DOS_Nov_2007

as well as the ophthalmic and central retinal arteries, are • For NAION, underlying predisposing factor (diabetes,
compromised by an idiopathic infiltration of the vessels walls by hypertension, hyperlipidemia, smoking) should be
inflammatory macrophages, lymphocytes, and multinucleate giant investigated for and treated, if present to prevent bilateral
cells. As most arteries are affected in GCA, there usually is a involvement which can occur in about 33% cases.
constellation of systemic symptoms. Due to the widespread
involvement in GCA, there is a very high chance for involvement Optic Neuritis (Figure 5)
of the fellow eye within days, therefore requiring immediate
intervention, if suspected. Optic neuritis (ON) is defined as acute inflammation of the optic
nerve. When the inflammation involves the disc, it is termed as
Management papillitis. When it involves the posterior part of the optic nerve,
the fundus appears normal and it is termed as retrobulbar neuritis.
• Complete ocular and systemic history
Etiologies
• Erythrocyte sedimentation rate (ESR).
Elevated in arteritic AION, normal in NAION The most common etiology is demyelination, which can occur
with or without evidence of multiple sclerosis (MS). Others include:
• C - Reactive Protein (CRP)
Elevated in arteritic AION, normal in NAION • Infection (syphilis, mumps, measles).

• Temporal artery biopsy - To rule out GCA • Infiltrative/ inflammatory disease (sarcoidosis, lupus).

• In Arteritic AION, 1-2g I.V. methylprednisolone should be Optic Neuritis and Multiple Sclerosis
given for two to three days, followed by oral steroids for two
to four years to prevent progression of visual loss to the ON is the initial presenting feature in 20 to 25 percent of MS
other eye. patients and occurs in about 50% of cases of MS. About 35% to
75% of patients who present with ON go on to develop clinical

Figure 3. HT retinopathy. All B/L disc edema are not papilledema;
BP was 220/110 at presentation.

Figure 4. U/L pale disc edema.

www.dosonline.org 67

MS. Although long term studies from the Asian population are • Pulfrich's stereo phenomenon (beer barrel appearance of the
not available, the risk of progression to clinical MS appears to be environment)
low. The risk of developing MS increases steadily during the first
10 years after the initial presentation of ON. • Systemic signs and symptoms may include headache, nausea

Clinical features Management

The clinical presentation of demyelinating optic neuropathy varies. The currently accepted management is with intravenous
methylprednisolone sodium succinate 250 mg every 6 hours or 1
• Sudden onset, moderate-severe loss of vision, which can be gram every day for three days followed by oral prednisone (1 mg/
progressive for about 10-14 days which then stabilizes and kg per day) for 11 days as per the Optic Neuritis Treatment Trial
begins to improve. (ONTT). At our centre we routinely give intravenous
dexamethasone 200 mg every day for three days followed by oral
• Periocular eye eyeache, increasing on eye movements. taper.

• Dyschromatopsia. The aim of this treatment is for the purpose of accelerating visual
recovery only and it does not affect visual outcome after one year.
• Decreased brightness sense. The ONTT also determined that the use of oral prednisone in
routinely prescribed doses (1 mg/kg per day) alone for 14 days is
• Relative afferent pupillary defect in the involved eye. contraindicated, and was associated with increased risk of
reccurrence. Patients receiving this therapy had a higher rate of
• Visual field defects (could be of variable severity and type new attacks of ON in both the initially affected and fellow eye,
though frequently central / cecocentral). than did the group receiving intravenous steroids and placebo.

• Disc swelling with or without vitreous cells.

• Uhtoff 's sign (decreased vision with or without limb weakness Treatment with intravenous methylprednisolone followed by oral

following increasing body temperatures i.e., a hot bath or corticosteroid regimen also reduces the two-year risk of

exercise) development of clinical MS, particularly in patients with

• Romberg's sign (patient falls when they close their eyes), demyelinating lesions on MRI of the brain at the time of episode

Figure 5. Unilateral papillitis: hyperemic disc edema.
68 DOS Times - Vol. 13, No.4, October 2007

Workup of

of ON. Though serious side effects of dexamethasone or methyl- weeks. The term should not be used to describe optic disc swelling
prednisolone therapy are infrequent, monitoring during I/V with underlying infectious, infiltrative, or inflammatory etiologies.
administration is necessary. Prior to giving steroids, a chest X-ray
and proper clinical examination to rule out tuberculosis or any Pathophysiology
other focus of infection is necessary.
• Increase in cerebrospinal fluid (CSF) pressure
Papilledema (Figure 6)
• Increase in peri-neural pressure (transmitted) around the optic
Papilledema is an optic disc swelling that is secondary to elevated nerve sheath
intracranial pressure. In contrast to other causes of optic disc
swelling, vision usually is well preserved with acute papilledema. • Impediment of axoplasmic transport at the level of the lamina
Papilledema almost always presents as a bilateral phenomenon cribrosa
though may be asymmetrical and may develop over hours to
• Intra-axonal edema in the area of the optic disc

www.dosonline.org 69

Figure 6. Severe papilledema.

• Swelling of the optic nerve head • Narrow and sheathed vessels.

Papilledema occurs only if there is continuation of the subarachnoid • Peri-papillary pigmentary changes / choroidal folds.
space of the brain with the spaces around the optic nerve sheath.
Causes
Papilledema does not occur in eyes with pre-existing optic atrophy.
• Any tumors or space-occupying lesions of the CNS.
Clinical features
• Idiopathic intracranial hypertension (IIH).
• H/o nausea, vomiting, headache, nerve palsies etc.
• Usually bilateral. • Decreased CSF resorption (eg, venous sinus thrombosis,
• No significant visual function loss in the early stages. inflammatory processes, meningitis, subarachnoid
hemorrhage).

• Transient obscuration of vision. • Increased CSF production (tumors).
• Enlarged blind spots and peripheral field constriction. • Obstruction of the ventricular system.
• Diplopia due to VI nerve underaction. • Cerebral edema/encephalitis.
Early • Craniosynostosis.
Diagnostic techniques
• Hyperaemia, indistinct margins (lower pole first). • Hemogram.
• Blurring of peri-papillary retinal nerve fiber layer. • Chest X ray.
• Splinter haemorrhages in the peri-papillary region. • MRI .
• Absence of SVP ( absent in 20% of normals).
Established

• Obvious swelling, numerous haemorrhages. • CT Scan (non contrast and contrast enhanced).

• Engorged veins, obscuration of surface vessels. • Lumbar puncture.

• Paton's lines, cotton wool spots, macular fan or star. Management

Chronic Treatment of the underlying cause.

• Haemorrhages and exudates resolve. Management of Idiopathic intracranial hypertension (IIH):

• Disc has rounded appearance, milky gray colour. The treatment of IIH is initially medical.

• Obliteration of cup, NFL defects (slit like). • The cornerstone of medical treatment is weight loss.

Atrophic • Diuretics (Lasix, furosemide).

• Pale disc. • Diamox (acetazolamide) is the most commonly used
medication.

70 DOS Times - Vol. 13, No.4, October 2007

Not associated with any retinal haemorrhages, exudates, cotton
wool spots.

No peri-papillary nerve fiber layer edema, so the surface arteries
close to the disc are clearly visible

On FFA: may see autofluorescence at disc. No disc leak.

USG may show high spikes at disc even with low gain settings due
to presence of drusen.

Compressive optic neuropathies (Figure 8)

Figure 7. FA of case of pseudopapilledema Lesions in the orbit, optic canal and rarely intracranial lesions may
Note tortuous vessels, no disc leak. cause compressive swelling of the optic nerve head. Most cases
have significant and progressive visual loss, however some cases
may present only as disc swelling (orbital hemangiomas near disc
and nerve sheath meningiomas)

Clinical Features

• Transient monocular visual loss, in a particular gaze (direct
pressure of optic nerve or interruption of blood supply).

• Enlargement of blind spot on field analysis.

• RAPD and color vision abnormalities.

• Chronic compression leads to a triad of visual loss, swelling
evolving into atrophy and optociliary shunt (shunting the blood
from retina to choroid)

• Rarely optic disc swelling may occur in intracranial lesions eg.
Sphenoid wing meningioma.

• Features of orbital disease: proptosis, limitation of ocular
movements, orbital congestion.

Diagnosis

Figure 8. Thyriod exophthalmos: At risk compressive Ultrasound of the orbit.
optic neuropathy
Radio imaging (CT or MRI).
Surgical treatment
• Provide more information than USG
The surgical treatments currently used are optic nerve sheath
fenestration and lumbar shunting procedures. These procedures • CT useful for imaging of bones and metallic foreign body
are used when patients do not respond adequately to medical (MRI contraindicated).
therapy. Optic nerve sheath fenestration is done first by an incision
into the orbit. The eyeball is moved to the side and the optic nerve • MRI more useful in cases of inflammatory lesion and lesions
sheath is exposed. Slits or a large hole are then placed in the optic of optic pathway.
nerve sheath to drain out fluid, thereby taking pressure off the
optic nerve and halting pressure induced optic atrophy. • Fat subtraction technique and gadoliniuim - DTPA contrast
aid in demarcation of optic nerve sheath meningioma.
Pseudopapilledema (Figure 7)
Essential to rule out thyroid ophthalmopathy and pseudotumor.
Ophthalmoscopic features
Although disc edema may be due to a large number of causes, a
proper history, detailed systemic and ophthalmic examination and
a systemic approach can lead to the correct diagnosis in a large
number of cases, and avoid unnecessary and expensive
investigations in most.

Usually associated with hyperopia. First Author
Small disc, with absent physiological cup. Rohit Saxena MD
Abnormal branching and tortuosity of retinal vessels. No dilated
capillaries on surface of the disc.
Increased number of central retinal vessels arising from optic disc
Scalloped margins/ irregular disc surface or visible optic disc drusen.

www.dosonline.org 71

Congenital Midline Facial Swellings Photo Essay

Madhu Karna MS

Case 1 Answers

This 8 day old female baby had firm, non-tender bilateral bluish Case 1
swellings at birth accompanied by discharge. What is your
diagnosis? This is bilateral congenital dacryocele/ amniontocele/
dacryocystocele. If not infected, it is treated with warm compresses,
Case 2 massage and topical antibiotics. If infected it is treated with IV
antibiotics in addition. If unresolved within 2 weeks of medical
This 20 day old female baby had soft, non-tender bilateral pulsatile management, it is probed and irrigated.
swellings at birth. What is your diagnosis?

a

Figure 1. Congenital Dacryocele b
c

Figure 2a,b,c. Meningocoele

Case 2 (a,b,c)
This is bilateral encephalocele characterized by soft pulsatile swelling
above the medial canthal tendon. It is confirmed by MR imaging
and requires neurosurgical intervention. Rarely it is associated
with Morning Glory syndrome or dysplastic disc.

Figure 2. Meningocoele Author
Madhu Karna MS
Pediatric Ophthalmologist,
Centre for Sight, Safdarjung Enclave, New Delhi. 73

www.dosonline.org

Industry News Industry News

Noopur Gupta MS, DNB

NASA Approves Advanced Lasik for Use on Astronauts The Stellaris system offers greater performance, control and
versatility than its predecessors, with optimized cutting to deal
AMO’s Advanced CustomVue(TM) LASIK with the IntraLase® with even the hardest nuclei. The improved fluidics are increasingly
Method Proves Ready for the Rigors of Space TravelAdvanced important for chamber stability in both biaxial and micro-coaxial
Medical Optics, Inc. (AMO) (NYSE: EYE), a global leader in phaco. Surgical control is improved in the wide range of lens
ophthalmic surgical devices and eye care products, announced on opacities,” commented H. Burkhard Dick, M.D., Universitäts-
Sept. 21in California that the National Aeronautics and Space Augenklinik, Center for Vision Science, Ruhr University.
Agency (NASA) has approved the company’s LASIK technologies
for use on U.S. astronauts. The NASA decision was made following In addition to the Stellaris system, Bausch & Lomb showcased new
review of extensive military clinical data using AMO’s Advanced advancements in refractive surgery during ESCRS 2007, including:•
CustomVue(TM) LASIK with the IntraLase® Method, which Zyoptix® ACE™ Advanced Control Eyetracking technology. Zyoptix
showed the combination of technologies provides superior safety ACE is designed to further improve the accuracy and predictability
and vision.Approved for use on consumers almost a decade ago, of refractive surgery outcomes by dynamically compensating for
more than 11 million LASIK procedures have been performed to- intraoperative cyclotorsion (eye rotation).
date, making it the most-common elective surgical procedure in
the U.S. But it wasn’t until LASIK developed into an all-laser Seeing Machines Receives FDA Clearance for Truefield
procedure that NASA approved it for use on pilots, mission and Analyzer
payload specialists who face extreme, physically demanding
conditions in space. The all-laser LASIK technologies, which utilize Seeing Machines (AIM: SEE), a leading developer of advanced
wavefront guided and femtosecond lasers, have also been cleared computer based imaging software systems, received marketing
for U.S. military personnel, including most recently Air Force clearance from the United States Food and Drug Administration
pilots.NASA followed the Naval Aviation clinical studies closely (FDA) for its revolutionary new medical device, the TrueField(R)
with a particular interest in both safety and quality of vision under Analyzer (TFA). The TFA helps doctors measure defects in a
extreme conditions. Wavefront guided and femtosecond lasers patient’s visual field, a crucial step in the detection and management
were proven to provide excellent safety with consistent visual results of diseases of the vision system, including glaucoma. The TFA
of 20/20 or better. LASIK was able to withstand even the most offers many outstanding new benefits to both the patient and the
extreme rigors of warfare and flight. All surgical procedures have doctor. The systems work in real-time, enabling the behaviour of
risks, but with this exceptional track record, the average consumer subjects to be tracked in real-time Most importantly the device is
has nothing to fear from. both objective and it is quick and easy for the patient and operator.

Bausch & Lomb Launches the Stellaris™ Vision Unlike traditional standard automated perimetry (SAP) devices,
the TFA measures both eyes concurrently, and does the entire test
Enhancement System in Europe at ESCRS 2007 of both eyes in approximately 5 minutes (including rest breaks
within the test). The objectivity of the TFA test offers doctors the
The Stellaris system is the cornerstone of Bausch & Lomb’s possibility of significant improvements over the test-retest
microincision cataract surgery (MICS™) platform, to which variability issues that impact SAP. For patients it means an end to
ophthalmologists around the world are transitioning. Delivering the button pressing associated with SAP - the only task required of
safety, efficiency and ease-of-use, the system is ideal for all the patient in the TFA test is simply to look at the display.
techniques, particularly 1.8 mm biaxial (B-MICS) and 1.8 mm
coaxial (C-MICS) procedures. The TrueField Analyzer(R) offers a new objective method to help
doctors diagnose and manage a range of eye diseases including
The Stellaris EQ™ fluidics management technology allows surgeons glaucoma, age related macular degeneration and diabetic
to choose either a flow-vacuum module (AFM) or an advanced retinopathy. It has the potential to become a new standard in the
vacuum module (AVM). Using the flow based module, surgeons measurement of visual field defects and thus in the diagnosis and
can switch between flow and vacuum modes for optimal surgical management of glaucoma.
flexibility and efficiency. The inherent safety of the Stellaris system
stems from the novel EQ technology, which balances aspiration
dynamics in flow and vacuum modes for exceptional chamber
stability. A new ergonomically-designed, six-crystal phaco
handpiece, Bluetooth wireless-enabled dual-linear foot pedal, and
high-definition touch-screen display have been designed to address
the demanding needs of today’s surgical environments.

Dr. Rajendra Prasad Centre for Ophthalmic Sciences, 75
All India Institute of Medical Sciences, New Delhi

www.dosonline.org

Association between cultures of contact lens and corneal scraping in Abstracts

contact lens related microbial keratitis

Das S, Sheorey H, Taylor HR, Vajpayee RB.

Centre for Eye Research Australia, University of Melbourne, Melbourne, Australia.

OBJECTIVE

To study the association between cultures of contact lens and corneal scraping in contact lens-related microbial keratitis.

METHODS

A retrospective analysis of the culture results of corneal scrapings and contact lenses of patients with contact lens-related microbial
keratitis who were initially seen at Royal Victorian Eye and Ear Hospital, Melbourne, Australia, between January 1, 2001, and December
31, 2004, was conducted. RESULTS: Fifty eye specimens of 49 patients were included in the study. Corneal scrapings and contact lenses
were culture positive in 17 eyes (34%) and in 35 eyes (70%), respectively. In 13 eyes, corneal scrapings and contact lenses yielded identical
organisms. Serratia marcescens was the most common organism isolated from the corneal scrapings and from the contact lenses.

CONCLUSION

Contact lens culture may sometimes give a clue to the organism involved in cases of microbial keratitis in which the corneal scraping is
culture negative and may help in choosing the appropriate antimicrobial therapy.

Application of Shape-based Analysis Methods to OCT Retinal Nerve

Fiber Layer Data in Glaucoma

Gunvant, Pinakin BS Optom, PhD, FAAO, Zheng, Yufeng PhD, Essock, Edward A. PhD, Parikh, Rajul S. MS, Prabakaran,
Selvaraj BS Optom, Babu, Jonnadula Ganesh BS Optom, Shekar, Garudadri Chandra MD, Thomas, Ravi MD

Journal of Glaucoma. 16(6):543-548, September 2007.

PURPOSE

To evaluate the performance of shape-based analysis [wavelet-Fourier analysis (WFA) and fast Fourier analysis (FFA)] applied to
retinal nerve fiber layer (RNFL) thickness values obtained from the optical coherence tomograph (OCT) to discriminate healthy and
glaucomatous eyes.

To compare the performance of the shape-based metrics to that of the standard OCT output measures (Inferior Average and Average
Thickness).

METHODS

RNFL values were obtained from 152 eyes of 152 individuals (83 healthy and 69 “mild”-stage perimetric glaucoma). WFA and FFA were
performed on the RNFL values and linear discriminant functions for both were obtained using Fisher linear discriminant analysis.
Performance was evaluated by calculating sensitivity, specificity, and area under the receiver operating characteristic (ROC) curve (ROC
area).

RESULTS

The ROC area of the shape-based methods [0.94 (WFA) and 0.88 (FFA)] was greater than that of OCT metrics [0.81 (Inferior Average)
and 0.74 (Average Thickness)]. Specifically, WFAs performance was significantly better than both the FFA (P=0.009) and the Inferior
Average (P=0.001). Inferior average performed significantly better than Average Thickness (P=0.006).

CONCLUSIONS

The ability to differentiate glaucomatous from healthy eyes using stratus OCT measurements is improved by using these analysis
methods that emphasize the shape of the RNFL thickness pattern.

www.dosonline.org 77

Low-Dose Mitomycin C as a Prophylaxis for Corneal
Haze in Myopic Surface Ablation

Ivey Thorntona,b, Ashok Puric, Meng Xud and Ronald R. Kruegera
aCole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio
bDepartment of Ophthalmology and Visual Sciences, University of Louisville, Louisville, Kentucky
cRajasthan Laser Eye Center, Jaipur, India
dDepartment of Quantitative Health Sciences, Cleveland Clinic Foundation, Cleveland, Ohio (M.X.)

PURPOSE
To evaluate the efficacy of low-dose (0.002%) mitomycin C (MMC) vs no prophylactic MMC (control) in reducing corneal haze after
surface laser ablation.
DESIGN
Two-year retrospective follow-up study performed in Jaipur, India.
METHODS
Ninety-two eyes with no MMC application and 83 eyes with 0.002% MMC application during laser epithelial keratomileusis (LASEK)
were analyzed in a retrospective chart review with one month, two months, three months, six months, one year, and two years of
postoperative follow-up. Postoperative haze, visual acuity, and efficacy ratio (EFFR) then were analyzed statistically.
RESULTS
The no-dose MMC and low-dose MMC groups were statistically similar except for a thinner corneal pachymetry (P < .001), higher
spherical equivalent error (P = .006), and smaller ablation zone (P = .009) in eyes not treated with MMC when subjected to univariate
analysis. Multivariate analysis was used to overcome the preoperative statistical differences among the two groups. Eyes treated with
low-dose MMC (0.002%) demonstrated statistically less haze at all postoperative time points and in each myopic subgroup (P < .001).
The postoperative uncorrected visual acuity (UCVA) and EFFR, however, showed no difference between the groups, except for better
EFFR with MMC at one month (P < .001) and two months (P = .034).
CONCLUSIONS
Low-dose MMC (0.002%) in eyes after LASEK results in less corneal haze than in eyes not receiving this agent. Concerns regarding the
potential toxicity of MMC make a 10-fold less concentration more desirable in refractive surgery. Further comparative study of low- vs
higher-dose MMC is recommended to characterize its clinical benefit fully.

78 DOS Times - Vol. 13, No.4, October 2007

Ophthalmoplegia: Looking Beyond the Obvious Clinical Meeting: Case 1

Sandeep Buttan MS, Suma Ganesh MS, Manish Sharma MS, Archana Gupta DNB

Ophthalmoplegia or anomalies of ocular movements may Three weeks after the IV IG therapy, the patient had recovered
present in a variety of settings and may have coexisting some vertical movements and was prescribed horizontal prisms
complex neurological features that often have no obvious relation. for diplopia. At last follow up (5 months) the patient has full
recovery of ocular movements with no diplopia (Figure 4).
To form a clinical diagnosis from these quanta’s of information is
like putting together the pieces of a jigsaw puzzle. A keen sense of Discussion
suspicion and a thorough neurological workup, keeping in mind
both the common and the not so common differentials are essential The patient is a young male who presents with acute progressive
to reach the right diagnosis. bilateral ophthalmoplegia unassociated with head or eye pain.
Examination reveals bilaterally symmetric limitation of both
Case History horizontal and vertical eye movements. Additional features include
bilateral ptosis, facial paresis and diminished deep tendon reflexes.
A 39-year-old non-Diabetic, normotensive male presented to us
with sudden onset diplopia since one day. The diplopia was The first question to address is whether this constellation of
horizontal and constant and not associated with ocular or facial findings could be the result of a single lesion.
pain. He also complained of paraesthesiae in his hands and mild
weakness of lower limbs off and on for past 3-4 days. There was In evaluating any patient with acquired ophthalmoparesis, one
no history of any headache, dysarthria, dysphagia, hearing must consider three main etiologies: myopathic, neuromuscular,
disturbances, bowel / bladder involvement, fever or upper and neurologic. In this patient, the presence of hyporeflexia (a
respiratory infection in the recent past. lower motor neuron sign), with normal strength eliminate most
of the myopathic and a neuromuscular etiology. The evaluation
On ophthalmic examination there was esotropia of left eye with should therefore focus on a neurologic cause. (Table 1)
limitation of abduction. There was horizontal uncrossed diplopia
with maximum separation of images in levoversion. Hess charting Supranuclear gaze palsy
also revealed left lateral rectus underaction and right medial rectus
overaction. (Figure 1) The pupils were symmetrical and well reacting A structural lesion extensive enough to impair both horizontal
with no RAPD. Posterior segment examination was unremarkable. and vertical gaze would of necessity cause a variety of other
MRI brain showed no abnormalities. neurologic deficits. Even multifocal brainstem disease, such as
brainstem encephalitis, would likely cause additional motor and
Three days later the patient developed ptosis of both eyelids, more sensory deficits as well as more severe changes in sensorium. It is
so in the left eye. There was gross limitation of all ocular hard to imagine a single intraxial lesion that could produce a bilateral
movements. The pupils were symmetrical and briskly reactive. generalized ophthalmoplegia, and hyporeflexia. Such a lesion would
(Figure 2,3) have to extend from the mesencephalon to the pons and involve
the corticospinal and cerebellar tracts as well and would leave the
The patient was referred to a neuro- physician for detailed patient much more neurologically impaired than he is.
neurological evaluation. The deep tendon reflexes were diminished
with normal motor power in all limbs. A provisional diagnosis of
Myasthenia Gravis was made and the patient was put on Tab.
Pyridostigmine 60 mg QID for 5 days but no clinical or subjective
improvement was noticed.

One week later, the patient developed facial weakness on the left
side with deviation of the angle of mouth. The patient was admitted
for investigations. The routine hematological and blood
biochemistry tests were within normal limits. Nerve conduction
velocity test was suggestive of facial demyelination and repetitive
nerve stimulation was negative. MRI thorax and Acetyl
cholinesterase antibodies were also negative. CSF analysis showed
elevated proteins (65.6 mg/dl) with near normal WBCs (7 / mm3)

A clinical diagnosis of Miller Fisher syndrome was made and the Figure 1: Hess Charting (Day 1) Smaller
patient was put on intravenous immunoglobulin (IV IG) therapy OS chart, OS under action of LR,
for five days. OD medial rectus overaction

Dr. Shroff's Charity Eye Hospital,
5027 Kedarnath Road, Daryaganj, New Delhi

www.dosonline.org 81

Figure 2. (Day 3), Bilateral Ptosis, Gross Table 1: (Acute ophthalmoplegia)
limitation of eye movements
Causes of Acute Bilateral Ophthalmoplegia
• Myasthenia gravis
• Pituitary apoplexy
• Demyelinating disease
• Miller Fisher syndrome
• Brainstem ischemia or hemorrhage
• Botulism
• Diphtheria
• Whipple's disease
• Wernicke's encephalopathy

Myasthenia Gravis

Multiple cranial nerve palsy A more likely cause of acute weakness with this pattern is disease
of the neuromuscular junction. Myasthenia could certainly present
The next cause to consider is multiple cranial nerve palsies. A with acute onset of painless, bilateral, symmetric ophthalmoplegia
process involving cranial nerves III, IV, and VI bilaterally would with ptosis, and it would fit some of the clinical features of this
cause horizontal and vertical ophthalmoplegia that could involve case. Myasthenia gravis should always be considered in a patient
lids and pupils. Several pathologic processes may sometimes with an external ophthalmoplegia; however, as noted above, the
involve both cavernous sinuses and, thus, could produce such a presence of hyporeflexia and absence of fatigability in this patient
clinical picture. Examples include intracavernous carotid makes a diagnosis of myasthenia gravis untenable. Various neuro-
aneurysms, dural-cavernous fistulas, cavernous sinus thrombosis, physiological tests like repetitive nerve stimulation test and single-
and large skull-base tumors. A negative Neuroimaging and fibre electromyography (SFEMG) are also helpful for confirmation
presence of lower motor neuron signs make these highly unlikely. of the diagnosis.

Figure 3. (Day 3), Gross limitation of all extra ocular movements
82 DOS Times - Vol. 13, No.4, October 2007

Figure 4. (5 months), Total recovery of extra ocular movements

Botulism Miller Fisher syndrome

Another condition that affects the neuromuscular junction, causing Miller Fisher syndrome (MFS) is one of a spectrum of acute
similar manifestations is botulism. Symptoms of food-borne demyelinating inflammatory polyneuropathies, which include
botulism usually begin 12 to 36 hours after ingestion of Guillain – Barré syndrome, acute ophthalmoplegia and
contaminated food and include weakness, lassitude, and decreased Bickerstaff ’s encephalitis. Originally described by Miller Fisher
lacrimation and salivation. (1956), MFS is a triad of ataxia, areflexia, and ophthalmoplegia.

Toxins elaborated by the organism Clostridium botulinum impair The male/female ratio is 2:1, with a mean age of 43.6 years at the
neuromuscular transmission by interfering with the release of onset of the disease. A viral infection which is seen preceding the
acetylcholine at the presynaptic side of the neuromuscular junction. neurological symptoms in 71.8% of the cases ,2,3 was not present in
The neuro-ophthalmologic findings typically include our case.
ophthalmoplegia and ptosis.
Diplopia is the presenting feature in 38.6% cases, with the remainder
This patient did not have any gastroenteritis, there is also no presenting with only ataxia (20.6%) or with both symptoms
evidence of generalized proximal motor weakness, and his pupils simultaneously.1, 2 The disease progresses over five to ten days,
are not dilated and non-reactive, findings that typically occur with sometimes up to three weeks. External ophthalmoplegia begins
botulism. Although ophthalmoplegia is prominent, bulbar and relatively symmetrically and most patients progress to have
extremity weakness are also characteristic and their absence speaks complete immobilization of the globes.
against botulism as the cause.
Additional features consistent with a peripheral neuropathy
Wernicke’s encephalopathy including paraesthesiae (50%), oropharyngeal weakness (26%), or
bi-facial weakness (32%). Bladder dysfunction (16%) or more
In 1881, Carl Wernicke described a syndrome primarily found in widespread dysautonomia is occasionally seen.2, 3
alcoholics characterized by nystagmus usually preceding complete
or incomplete ophthalmoplegia, gait ataxia, and mental confusion The diagnosis of MFS is still descriptive, depending on the
that may develop acutely or subacutely. Many of these patients presentation of the triad of MFS. Although, almost half of the
are hyporeflexic. Although most patients with the so-called cases are not the pure syndrome, it is important to emphasize that
Wernicke syndrome have significant mental confusion, the diagnosis of MFS should be considered in any patient who
confabulation, or amnesia, in which case the condition is called the develops an acute ophthalmoparesis with or without either ataxia
Wernicke-Korsakoff syndrome. Although Wernicke syndrome is or hyporeflexia, or even acute onset of either ataxia or areflexia
typically associated with a nutritional deficiency of thiamine and without ophthalmoplegia.3
usually found in alcoholics, it can also occur in patients on fad diets
or under other circumstances. Cranial nerves other than the oculomotor nerve may be involved
in more than half of the cases (56 .9%), most commonly the facial
Wernicke syndrome is a medical emergency with 17% mortality if nerve (45.7%) followed by IX and X (39.9%), and XII (13%). 4
left untreated and, once suspected, requires the immediate
administration of thiamine. Recovery of neurologic deficits can be CSF examination may show an elevated protein value with a normal
dramatic, often with improvement of the ocular motor cell count. A tetrasyaloganglioside (GQ1b) antibody in patient
abnormalities within hours following the administration of serum may give clues in the diagnosis of MFS variants .Due to the
thiamine. As there is no evidence that this patient has a history of linkage between this antibody and MFS, especially
alcohol abuse or was on a fad or starvation diet, this diagnosis was ophthalmoplegia; it may prove a highly sensitive and specific clinical
excluded.

www.dosonline.org 83

marker for the diagnosis of typical and atypical MFS. It would also diagnosis of MFS, and therefore the diagnosis needs to be
differentiate MFS ophthalmoplegia from ophthalmoplegia of other established with the combination of serologic studies, CSF, and
causes. GQ1b antibody is supportive but not essential for the clinical electrophysiology. The authors present this case to highlight the
diagnosis of MFS.3, 5 existence of this acute neurological illness with a relatively benign
course if recognized and managed appropriately.
Because of the relative scarcity of MFS, it is usually incorporated
with GBS in the evaluation of therapy. The treatment options are References
steroids, plasma exchange (PE) and intravenous immunoglobulin
(IVIG).3 1. Berlit P, Rakicky J.The Miller Fisher syndrome. Review of the literature.
J Clin Neuroophthalmol 1992; 12:57-63
Prognosis is good with recovery after a mean of 10 weeks, 2, 3
although as in the present case the total recovery may be delayed 2. Mori M, Kuwabara S, Fukutake T, Yuki N, Hattori T. Clinical features
up to several months. Prisms may be prescribed in the meantime and prognosis of Miller Fisher syndrome. Neurology. 2001 Apr 24;
for the diplopia. Most patients show a complete remission without 56(8): 1104-6.
any residual symptoms.
3. LI Haifeng. Miller Fisher syndrome: toward a more comprehensive
In summary, the importance of recognizing the significance of the understanding. Chinese Medical Journal, 2001, Vol. 114 No. 3 :
triad of acute ophthalmoparesis, ataxia, and hyporeflexia, especially 235-239
following either a gastroenteritis or upper respiratory infection,
greatly limits the differential diagnosis. As discussed above, 4. Michael S. Vaphiades, DO, The Double Vision Decision Surv
ophthalmoparesis without ataxia or areflexia does not eliminate a Ophthalmol 48 (1) January–February 2003

5. M Odaka, N Yuki, K Hirata Anti-GQ1b IgG antibody syndrome:
clinical and immunological range J Neurol Neurosurg Psychiatry
2001; 70:50-55 (January)

First Author
Sandeep Bhuttan MS

84 DOS Times - Vol. 13, No.4, October 2007

Bevacizumab (Avastin) in the Management of Clinical Meeting: Case 2
Neovascular Glaucoma

Suneeta Dubey MS, M.Agarwal MS, Monica Gandhi MS, Gaurav Sood MS, A.Pandey MS, Julie Pegu MS

Neovascular glaucoma (NVG) is defined as rubeosis irides with visual acuity was perception of light with accurate projection in her
secondary angle closure glaucoma1 and is characterized by right eye and 6/36 in her left eye. Florid neovascularization of iris
widespread retinal ischemia most commonly associated with (INV) extended from pupillary margin to angle in her right eye
anterior segment neovascularization and subsequent raised with 270 degrees of synechial angle closure (Figure 1,2a, 2b). The
intraocular pressure (IOP). The increased IOP is often difficult to pupil was central, round and fixed with ectropion uveae involving
control and frequently results in loss of vision.2 Prompt diagnosis more than 270 degrees (Weiss and Gold classification grade-4).4
and treatment of the underlying etiology is essential. There are Dense cataract obscured visualization of the vitreous, optic nerve,
two key aspects to the management of NVG: namely, treatment of and retina. Fluorescein angiography of the iris (IFA) revealed
the underlying disease process responsible for rubeosis and marked leakage from rubeotic vessels (Figure 3). There was no iris
treatment of the increased IOP. The standard treatment for NVG neovascularization in the patient’s left eye, the ocular media were
includes retinal photocoagulation and cyclodestructive or drainage clear and there was evidence of prior panretinal photocoagulation.
procedures. Studies have shown that iris neovascularization (INV) The patient’s IOPs were 48 mm Hg in the right eye and 12 mm Hg
is highly correlated with retinal ischemia which stimulates the
production of vascular endothelial growth factor (VEGF), a key
molecule in ocular neovascularization.3 Direct targeting of VEGF
might be another possible therapeutic strategy to treat
neovascularization

Case Report

A 60 year old female presented to us in October 2006 with a ten-
month history of gradual decrease of vision, which was more in
her right eye . She had a 30- year history of diabetes with coexisting
hypertension. The patient had undergone panretinal
photocoagulation bilaterally in 2003 for proliferative diabetic
retinopathy. She had also undergone vitrectomy in her right eye in
2004 and cataract surgery in her left eye in 2005. The patient’s

Figure 2a. Extensive PAS of the
angle 270 Degrees

Figure 1. Extensive NVI – Grade IV Figure 2b. Neovascularization
(Weiss & Gold Classification) of inferior angle

Dr. Shroff's Charity Eye Hospital, 87
5027 Kedarnath Road, Daryaganj, New Delhi

www.dosonline.org

Figure 3. Extensive Leakage from INV on Figure 5. Post Phaco trabeculectomy
iris fluorescein angiography

phacotrabeculectomy with MMC (0.4 mg for 2 minutes) ( Figure5).
Additional laser photocoagulation was performed two weeks after
the surgery for the anterior non ablated retina. At the most recent
follow-up (16 weeks after the injection), best corrected visual acuity
was 6/24, the IOP was 16.0 mm Hg with no clinically evident
rubeosis.

Discussion

Figure 4. Regression of INV post avastin The visual prognosis and control of neovascular glaucoma still
injection on Iris fluorescein angiography remains a challenge despite many advances. Although PRP is
considered the standard treatment of retinal ischaemia, the best
alternative method is still undetermined. Consideration of visual
potential is also important. If there is no useful vision, the goal of
therapy becomes patient comfort and the management protocol
may differ. In conditions precluding PRP due to media opacities,
other modalities should be considered including pan-retinal
cryotherapy, and trans-scleral diode laser retinopexy.2

in the left eye. An ultrasound B-scan performed on her right eye If NVG follows its natural course to the angle closure glaucoma
demonstrated that the retina was attached, and there were multiple stage, medical therapy usually becomes ineffective and surgical
dot opacities in vitreous suggestive of vitreous hemorrhage. intervention is required. It is a general belief that standard filtering
procedures in eyes with NVG are rarely successful primarily
The patient was immediately started on medical management. because of the high risk of intraoperative bleeding and post
Topical steroids, cycloplegics and anti-glaucoma drugs in the form operative progression of the neovascular membrane. Therefore
of tab acetazolamide 250 mg (QID), timolol 0.5% (BID) and there is a need to achieve complete regression of neovascularization
brimonidine 0.2% eye drops (BID) were started. The patient was in order to have a better outcome of the surgical procedure.
offered an off-label intravitreal and intracameral injection of
Bevacizumab (Avastin; Genentech, San Francisco, California). After Advances in the understanding of the angiogenic process have led
discussion of the risks and benefits of the treatment, the patient to the development of compounds that are approved for the
signed consent for the off-label use of injection. The Injection was treatment of neovascularization. Bevacizumab is a humanized
given in a dose of 1.25 mg in 0.05 ml intravitreally and 0.25 mg in recombinant antibody that binds all isoforms of VEGF-A and its
0.02 ml Intracamerally. It was given under topical anesthesia under off label use has been reported by a few authors to be of benefit in
aseptic conditions. The injection was well tolerated without regression of iris and retinal neovascularization. Cases of intraocular
observed side effects. At a follow-up examination 5 days later, the inflammation after intravitreal bevacizumab were low, suggesting
visual acuity of her right eye was perception of light with accurate that intravitreal bevacizumab seems safe over the short term.
projection of rays with an IOP of 20.0 mm Hg on maximal tolerable
medical therapy for glaucoma. Slit-lamp examination revealed It’s role has also been evaluated in patients with NVG. In a case
dramatic regression of the previously visible rubeotic vessels, and series of six patients of CRVO with NVG reported by Iliev et al 5,
IFA showed substantial reduction in iris neovascularization with Intravitreal Bevacizumab (IVB) resulted in a marked regression of
minimal leakage (Figure 4). Three weeks after the bevacizumab anterior segment neovascularization and relief of symptoms within
injection, the patient underwent an uncomplicated 48 hours with no side effects. Similarly, Avery 6 has reported a
single case of regression of retinal and iris neovascularization, due
to PDR, one week after IVB without any observed side effects.

88 DOS Times - Vol. 13, No.4, October 2007

Paula et al 7 also have a single case report with positive results of References
IVB. Davidorf et al 8 have described a one-eyed patient with PDR
and NVG who showed rapid improvement of rubeosis irides from 1. Chen KH, Wu CC, Roy S, Lee SM, Liu JH. Increased interleukin-6
a single bevacizumab injection. This patient subsequently in aqueous humor of neovascular glaucoma. Invest Ophthalmol Vis
underwent a remarkably routine trabeculectomy three weeks after Sci. 1999 Oct;40(11):2627-32.
the IVB without any hemorrhage leading the authors to conclude
that anti – VEGF therapy may have application in the preoperative 2. Sivak-Callcott JA, O’Day DM, Gass JD, Tsai JC. Evidence-based
preparation of trabeculectomy for NVG. In a series of three recommendations for the diagnosis and treatment of neovascular
patients with NVG reported by Mason et al, 9 IVB resulted in total glaucoma.Ophthalmology. 2001 Oct;108(10):1767-76
regression of INV with control of IOP surgically in one case and
medically in two cases. The tube drainage surgery done in one 3. Oshima Y, Sakaguchi H, Gomi F, Tano Y. Regression of iris
case was without bleeding complications resulting in less operative neovascularization after intravitreal injection of bevacizumab in
time and quicker recovery for the patient. patients with proliferative diabetic retinopathy.Am J Ophthalmol.
2006 Jul;142(1):155-8.
Although the optimal approach for management of NVG
4. Weiss DI, Gold D. Neofibrovascularization of iris and anterior
can only be determined chamber angle: a clinical classification. Ann Ophthalmol. 1978
Apr;10(4):488-91.
through future research, IVB might be able to open a therapeutic
window for PRP and also surgical intervention for IOP control can 5. Iliev ME, Domig D, Wolf-Schnurrbursch U, Wolf S, Sarra GM.
be performed in a quieter eye with less operative time, decreased Intravitreal bevacizumab (Avastin) in the treatment of neovascular
risk of hemorrhage and quicker recovery. PRP takes time to achieve glaucoma. Am J Ophthalmol. 2006 Dec;142(6):1054-6.
regression of INV and alone it does not achieve complete success
in halting INV in every patient. Literature suggests that IVB is well 6. Avery RL. Regression of retinal and iris neovascularization after
tolerated and might be an emergent treatment of choice for INV intravitreal bevacizumab (Avastin) treatment. Retina. 2006
that is poorly responsive to conventionally approved treatments. Mar;26(3):352-4.
Also, IVB may be an advantageous treatment option rather than
PRP, especially in eyes with fundus- obscuring cataract or vitreous 7. Silva Paula J, Jorge R, Alves Costa R, Rodrigues Mde L, Scott IU.Short-
hemorrhage. term results of intravitreal bevacizumab (Avastin) on anterior segment
neovascularization in neovascular glaucoma. Acta Ophthalmol
In conclusion, injection Bevacizumab shows promise as an adjunct Scand. 2006 Aug;84(4):556-7.
in the treatment of refractory NVG. How long this regression will
persist is unknown, but even a transient effect could be of benefit 8. Davidorf FH, Mouser JG, Derick RJ. Rapid improvement of rubeosis
as a surgical adjuvant in the preoperative preparation of filtering iridis from a single bevacizumab (Avastin) injection. Retina. 2006
surgery for NVG. However, randomized case control studies are Mar;26(3):354-6.
necessary to evaluate the long term effectiveness and safety of
IVB for wide spread use in the management of NVG. 9. Mason JO 3rd, Albert MA Jr, Mays A, Vail R. Regression of
neovascular iris vessels by intravitreal injection of bevacizumab.
Retina. 2006 Sep; 26(7):839-41.

First Author
Suneeta Dubey MS

www.dosonline.org 89

Determining Progression of Glaucoma on Perimetry Clinical Meeting: Clinical Talk

Gaurav Sood MS, Suneeta Dubey MS, Monica Gandhi MS, Julie Pegu MS

Primary open angle glaucoma is a chronic, progressive optic Strategies for judging progression on perimeter (White on
neuropathy characterized by morphological changes at the White Perimetry)
optic nerve head and retinal nerve fibre layer in the absence of
other ocular disease or congenital anomalies(with or without raised • Clinical judgment- overview
IOP)
• Defect classification system by various landmark studies-
Why We Want To Know Progression? AGIS, CIGTS, EMGT

The important tool for treatment in primary open-angle glaucoma • Box plot
(POAG) is a documented progression of glaucomatous optic
neuropathy (GON). Retinal ganglion cell loss is a continuous • Event analysis- GPA
physiological process. But in glaucoma, this loss is exaggerated. So
knowing progression at the earliest can help to modify treatment • Trend analysis-Progressor
strategies and the new target intraocular pressure (IOP) can be
set. Overview

The ganglion cell loss can be monitored structurally as well as Overview presents all the single field analysis examinations of up
functionally. Structural changes can be assessed by optic nerve to 16 tests on a single page for comparison. But, the most important
head evaluation using stereophotography or newer machines like thing to know is that it does not give any additional information
HRT, GDx, OCT whereas functional changes can be judged by over the single field analysis printout.
perimetry.
Overview printout showing stable fields over 3 years
Perimetry in Progression
Fluctuation
Although structural damage can usually be detected in simple
glaucoma before functional damage, evaluation of a longitudinal If an abnormality is found, it needs to be confirmed on repeated
series of visual fields remains one of the most frequently used visual field examination. But worsening of fields is not always
methods to detect early evidence of glaucoma and to observe progression. There exists Test-Retest Variability in Perimetry called
patients. The perimetry methods are used to chart the course of
disease in patients with glaucoma, wherein progressive visual field
loss is taken to reflect the worsening of the disease and is therefore
usually regarded as a strong indication that the treatment regimen
should be intensified (therapeutic impact).

Figure 1. Ganglion cell loss in a normal individual Figure 2. Overview printout showing
and in a patient with Glaucoma stable fields over 3 years

Dr. Shroff's Charity Eye Hospital, 91
5027 Kedarnath Road, Daryaganj, New Delhi

www.dosonline.org

Figure 3. Short term fluctuation measurement
at 10 points in Humphrey machine

Figure 4. Box plot

fluctuation. Also abnormal and peripheral points fluctuate more.
Always remember to follow patient by same strategy (SITA
Standard or Full threshold)

Fluctuation can be of two types

Short term fluctuation

This is intra -test variability.Visual field variability increases in and
around a scotoma. Short-term fluctuation (STF) represents the
average of the local scatter over the entire visual field.Values greater
than > +2.00 db are usually abnormal.

Short term fluctuation measurement at 10 points in Humphrey
machine

Long term fluctuation Figure 5. Findings of Box Plot

It is a reversible, physiological variation of visual field thresholds Suggested criteria for visual field defect progression
over two or more examinations, which is exclusive of reproducible For a new defect in a previous normal area
deterioration, improvement or artifacts.

(Hodapp et al, clinical decision in glaucoma 1993, Eugs 2003)

First step is to establish a baseline visual field for further A cluster of three or more non edge points, each of which declines?
follow up tests 5db compared to baseline on two consecutive fields or

• What will not form baseline? A single non edge point that declines ? 10 db compared to baseline
• Learning curve on two consecutive fields
• High false positive
• High false negative Deepening of a preexisting defect
• Rim artifacts
• Small pupil A cluster of three non-edge points, each of which declines >10 db
• Clover leaf deformity compared to baseline on two consecutive fields.
• Scotomas d/t congenital anomalies
• Wrong prescription How is technology helping us?

Box plot

The box plot is a modified histogram of the threshold values. It is
based on total deviation numerical plot. The box represents the
range of deviation for the middle 70% of points (sd).Upper tail
represents the range of the 15% best points. Lower tail represents
the range of the 15% worst points.

92 DOS Times - Vol. 13, No.4, October 2007

Figure 6. GPA single-page summary printout Figure 8. Legend for Progressor

What are important deductions from Box Plot? Two-tests are averaged to establish a baseline, and up to 14 follow-
up tests may be compared to averaged thresholds of 2 baseline
Same shape as normal but graph at a lower point = depression in exams
height.
GPA single-page summary printout
Bottom of box same positioned, elongating tail = localized loss/
scotomas deepening. GPA Symbols

Event analysis (GPA) • A single solid dot indicates a point not changing by a significant
amount.
Event analysis uses the first few visual fields in a series as a baseline,
then compares subsequent visual fields to that baseline to • A small open triangle identifies degree of deterioration that is
determine whether change has occurred. significant at the 5%level (p<0.05).

Event analysis is implemented in the glaucoma progression analysis • A half filled triangle indicates deterioration at that point in 2
(GPA) software for the humphrey field analyzer. It is based upon consecutive tests.
significance limits for test-retest variability on pattern deviation. It
helps accurately identify clinically significant progression of visual • A solid triangle indicates deterioration at that point in 3
field loss in glaucoma patients. It is compatible with consecutive tests.

• Sita standard • An X signifies that the point is out of range for analysis.

• Sita fast GPA Alert

• Full-threshold tests (only for baseline) Possible progression: same 3 or more points show deterioration
in at least 2 consecutive tests.
Requisites for GPA
Likely progression: same 3 or more points show deterioration in
Minimum of three tests required: two baseline and 1 follow-up at least 3 consecutive tests.
exam

Figure 7. Image of Grey Scale printout on Progressor

www.dosonline.org 93

Trend analysis Defect Classification System developed by different landmark
studies are complex and not very practical to use.
Trend analysis measures the rate of change of the visual field and
the statistical significance of that rate. Measurement may be made To conclude,Visual fields is still considered to be the gold standard
for each test point (pointwise linear regression [PLR]) or on a in the diagnosis and management of glaucoma. It is a cost effective
cluster basis. and easily available means to judge progression and it's parameters
can be helpful to modify therapy in glaucoma.
Trend analysis is implemented in the Progressor software
(Moorfields eye hospital/ medisoft ltd.). References

Progressor is a trend analysis for identifying progression in serial 1. Properties of Perimetric Threshold Estimates from Full Threshold,

visual software package which analyses visual field progression SITA Standard, and SITA Fast Strategies Paul H. Artes et al IOVS.

using point wise linear regression of sensitivity on time. 2002;43:2654-2659.

Image of Grey Scale printout on Progressor 2. Lee AC, Sample PA, Blumenthal EZ, Berry C, Zangwill L, Weinreb
RN. Infrequent confirmation of visual field progression.

The image indicates the significance of change for each point tested Ophthalmology. 2002;109(6):1059-65.

in the visual fields. Each bar represents a Humphrey field analyser 3. Fitzke et al, analysis of vf progression in glaucoma Br. J.
test. The length of the bars indicate the amount of change in visual
Ophthalmology 1996 80; 40-48.

field sensitivities. 4. Wilkins MR, Fitzke FW, Khaw PT. Pointwise linear progression

The legend provides the color key for the significance of change, criteria and the detection of visual field change in a glaucoma trial.

where a positive slope indicates improvement, a negative slope Eye. 2006; 20(1):98-106 Anderson's perimetry.

deterioration and grey indicates no change.

First Author
Gaurav Sood

94 DOS Times - Vol. 13, No.4, October 2007

DOS Quiz Columns

Anagram Time

Each of the following words is a jumbled ophthalmic or related term. There is, however, an extra letter in every set of letters. These
extra letters will also form a eight letter ophthalmic word when unjumbled.

So get cracking.

1. MIGOALO ___ ___ ___ ___ ___ ___ ____

2. SPOOKIA ___ ___ ___ ___ ___ ___ ____

3. MEANOMALY ___ ___ ___ ___ ___ ___ ___ ___ ____

4. GREATMOTA ___ ___ ___ ___ ___ ___ ___ ___ ____

5. KEANULIME ___ ___ ___ ___ ___ ___ ___ ___ ____

6. OEPRIMALMOLD ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ____

7. RAAMBETIONSTOOL ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ____

8. BARAOMOOCHSYMCARD ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ____

Answers on page number 103 Saurabh Sawhney DO, DNB Ashima Aggarwal MS, DNB
Insight Eye Clinic, New Delhi

Dr. Shroff’s Charity Eye Hospital

Presents an

“Update on Retinopathy of Pre-maturity (ROP)”

At
Gulmohar Hall, India Habitat Center, 13th January’ 2008, 9am-5pm.

Faculty
Dr. Lingam Gopal – Sankara Nethralaya, Chennai.
Dr. R.V. Azad – R.P. Center, AIIMS, Delhi.
Dr. Subhadra Jalali – LVPEI, Hyderabad
Dr. Mahesh P Shanmugam – Retina Clinic, Bangalore
Dr. Mangat Dogra – PGI, Chandigarh
Dr. Arvind Taneja & Dr.Manish Malik – Max Hospital, Delhi.

Dr. Anand Subramanyam – Wockhardt Hospital, Mumbai

Dr. Manisha Agarwal Dr. Nishant Taneja

Organizing Secretary Co-organizing Secretary

For Registration Contact: Mr. A. K. Singh
Dr. Shroff’s Charity Eye Hospital
5027, Kedar Nath Road, Daryaganj
Delhi-110002
Email: [email protected]
Ph: 9811009434, 011-41564319

www.dosonline.org 99

Journal of Current Glaucoma Practice with DVD

Publisher : Jaypee Brothers Medical Publishers (P) Ltd.

Chief Editors: Dr Tanuj Dada (Glaucoma Service, RP Centre for Ophthalmic Sciences,AIIMS, New Delhi)
Prof. Kuldev Singh (Director Glaucoma Service - Stanford University, USA)
Prof. Roger Hitchings (Moorefield Eye Hospital - London, UK)

Delhi), Sushmita Kaushik (PGIMER, Chandigarh), P Sathyan
(Aravind eye hospital, Madurai)

This is the world's first international review journal
incorporating a video DVD. The journal publishes invited
review articles from top glaucoma experts worldwide and
also includes diagnostic and surgical videos in the DVD.

The journal covers each subspeciality of glaucoma including :
basic and clinical research, epidemiology, biostatistics, genetics,
pathophysiology, laboratory methods, clinical examination,
perimetry, new structural and functional tests, anterior
segment imaging, ocular blood flow, pediatric glaucoma, angle
closure glaucoma, open angle glaucoma, secondary glaucoma,
medical management, laser therapy, glaucoma and combined
cataract glaucoma -surgical techniques, neuroprotection,
health economics, quality of life and visual rehabilitation.

The journal has a unique video section in the DVD which
show-cases basic and advanced glaucoma surgical techniques,
management of complications, includes diagnostic techniques
and video assisted instruction courses and lectures.

Senior Editorial Advisors : Anders Heijl (Sweden),Erik Greve The first issue covers epidemiology of angle closure glaucoma
(Netherland), George Spaeth (USA), Graham Trope (Canada), (David Friedman), the glaucoma vaccine (Michal Schwartz),
Ivan Goldberg (Australia), Michael Belkin (Israel), Paul importance of disc size (Robert Ritch), anterior segment
Kaufman (USA), Paul Palmberg (USA), Ravi Thomas (India), imaging (Jovina See), Ab interno Trabeculotomy (Don
Robert Weinreb (USA), Sohan Singh Hayreh (USA), Yoshiaka Minckler) and many others. The DVD includes non-
Kitzawa (Japan) penetrating surgery (Andre Mermoud), surgical caveats for
implanting Ahmed glaucoma Valve (Lama-Al-Aswad), repair
Associate Editors: Dr Ronnie George (Sankara Netralaya, of cyclodialysis cleft (Peter Shah), managing an overhanging
Chennai), Dr Jovina See (National University Hospital, bleb (Arun Narayanaswamy) etc etc.
Singapore), Rajul Parikh (LV Prasad Eye Institute, Hyderabad)
and Robert Campbell (University of Toronto, Canada) This new journal serves as a unique teaching resource for all
ophthalmologists and especially for trainee surgeons and
Managing Editor: Dr Ritu Gadia (RP Centre, AIIMS, New glaucomatologists.

The combination of practical knowledge provided by the
experts combined with video assisted teaching offers an
excellent learning experience for the reader. It helps the reader
by updating knowledge on current practice and recent
advances in the field of glaucoma, and at the same time
provides an opportunity to learn new surgical skills and
improve existing surgical standards.

For details contact:
[email protected] [email protected]

www.jaypeebrothers.com

www.dosonline.org 101

Forthcoming Events : National

November 2007 December 2007
3-4 DHANBAD, JHARKHAND 7-9 KOLKATA, WEST BENGAL

22nd Easter India Zonal Ophthalmic Congress 17th Annual Conference of Glaucoma Society of India
(EIZOC) & 5th Jharkhand Ophthalmological Society Contact Person & Address
(JOS) Conference “EYEFEST-007” Dr. Chandrima Paul
Contact Person & Address B.B. Eye Foundation
Dr. B.N. Gupta, Organising Secretary 2/5, Sarat Bose Road, Sukhsagar
Navjyoti Netralaya & Research, 1st & 2nd Floors, Kolkata-700020
Joraphatak Road, Dhanbad, JHARKHAND Ph: 033-24746608, 24748816
Ph.: 0326-2306030 (R), 2305055 (C) Email: [email protected]
(M): 09431121030, 09431726030, 09334018182
E-mail: [email protected] 14-16 HYDERABAD, ANDHRA PRADESH
Annual Meeting of
17-18 NEW DELHI the Oculoplastic Association of India
Midterm Conference of Contact Person & Address:
Delhi Ophthalmological Soceity Dr. Milind Naik, Dr. Santosh G Honavar
Contact Person & Address LV Prasad Eye Institute
Dr. Namrata Sharma LV Prasad Marg, Banjara Hills,
Room No. 474, 4th Floor, Hyderabad 500034
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, Website: http://www.opai.in,
All India Institute of Medical Sciences, E-mail: [email protected],
Ansari Nagar, New Delhi – 110029
Ph.: 011-65705229, Fax: 26588919 22nd NEW DELHI
E-mail: [email protected], Website: www.dosonline.org Clinical Meeting of Madan Mohan Cornea Society
on “Surgical Management of Corneal Disorders”
23-25 KERALA Contact Person & Address:
34th Annual Conference of Dr. Rishi Mohan, Joint Secretary
Kerala Society of Ophthalmic Surgeons 29, Link Road, Room No. 106, Lajpat Nagar-III,
Contact Person & Address New Delhi - 110 924
Dr. Anup Chirayath Ph.: 29847800/7900, Fax: 29847600,
Ahalia Foundation Eye Hospital Email:[email protected]
Near Kanalpirivu, Walayar, Palakkad, Kerala
Ph: 04923-235999, Tele-Fax: 235900, Cell: 9447774439 23-24 NEW DELHI
Email: [email protected] Workshop "Knowbology- know your machine"
Contact Person & Address:
30 Nov., 1-2 Dec. BAREILLY, U.P. Prof. Kirti Singh, Organizing Secretary
Annual Conference of Mob. 09968225285 or
U.P. State Ophthalmological Society E-mail: [email protected].
Contact Person & Address
Dr. Kapil Agarwal January 2008
B-39/B, Rajendra Nagar 13th NOIDA, U.P.
Bareilly-243122 (U.P.) Ph: 2442592, 2455353
3rd Annual Conference of Noida
December 2007 Ophthalmological Society
1-2 HYDERABAD, ANDHRA PRADESH Contact Person & Address:
Dr. Mohita Sharma
International Pediatric Ophthalmology Symposium Tripati Eye Centre
Contact Person & Address: C-8, Sector-19, Noida-201301 (U.P.)
Dr. K. Ramesh Ph.: 0120-4266642, 2444349 (M): 9810045425
Pediatric Ophthalmology, Strabismus & E-mail: [email protected]
Neuro-Ophthalmology Website: www.nos2004.org
L.V. Prasad Eye Institute
L.V. Prasad Marg, Banjara Hills
Hyderabad - 500 034 A.P. INDIA
Tel : +91-40-30612 644/ 345, Fax : +91-40-2354 827
Email : [email protected], Web : www.lvpei.org

102 DOS Times - Vol. 13, No.4, October 2007

Forthcoming Events : International

October, 2007 May, 2008
13-17 VIENNA, AUSTRIA 21-24 JAPAN

20th ECNP Congress 18th International Visual Field &
VIENNA, AUSTRIA Imaging Symposium (IPS2008)
Tel: +31 20 504 0200 / Fax: +31 20 504 0225 Nara, Japan
Email: [email protected] Contact: Chota Matsumoto
Phone: 81-72-366-0221 ext 3335
24-27 TAMPA, FLORIDA Fax: 81-72-368-2559
American Academy of Optometry Meeting E-Mail: [email protected]
Tampa Florida
http://www.aaopt.org/meetings 28-31 BELGIUM

November, 2007 XI International Orthoptic Congress 2008
10-13 NEW ORLEANS, UNITED STATES ANTWERP, BELGIUM
Contact: Daisy Godts
American Academy of Ophthalmology 2007 Tel: +32 3 8214845 / Fax: +32 3 8251926
Annual Meeting Email: [email protected]
New Orleans , Province: LA (United States) Web: www.ioacongress2008.org
Contact: American Academy of Ophthalmology,
P.O. Box 7424 San Francisco, CA 94120-7424 June, 2008
Phone: 415-561-8500, Fax: 415-561-8533 19-22 WURZBURG, GERMANY
E-Mail: [email protected]
21st Annual Congress of
December, 2007 the German Retina Society/
1-5 CALIFORNIA 8th Symposium of Intl Society
of Ocular Trauma,
25th Annual Meeting of the American Society of Main Topic: Ocular Trauma
Retina Specialists Wurzburg, Germany
Palm Springs area, city of Indian Wells, California. http://www.retinologie.de
Tel: (914) 722-0664, Fax: (914) 722-0465
[email protected] July, 2008
7-10 MONTREAL, CANADA
March, 2008
28 Mar. - 2 Apr. HUNGARY 9th International Conference on Low Vision
Rehabilitation - Vision 2008
7th International Symposium on Ocular Montreal, Province: QC (Canada)
Pharmacology and Therapeutics Contact: Beatrice Laham
Budapest, Hungary Phone: 514-906-1979, Fax: 514-395-1801
Contact: Robert Nesbitt E-Mail: [email protected]
Phone: 44-229-080-488
Fax: 44-227-322-850 September, 2008
E-Mail: [email protected] 5-6 NEW DELHI, INDIA

April, 2008 Biennial Meeting SAARC Academy
12-16 CHICAGO of Ophthalmology
India Habitat Centre,
ASCRS/ASOA Symposium and Congress New Delhi
CHICAGO, IL, USA Contact: Dr. Namrata Sharma
Contact: ASCRS Phone: 011-26589810
Tel: +1 703 591 2220 E-Mail: [email protected]
Fax: +1 703 591 0614
Web: www.ascrs.org

Answer Quiz No. 4

Extra Word: ONCOLOGY

4. TERATOMA 7. RETINOBLASTOMA 6. DERMOLIPOMA 1. GLIOMA
8. RHABDOMYOSARCOMA 5. LEUKEMIA
3. MELANOMA 2. KAPOSI

www.dosonline.org 103

Delhi Ophthalmological Society

(LIFE MEMBERSHIP FORM)

Name (In Block Letters) ___________________________________________________________________________
S/D/W/o _____________________________________________________________ Date of Birth _____________
Qualifications __________________________________________________________ Registration No. __________
Sub Speciality (if any) ____________________________________________________________________________
ADDRESS

Clinic/Hospital/Practice _______________________________________________________________________
________________________________________________________________ Phone __________________
Residence _________________________________________________________________________________
________________________________________________________________ Phone __________________
Correspondence ____________________________________________________________________________
________________________________________________________________ Phone __________________
Email ___________________________________________________________ Fax No. _________________
Proposed by
Dr. _____________________________________ Membership No. ________ Signature ___________________
Seconded by
Dr. _____________________________________ Membership No. ________ Signature ___________________
[Must submit a photocopy of the MBBS/MD/DO & State Medical Council / MCI Certificate for our records.]

I agree to become a life member of the Delhi Ophthalmological Society and shall abide by the Rules and
Regulations of the Society.
(Please Note : Life membership fee Rs. 3100/- payable by DD for outstation members. Local Cheques acceptable, payable
to Delhi Ophthalmological Society)
Please find enclosed Rs.___________in words ____________________________________________________ by Cash
Cheque/DD No.____________________ Dated_____________ Drawn on______________________________________

Three specimen signatures for I.D. Card. Signature of Applicant
with Date

FOR OFFICIAL USE ONLY

Dr._______________________________________________________________has been admitted as Life Member of

the Delhi Ophthalmological Society by the General Body in their meeting held on________________________________

His/her membership No. is _______________. Fee received by Cash/Cheque/DD No._______________ dated_________

drawn on __________________________________________________________________.

(Secretary DOS)

www.dosonline.org 105

INSTRUCTIONS

1. The Society reserve all rights to accepts or reject the application.

2. No reasons shall be given for any application rejected by the Society.

3. No application for membership will be accepted unless it is complete in all respects and accompanied by a Demand Draft of Rs.
3100/- in favour of “Delhi Ophthalmological Society” payable at New Delhi.

4. Every new member is entitled to received Society’s Bulletin (DOS Times) and Annual proceedings of the Society free.

5. Every new member will initially be admitted provisionally and shall be deemed to have become a full member only after formal
ratification by the General Body and issue of Ratification order by the Society. Only then he or she will be eligible to vote, or apply
for any Fellowship/Award, propose or contest for any election of the Society.

6. Application for the membership along with the Bank Draft for the membership fee should be addressed to Dr. Namrata Sharma,
Secretary, Delhi Ophthalmological Society, R.No. 474, 4th Floor, Dr. R.P. Centre for Ophthalmic Sciences, AIIMS, Ansari Nagar,
New Delhi - 110 029.

7. Licence Size Coloured Photograph is to be pasted on the form in the space provided and two Stamp/ Licence Size Coloured
photographs are required to be sent along with this form for issue of Laminated Photo Identity Card (to be issued only after the
Membership ratification).

Situation Vacant

Muzaffarpur Eye Hospital, the only eye hospital of Bihar
with 151 indoor beds and all modern and sophisticated
equipments, treating over 1,60,000 outdoor eye patients
and performing over 18,000 surgeries annually, needs
suitable candidates for the following posts.

1. Chief Medical Officer : 1 Post (Ms/DNB with
minimum 10 years
experience)

2. Ophthalmologist : 1 Post (Retina & Vitreous
Specialist)

3. Ophthalmologist : 3 Post (MS/DNB)

4. Hospital Administrator : 1 post (Degree Hospital
Management)

The posts are non-practicing and they carry competitive
salaries, furnished/semi furnished accommodation and
other incentives.
Interested candidates should send their resume to:-

The Secretary,

Muzaffarpur Eye Hospital

Juran Chapra, Road No. 2,
Muzaffarpur - 842001

E-mail to:- [email protected]

Mob. No.: 09334910514

106 DOS Times - Vol. 13, No.4, October 2007

DOS Credit Rating System (DCRS)

DOS has always been in the forefront of efforts to ensure that its members remain abreast with the latest developments in
Ophthalmology. Among the important objectives formulated by the founders of our constitution was the cultivation and promotion
of the Science of Ophthalmology in Delhi.

The rapid strides in skills and knowledge have created a need for an extremely intensive Continuing Medical Education programme.

In a bid to strengthen our efforts in this direction DOS had DOS Credit Rating System (DCRS), the details of which are given below.
Our Primary objective is to promote value-based knowledge and skills in Ophthalmology for our members and give recognition and
credit for efforts made by individual members to achieve standards of academic excellence in Ophthalmic Practice.

DOS CREDIT RATING SYSTEM (DCRS)

1) Attending Monthly Clinical Meeting* † (For full attendence) DCRS Max.
2) Making Case Presentation at Monthly Meeting** 10 90
3) Delivering a Clinical Talk at Monthly Meeting** 10 10
4) Free Paper Presentation at Annual Conference (To Presenter)** 10 10
5) Speaker/Instructor** in : Monthly Symposium 10 20
10 10
: Mid Term Symposium 15 10
: Annual Conference 15 30
6) Registered Delegate at Mid Term DOS Conference 10 10
7) Registered Delegate at Annual DOS Conference 10 10
8) Full Article publication in Delhi Journal of Ophthalmology/DOS Times 15 45
9) Letter to editor in DOS Times 5 10
10) Letter to editor in DJO 5 10
11) > 3 Bonus points for Monthy Clinical Meeting: 10 bonus points — —
12) > 5 Bonus points for Monthy Clinical Meeting: 30 bonus points — —
13) All Monthly Clinical Meeting: 50 Bonus Points — —

If any of the presentations is given an Award – attendance at its meeting is higher (i.e. more than the average

Additional 20 bonus Credits. attendance of the eight monthly meetings).

Member who have earned 100 Credits, are entitled * Based on Signature in DCAC
** Subject to Submission of Full Text to Secretary, DOS
a) Certificate of Academic Excellence in Ophthalmic † Credits will be reduced in case attendance is only for part of
b) Eligible for DOS Travel fellowship for attending the meeting.

conference. DCRS !! Attention !!
If any member earns 200 Credits, he/she shall, in addition to
above, be awarded Certificate of Distinguished Resource- * Members are requited to sign on monthly meeting
Teacher of the Society. attendance register and put their membership number.

Institutional assessment for best performance will be based * The DCRS paper will be issued only after the valid signature
on the total score of members who attend divided by number of the member in the attendance register.
of members who attended. Institutional assessment regarding
decision to retain the institute for the next year will be based * Please submit your DCRS papers to the designated DOS
on total score. Staff only.

Please note that the Institutions’ grading increases if the * The collected DCRS papers will be countersigned by
President and Secretary and sealed immediately after the
meeting is over.

www.dosonline.org 107

Proceeding Protocol for Monthly Clinical Meetings

1. The Host (usually the ophthalmic chief of the Hosting Institution) will welcome the DOS and request the President
and Secretary of the DOS to come to the Dais and start the Meeting.

2. The President and the Secretary will take up their seats on the side of the Dais, which is opposite to the Lectern.
(They would continue to be in the same position through out the Meeting, including the Mini Symposium.) The
Chairman of the Symposium will be invited to a Third seat next to the President on the same table, after the ‘Clini-
cal Talk’. The Speakers, who if they form a Panel would be seated on the same side as the Lectern.

3. The President will declare the Meeting open.

4. The President and the Secretary will then conduct the meeting.

5. The case presentations (2 in no.) will form the first part of the clinical meeting. Each presenter will be allotted 10
min. time for his/her presentation. This will be followed by discussion with the audience on both the cases (Total
time allotted is 15 min.). The case presentation will be followed by a Clinical Talk of 15 min. duration. This will be
followed by discussion with the audience on the topic for 10 min.

6. After the first part of the meeting is over, the President will introduce the subject of the Mini Symposium (which will
be of 1 hour duration) and invite the Chairperson of the Symposium to the Dais to conduct the Symposium. All the
speakers may be invited to assume their seats on the Dais at this time or one by one after they have presented their
Talks (at the discretion of the chair person of the symposium).

7. After the Symposium is over, the President will thank the Speakers and the Chair person and request Secretary to
make any Announcements, including the Prizes etc.

8. By the time, the Clinical Meeting is to be declared closed by the President, the Host or his representative would be
at the Lectern to (take the floor immediately after the Meeting is closed) thank people, firms who had helped him
in hosting the Meeting and invite the Members of the DOS for Refreshments.

9. Venue : The monthly clinical meeting will definitely be held in the premises of the allotted institution.

10. Day : The meeting shall be held on the last Saturday / Sunday of the month, whichever the institution deems fea-
sible.

11. Presenter : The presenting faculty / resident / fellows should be from the same institute for clinical case presenta-
tions and the clinical talk.

12. One person will be allowed only one-presentation for the award-wining session in the same academic year.

13. Exchange of dates : In case two institutions want to exchange the date of the meeting, it can be done with mutual
agreement by the heads of the department and with information to the secretary’s office, well in advance.

14. Mini Symposium : It shall be organized by the institution but other DOS members can be invited to participate, if
required. There should not be more than 3 speakers in the mini symposium.

15. To qualify for the retention in the monthly meeting calendar, a minimum attendance of 70 members is required
(inclusive of the members of the host institute).

16. For the Best Clinical Meeting award i.e. Bodhraj Sabharwal Trophy, the overall assessment of the meeting will be
made purely on the overall marks by outside delegates and for Dr. Minoo Shroff Trophy the award will be given to
the most popular meeting (based on total attendance including outside and inside delegates as per the attendance
register).

17. The attendance will be marked in the register which will be at a separate counter and will be managed by the DOS
Staff. At the close of the clinical meeting, the attendance register will be signed by the Secretary and the President on
the same day.

18. Meetings in the month of May and June may be opened from the next year (2008) if there are applications for the
same.

19. No alcoholic drinks will be served during or after the meeting; only refreshments / snacks/ lunch will be served.

108 DOS Times - Vol. 13, No.4, October 2007

Tearsheet

www.dosonline.org 109

110 DOS Times - Vol. 13, No.4, October 2007