cancers, and out of them 60% report in advanced stage which is due to lack of awareness, poverty, social and cultural taboos. Globally speaking the number of cancer patients have arisen from 12.7 million in 2008 to 14.1 million in 2012 and it is expected to rise further to 19.0 million in 2025. Multiple risk factors are smoking, obesity, lack of physical activity and indiscriminate use of hormones and reluctance of our female population to consult a doctor. As such we need many clinics almost in every teaching hospital of Pakistan where we can provide the state-of-art facilities to our people. Keeping in view of this fact, Rawalpindi Medical College and its Allied Hospitals has always been torch-bearer in taking the health facilities to higher level. It is worth mentioning here that Prof. Muhammad Umar who is a very humble, helpful, cheerful, energetic and an untiring personality has already established a most modern Liver diseases Clinic, providing latest treat-ment for Hepatitis ‘C’ patients and other liver diseases.He held a Workshop on Clinical Audit, which goes a long way in improving the health services and now a Breast Cancer Clinic with state-of-the -art services to the Public. Realizing the difficulties of our people Prof. Umar has gone a long way to undertake this project on pri-ority basis. Other professors who are helping this pro-ject are Prof. Hamamatul Bushra, Prof. Idrees and Dr. Jahangir Sarwar as active members of the team. Prof. Bushra highlighted to the audience the major causes of



increasing incidence of Breast cancer. Patients mostly depend on unqualified and untrained healers. Our fe-male population always think that it is immoral to get examined especially in the rural areas. Dr. Sarwar indicated that the newly established clinic will greatly increase the awareness in our fe-male population and stressed the need for early detec-tion of the disease. We need to educate our womenfolk regarding the importance of early detection of cancer in case they happen to suspect any small lump in the breast, which will ultimately help in saving the lives of millions. Young mothers should be encouraged to breast feeding and to adopt a healthy life style.

Chief Editor

Letter to the Editor

Dear Prof. Durrani, We gratefully acknowledge the receipt of your esteemed quarterly journal ‘International Ophthalmol-ogy update’Vol 12 No:4, Ocober-Decmeber,014. We are sure that this is going to provide useful additional in-formation for our postgraduate students involved in re-search project for their M.Phil and PhD programs. I am sure that your support in academic field will continue to enrich the knowledge of the student population and the faculty at the University. We thank you once again for the complimentary copy of the journal. With best regards,

Yours sincerely,Assistant Librarian.University of Health Sciences, Lahore.

Dear Prof. Yasin Durrani Keeping my words, I have just finished my pa-per“ General impact of ocular anti-angiogenic therapy” and I am sending it to your attention. Today I have re-ceived a hard copy of the Ophthalmology Update and just have read about your new Guidebook. I am very impressed with a wide field of your professional inter-est. My cordially congratulations to you on new book, Why should I become a doctor’ Taking this opportu-nity I would like to express my deep gratitude to you for sending me the Journal and I wish you once more continued successful and fruitful work and all the very best. Best regards,

Prof. Marianne Shahsuvaryan Prof. of Ophthalmology, Yerevan State Medical University, Republic of Armenia

Dear Prof. Yasin Durrani, AOA. I hope you are in the best of your health. Today I received in the mail the Ophthalmology Update maga-zine . I was very delighted to see my article “ Are we on Right Path in Glaucoma”. I have no words to say my thanks for your kindness and support. I am certain, one day by Grace of Allah, my colleagues would listen to me. I always enjoy Iqbal’s poetry in your magazine which really makes your magazine even more colorful. I really admire your dedication that you are so actively involved in publication of Ophthalmology Update in your age. I pray to Allah to bless Pakistan with more persons like yourself. My best regards.

Syed S. Hasnain M.D.General Ophthalmology 560 W. Putnam Ave. Suite #6Porterville, CA 93257 Tel: 559.781.7482 Fax: 559.781.8446 Email: [email protected]

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Abstract: Abstract of original article should be in structured format with the following sub-headings:Objective, Design, Place and duration of Study, Patients & Methods, Result and Conclusion. Introduction: This should include the purpose of the article. The rationale for the study or observation should be summarized. Methods: Study design and sampling methods should be mentioned. The selection of the observational or experimental subjects (patients or experimental animals, including controls) should be described clearly. The methods and the apparatus used should be identified and procedures described in sufficient details to allow other workers to reproduce the results and references to established methods. All drugs and chemicals used should be identified precisely, including generic names, doses, routes of administration. Results: These should be presented in a logical sequence in the text, tables and illustrations. Only important observations should be emphasized or summarized. Discussion: The author’s comments on the result, supported with contemporary references, including arguments and analysis of identical work done by others. Brief acknowledgement may be made at the end. Conclusion: Conclusion should be provided under separate heading and highlighting new aspects arising from the study. It should be in accordance with the study. Copyright: Material printed in this journal is the copyright of the publisher of Ophthalmic Newsnet/Ophthalmology Update and may not be reproduced without the permission of the editor/publisher. The publisher only accepts the original material for publication with the understanding that except for abstracts, no part of the data has yet been published or will be submitted for publication elsewhere before appearing in the journal. The Editorial Board makes every effort to ensure the accuracy and authenticity of the material printed in the journal. However, conclusions and statements expressed are the views of the authors and do not necessarily reflect the opinions of the Editorial Board. Publishing of advertising material does not imply an endorsement by the Ophthlmic Newsnet /Ophthalmology Update. Address for Correspondence: The Chief Editor, Ophthalmology Update, 267-A, St: 53, F-10/4, Islamabad, Pakistan. E-mail: [email protected]

Instructions to the Authors

Instructions to the authors

POSTGRADUATE DIARYprime.edu.pk/ophthalmology/2015/jan_mar_2015.pdf · 2015-08-06 · bolic pathway...

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Transcript of POSTGRADUATE DIARYprime.edu.pk/ophthalmology/2015/jan_mar_2015.pdf · 2015-08-06 · bolic pathway...