dos_mar_2014

Miscellaneous

it is a very uncommon association. Table 1 illustrates fasting blood glucose levels, urine for reducing sugars after
the syndromes commonly associated with cataracts and a feed, red blood cell transferase and galactokinase levels
systemic malignancies. and TORCH titres. Investigations are usually not required
Pediatric cataract and intrauterine infections in the case of unilateral cataracts.
Maternally transmitted intrauterine infections may result With a careful history and meticulous evaluation of the eye
in congenital cataracts. The incidence of intrauterine and other organ systems it is always possible to achieve
infection induced cataract is less than 1% in developed an etiological diagnosis in a case of pediatric cataract. This
countries which has been significantly lowered due to the not only allows for visual recovery of the child but also
introduction of the rubella vaccine in 19871. However helps in identifying concurrent disorders. An appropriate
it is still common in India with around 25% of infants and timely referral to a pediatrician is warranted in all cases
having congenital rubella associated cataracts4. The most with systemic involvement before the surgical removal of
common causative infections are known by the acronym the cataract is planned. Even after treatment of the cataract
TORCHS for toxoplasmosis, rubella, cytomegalovirus, these children may require long term follow up and
herpes simplex and syphilis. Routine testing of all bilateral multisystem rehabilitation.
cataracts for TORCHS is classically taught but has an References
extremely low yield without a history of maternal fever/
rash during pregnancy or systemic clinical indicators in the 1. Rahi JS, Dezateux C, British Congenital Interest Group. Congenital
child such as microcephaly, hearing loss, developmental and Infantile Cataract in the United Kingdom: Underlying or
delay, thrombocytopenia, hepatosplenomegaly or skin associated factors. Invest Ophthalmol Vis Sci 2000;41:2108-14.
abnormalities.
Investigations 2. Michael Eckstein, P Vijayalakshmi, Milind Killedar, Clare Gilbert,
The investigations should be directed towards the suspected Allen Foster. Aetiology of childhood cataract in south India. Br J
systemic syndrome. In the absence of any obvious hereditary Ophthalmol 1996;80:628-32.
etiology all infants with bilateral congenital cataracts
should undergo serum calcium and phosphorus levels, 3. Haargaard B, Wohlfahrt J, Fledelius HC, Rosenberg T, Melbye M.
A nationwide Danish study of 1027 cases of congenital/ infantile
cataract. Ophthalmol 2004; 111:2292-8.

4. Evaluation of pediatric cataracts and systemic disorders Anya A.
Trumler Curr Opin Ophthalmol 22:365–379.

64 l DOS Times - Vol. 19, No. 9 March, 2014

EvoElvuoltuitoionn

Evolution of Anti-Microbials

Hemant Kamble
MD

Hemant Kamble MD

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

Antimicrobials is a general term for natural or synthetic was patented by Lloyd Conover, which became the most
compounds which at certain concentrations inhibit prescribed broad spectrum antibiotic in the United States.
growth of or kill micro-organisms. Bacterias were identified In 1957 Nystatin was patented and used to cure many
as early as 1670s by van Leeuwenhoek, after his invention disfiguring and disabling fungal infections.
of microscope. However it was only in the ninteenth Fluroquinolones
century that there link with the disease were appreciated. In 1963, during chloroquine synthesis Nalidixic acid was
The search for antibiotics began in the late 1800s, with discovered and was noted to have antibacterial properties.
the growing acceptance of the germ theory of disease, a But it was found to be excreted too quickly to have any
theory which linked bacteria and other microbes to the significant systemic antibacterial effects. Fluorinating the
causation of a variety of ailments. As a result, scientists quinolones solved this problem and fluoroquinolones were
began to devote time to searching for drugs that would formed. These compounds had far greater antibacterial
kill these disease-causing bacteria. An early advocate of a activity, therapeutic blood levels, and low toxicity.
‘germ theory of disease’ was the Edinburgh surgeon Lister. Second- and third-generation fluoroquinolones
In 1871, he began researching on the phenomenon that Ciprofloxacin and Ofloxacin are second generation
urine contaminated with mould would not allow growth fluoroquinolones, which have broadspectrum coverage
of bacterias. against gram-positive and gram- negative bacteria. They
By 1910, Ehrlich had successfully developed the first example were initially used to treat corneal and conjunctival
of a purely synthetic antimicrobial drug, Salvarsan. It proved infections; however, they have also gained wide
effective against trypanosomiasis and the spirochaete disease acceptance in the prophylaxis of bacterial endophthalmitis
of syphilis. In 1928, Sir Alexander Fleming observed that
colonies of the bacterium Staphylococcus aureus could be Sir Alexander Fleming
destroyed by the mold Penicillium notatum, demonstrating
antibacterial properties. In the early 1930s, Domagk found
a chemical named Prontosil. It was safe enough to be used
therapeutically and constituted the first clinically useful
chemotherapeutic agent for bacterial infections. Later, it
was discovered that prontosil was hydrolyzed in vivo to
release SULFANILAMIDE, the active ingredient. Thus,
prontosil was a Prodrug. Though Sir Alexander Fleming
had discovered penicillin in 1928, it was not until 1940s
that an effective way of isolating it was discovered by
Howard Florey and Ernst Chain. Fleming, Florey, and
Chain shared the 1945 Nobel Prize for medicine for their
work on penicillin.
In 1943, American microbiologist Selman Waksman made
the drug streptomycin from soil bacteria, the first of a new
class of drugs called aminoglycosides. In 1955, Tetracycline

www. dosonline.org l 65

Evolution

after intraocular surgery. Ciprofloxacin, was approved in converted into acyclovir and has a bioavailability three to
1990 and is a solution of ciprofloxacin 0.3% with 0.006% five times greater than acyclovir. Famciclovir is a prodrug
BAK as a preservative and a pH of 4.5. Ofloxacin, contains of penciclovir that has also been shown to be as efficacious
ofloxacin 0.3% and 0.005% BAK and has a pH of 6.41. as valacyclovir in treatment of HZV.
Levofloxacin, the l-isomer of ofloxacin, is considered a Valganciclovir was approved by the FDA in 2001 and
third-generation fluoroquinolone. It was FDA approved in has supplanted ganciclovir in the oral treatment of
2000 and has a higher solubility at neutral pH, allowing for cytomegalovirus (CMV) retinitis. Valganciclovir is a prodrug
a higher concentration of medication, 0.5%. It has a pH of and is rapidly converted to ganciclovir when administered
6.5 and is preserved with 0.005% BAK2. orally. Oral bioavailability is high (approximately 60%),
and a 900-mg dose provides serum levels equivalent to a
Fourth-generation fluoroquinolones 5-mg/kg dose of intravenous ganciclovir.
Moxifloxacin and Gatifloxacin, were approved by the US
Food and Drug Administration in 2003. The former is Antifungals
moxifloxacin 0.5% with a pH of 6.8 and contains boric acid The first report of antifungal property of azole compound,
but no BAK. The latter is gatifloxacin 0.3% with a pH of 6 benzimidazole, was described in 1944 by Woolley. In
and 0.005% BAK. The older fluoroquinolones had more the late 1960s, three new antifungals were introduced,
affinity for topoisomerase II (DNA gyrase), an enzyme more Clotrimazole developed by Bayer Ag and Miconazole and
important in gram-negative bacteria. With the addition of a Econazole, both developed by Janssen Pharmaceutica. In
methoxy group on carbon 8, the newer fluoroquinolones 1981, the FDA approved the systemic use of Ketoconazole,
bind more effectively to topoisomerase II and IV, giving an imidazole derivative synthesised and developed b
these medications better clinical efficacy against gram- Janssen Pharmaceutica. For over a decade it was the
positive organisms. only available oral antifungal drug. Fluconazole, a broad
spectrum antifungal triazole was approved for use in early
Oxazolidinone antibiotics 1990. It was developed by Pfizer. It could be given both
In 2000, linezolid became the first antibiotic, in a new orally as well as intravenously. Itraconazole, also abroad
class of drugs called oxazolidinones, to be FDA approved. spectrum antifungal triazole was approved by FDA in 1992.
It binds to the 50S ribosomal subunit and inhibit bacterial In 2002, Voriconazole was approved by the FDA for the
protein synthesis. It is available for oral or intravenous use treatment of invasive aspergillosis and Fusarium species
and is active primarily against gram-positive bacteria but in patients intolerant or refractory to other treatments.
has minimal activity against gram-negative bacteria. It is a triazole antifungal agent, a synthetic derivative
of fluconazole, and is available in oral and intravenous
Streptogramin antibiotics preparations.
Quinupristin-dalfopristin, which received FDA approval in Posaconazole is a triazole antifungal agent, approved by
1999. They bind sequentially to separate sites on the 50S FDA in September 2006. It blocks the synthesis of ergosterol,
ribosome, thus inhibiting protein synthesis3. Individually, a key component of the fungal cell membrane, through
they have only modest antibacterial activity. When dosed the inhibition of the enzyme lanosterol 14a-demethylase
together in a fixed 30:70 weight-to-weight ratio, however, and accumulation of methylated sterol precursors. It
a synergistic effect creates an antimicrobial activity 8 to 16 is specifically indicated for the prophylaxis of invasive
times greater than the components alone. Aspergillus and Candida infections in subjects, 13 years of
age and older, who are at high risk of developing these
Antivirals infections due to being severely immunocompromised.
Acyclovir is the ‘‘gold standard’’ for the treatment and Recently posaconazole has been FDA approved for
prophylaxis of herpes simplex virus and herpes zoster virus intravenous use also.
infections. It was originally synthesized in 1974 by Howard Ravuconazole is a triazole structurally related to fluconazole
Schaeffer at Welcome Research Laboratories. Acyclovir got and voriconazole. It is being developed by Bristol-Myers
FDA approval and was released commercially in 1982. Squibb for oral use. It is currently in Phase II clinical trials
Initially available as topical ointment, oral formulation
became available in 1985. Valacyclovir is a prodrug of References
acyclovir. It was initially approved by the FDA in June
1995 for the treatment of herpes zoster (shingles). In 1. Rhee MK, Kowalski RP, Romanowski EG, et al. A laboratory
December 1995 the FDA approved this drug for the evaluation of antibiotic therapy for ciprofloxacin-resistant
treatment of recurrent herpes genitalis and then for the Pseudomonas aeruginosa. Am J Ophthalmol 2004;138(2):226– 30
treatment of initial infections of herpes genitalis in October
1996. Maintenance (suppressive) use of valacyclovir for 2. Rhee D, Rappuano CJ, Weisbecker CA, et al. Physicians’ desk
herpes genitalis was approved in September 1997. Its use reference for ophthalmic medicines, vol. 32. Montvale, NJ7
for herpes labialis was approved in September 2002. After Thomson PDR; 2004. p. v
oral administration, it is rapidly and almost completely
3. Aguilar HE, Meredith TA, Shaarawy A, et al. Vitreous cavity
penetration of ceftazidime after intravenous administration. Retina
1995;15(2):154– 9

66 l DOS Times - Vol. 19, No. 9 March, 2014

Common Ophthalmic PG PCGoCronrneer
Emergencies
Vineet Seghal
MD

Vineet Sehgal MD1 Tarun Arora MD2, Vijay Kumar Sharma MS2

1. Centre For Sight Safdarjung, New Delhi
2. Dr. Rajendra Prasad Centre for Ophthalmic Sciences,

All India Institute of Medical Sciences, New Delhi

Aproper diagnosis in emergency leads to optimal absolute provides an arterial pO2 of 1000-1200 mm Hg,
management of the ocular condition, relieving the resulting in a 3 - fold increase in oxygen diffusion distance
patient of its symptoms and salvaging the eye in certain through ischemic retinal tissues. Ocular massage has also
scenarios. It is of paramount importance to be able to been described however none of the above treatment alter
recognize the clinical signs and to deliver the timely the natural history of disease definitively.
intervention and at the same time not compromise eye Chemical Burns
care at expense of speed. Hence we highlight certain very Presentation: Presentation varies from patient to patient and
common ocular emergencies with their symptoms, signs depends upon the nature of chemical, amount and duration
and appropriate treatment. of exposure and delay in bringing to the casuality room.
Central Retinal Artery Occlusion Patient can present with excessive watering, photophobia,
Presentation: Sudden, painless, loss of vision in one eye. redness, pain and swelling of eyelids and adjoining skin.
Some patients may reveal transient loss of vision lasting Examination: A thorough physical examination should
seconds to minutes. Mean age of presentation is 60 years
and males are more affected then females. Patient may have Figure 1: Central Retinal Artery Occlusion
history of temporal arteritis, hypertension, atrial fibrillation
and coagulopathies.
Clinical Appearance: The main findings during the
examination CRAO are retinal opacity in the posterior pole,
cherry-red spot, box-carring , retinal arterial attenuation,
and optic disk edema and pallor (Figure 1). Intra-arterial
emboli are also observed in few patients. Carotid
Doppler evaluation identify carotid vascular plaques and
hemodynamically significant obstruction. Only a few
patients of CRAOs present with simultaneous bilateral
onset.
Emergency Management: Immediate lowering of
intraocular pressure includes acetazolamide 500 mg IV or
500mg PO once. Carbogen therapy (5% CO2, 95% O2):
CO2 dilates retinal arterioles, and O2 increases oxygen
delivery to ischemic tissues. Perform for 10 minutes every
2 hours for 48 hours. Hyperbaric oxygen therapy (HBOT)
may be beneficial if begun within 2-12 hours of symptom
onset. Inhalation of 100% oxygen at 2 atmospheric

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PG Corner

Figure 2: Chemical injury Figure 3: Open globe injury

be done after eye is affected eye is irrigated copiously, Adequate lubricating eye drops hourly, ascorbate and
and the pH of the ocular surface is neutralized. Topical therapeutic bandage contact lens are used over corneal
anesthetic drops may be used to aid in patient comfort and surface3. Controlling inflammation- Citrate both promotes
cooperation. After irrigation, a thorough eye examination corneal wound healing and inhibits PMNs via calcium
is performed with special attention given to clarity and chelation. Acetylcysteine also inhibits collagenase to
integrity of the cornea, degree of limbal ischemia, and IOP. reduce corneal ulceration. Topical steroids should be used
Double eversion of eyelids should be undertaken if possible very carefully as it can both decrease inflammation and
to wash any chemical residue. Particles in the conjunctival hasten corneal melting, acting as double edged sword4
fornices are more common with particulate injuries, such Preventing infection - Prophylactic topical antibiotics are
as plaster. Corneal epithelial damage can range from mild warranted during the initial treatment stages5. Controlling
diffuse punctate epithelial keratitis (PEK) to a complete Pain - Severe chemical burns can be extremely painful.
epithelial defect (Figure 2). A complete epithelial defect Ciliary spasm can be managed with the use of cycloplegic
may not take up fluorescein dye as rapidly as in a routine agents; however, oral pain medication may be necessary
corneal abrasion; therefore, it may be missed. If an epithelial initially to control pain.
defect is suspected but not found on the initial evaluation, Open Globe Injury
the eye should be reexamined after several minutes. The Presentation: Depending upon the extent and type of injury
size of the defect should be recorded so as to document patient can present with variable amount of loss of vision,
response to treatment on subsequent visits. Corneal pain, hyphema, swelling of extra-ocular tissues.
perforation is a very rare finding at presentation, it is more Examination: A detailed history and examination should
likely to occur after the initial presentation (from days to be noted meticulously as medicolegal opinion can be
weeks) in severely injured eyes that have poor healing asked. Visual acuity, pupillary reactions, nature of injury
capacity. Anterior chamber inflammatory reaction can vary (laceration, perforation or intraocular foreign body), trauma
from trace cell and flare to a vigorous fibrinoid anterior to various ocular tissues checked (Figure 3). Gentle handling
chamber reaction. Generally, this finding is more common of the ocular tissue has to be done. Loss of consciousness
with alkaline injuries because of the greater depth of and vomitting should be specifically asked.
penetration. Adnexal damage/scarring similar to chemical Emergency Care: Exploration and repair under general
injuries on other skin areas can lead to severe exposure anesthesia can be warranted. So proper fasting and systemic
problems if eyelid scarring prevents proper closure, thereby clearance has to be ensured. Till the time patient is to be
exposing an already damaged ocular surface. operated, a cartella shield or pad to the eye can be done.
Emergency Treatment: Regardless of the underlying Tetanus and antibiotic prophylaxis is warranted in case of
chemical involved, common goals of management include suspected injury. Proper consent has to be taken explaining
the following:1 removing the offending agent - ideally, the visual prognosis to the patient.
eye should be irrigated with a sterile balanced buffered Angle Closure Glaucoma
solution, such as normal saline solution or Ringer’s Lactate Presentation: Patient comes with sudden painful diminution
solution. However, immediate irrigation with even plain of vision which can be associated with nausea, vomitting or
tap water is preferred without waiting for the ideal fluid.
Irrigating the fornices for adequately sufficient period
(30 min) is important2. Promoting ocular surface healing-

68 l DOS Times - Vol. 19, No. 9 March, 2014

PG Corner

Figure 4: Angle closure glaucoma Figure 6: Corneal abrasion

Figure 5: Orbital cellulitis anti-glaucoma drugs can be used when the corneal edema
headache. History of going in a dark room can be elicited. resolves first.
Specific drug history like topiramate should also be asked. Orbital Cellulitis
Examination: Signs of angle closure glaucoma are Presentation: Patient presents with either subtle onset or
pathognomic. Vertically dilated pupil, corneal edema, abrupt onset of painful swelling in ocular adnexa. The
shallow anterior chamber and high IOP indicate towards presentation can be varied that ranges from discharge,
it (Figure 4). Pupillary reactions are sluggish and other eye restriction of ocular movement to visual acuity deterioration,
can also have signs of angle closure. proptosis and exposure keratopathy can be its presentation
Emergency Care: Rapid lowering of intraocular pressure (Figure 5). Fundus examination should be undertaken to
has to be done. Intravenous mannitol (10 mg/kg) is rule out any possible extension of intraocular tumor.
a rapidly acting diuretic that is often the first line of Examination: Complete hematological investigation and
management. We should rule out hypertension or any systemic examination is warranted, more so in pediatric
signs of raised intracranial tension before administering case. Ocular movements, visual acuity and pupillary
it. Patient should be kept in a dark and quite room. IOP reactions should be recorded. Ultrasound orbit and
measurement after thirty minutes of giving intravenous posterior segment should be undertaken to find out the
mannitol should be recorded. Similarly syrup glycerol can etiology and extent.
also be used. Intravenous or oral acetazolamide is also very Management: Adequate hydration maintenance combined
useful in lowering down the intra-ocular pressure. Topical with broad spectrum antibiotics is initiated. The patient
can be admitted till patient is afebrile and the swelling
has reduced. Surgical drainage is indicated if there is
subperiosteal or intraorbital abscess. In case of malignancy,
proper and urgent oncology referral has to be done.
Corneal Abrasion
Presentation: Patient presents with photophobia, painful
diminution of vision. He typically gives history of accidental
or incidental trauma with a foreign body or nail. Rule out
history of use of contact lens. It can be associated with lid
swelling.
Examination: Patient can be given symptomatic relief by
putting few drops of pro-paracaine before examination.
Visual acuity, pupillary reactions and any superficial

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PG Corner

Figure 7: Hyphema Hyphaema
Presenting complaints: Patient usually comes with history
Figure 8: Lid canalicular injuries of trauma. If the hyphaema is significant and crosses the
corneal foreign body if present should be mentioned in pupillary axis it can cause severe diminution of vision.
findings (Figure 6). Detailed slit lamp examination should Increased intraocular pressure can give rise to pain in
be carried out and the epithelial defect is measured. eyeball. There can be associated signs of symptoms of
Management: Prophylactic topical antibiotics and ocular trauma.
preservative free lubricants are given in patients with Examination: Patient should be seated comfortably and
abrasions. Patching the eye has been used to help relieve asked about any trauma or surgical intervention that can be
the pain associated with corneal abrasion. Patching should inciting event. The systemic history of the patient is asked
not be performed in patients at high risk of infection, such for any hematological disorder and bleeding diathesis.
as those who wear contact lenses and those with trauma Associated signs of ocular trauma like corneal abrasions,
caused by vegetable matter, because of potential incubation iridodialysis, lens subluxation, traumatic mydriasis are
of infecting organisms and promoting subsequent looked upon and if possible fundus evaluation is done to
infectious keratitis. Some ophthalmologists advocate the look into the vitreous cavity (Figure 7). Intraocular pressure
use of diclofenac or ketorolac drops with a disposable soft is recorded and slit lamp examination of the patient is done
contact lens in addition to antibiotic drops. This therapy to detect any presence of corneal blood staining. If there is
may be an effective alternative to patching, as it allows the spontaneous hematoma presence of intraocular tumors has
patient to maintain binocular vision during treatment and to be ruled out.
reduces inflammation. Patient should be reviewed after 48- Emergency cure: Patient admission is considered if the
72 hours. hyphaema is more than 50% of the anterior chamber,
severe loss or decrease in vision, intractable IOP, non
compliant patients, extremes of age, suspected child
abuse, positive sickle cell anemia or trait. Long acting
topical cycloplegic, topical corticosteroids are given to
control inflammation. beta adrenergic antagonist, carbonic
anhydrase inhibitors and intravenous & oral hyperosmolar
agents reduce intraocular pressure. Analgesics that do
not contain aspirin can be given to relieve pain. Surgical
drainage of the hyphaema is considered in some special
situations like intractable intraocular pressure and corneal
blood staining. If there is associated retinal detachment
immediate vitreoretinal intervention is required.

Canalicular Injuries
Presentation: Lacerations of the canalicular system often
occur in the setting of trauma. Injuries to the canalicular
portion of the tear drainage system can occur as isolated
injuries or as one component of more extensive injuries,
including multiple marginal lid lacerations, orbital fractures,
and globe injuries. Because of its superficial location in the
medial lid, the canalicular system is vulnerable to trauma.
Patient comes in emergency with presenting symptoms of
associated trauma and epiphora.
Examination: A complete ophthalmic examination must
be performed, including visual acuity, pupil reaction (with
specific mention of whether a relative afferent pupillary
defect is present), visual fields, extraocular movements,
intraocular pressure, external examination, slit lamp
examination, and dilated examination of the optic nerves
and posterior pole. Injuries of the lacrimal system can occur
in the setting of major head trauma, in which case, dilation

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PG Corner

of the pupils may not be permissible from a neurologic variety of methods, such as instilling various fluids (eg,
standpoint. Any lid laceration medial to the pupil should be saline, boiled milk, antibiotic solutions, methylene blue,
considered to involve the canalicular system until proven sodium hyaluronate, fluorescein), have been suggested.
otherwise. To check for disruption of the system, the puncta Puncta must be dilated, and a Bowman probe must be
can be dilated, followed by insertion of a Bowman probe passed delicately through the canaliculus. The severed end
(Figure 8). Another method of confirming a canalicular of the canaliculus is a shiny white cuff of tissue at the edge
laceration includes irrigating substances, such as fluorescein of the lumen. Most surgeons favor silicone intubations
stained balanced saline solution, through the system with of the system, with repair of the pericanalicular injury.
visualization of the dye in the wound. Examination of the Intubation can be accomplished with either bicanalicular
orbit for any associated injuries (eg, orbital fractures) must intubation (either by passing the stent ends through the
be performed. Fractures of the maxillary bone in the area nasolacrimal duct or by using a modified eyed pigtail
of the nasolacrimal duct can cause difficulty in silicone probe) or monocanalicular intubation. The pericanalicular
intubation through the nasolacrimal duct. tissue can be opposed with 7-0 Polyglactin 910 suture.
Emergency Care: Tetanus prophylaxis must be confirmed References
in any contaminated injury. Rabies prophylaxis with both
active and passive immunization may be necessary in 1. Rudkin AK, Lee AW, Aldrich E, Miller NR, Chen CS. Clinical
certain carnivore bites; in most domestic dog bites, it is characteristics and outcome of current standard management of
not necessary. Postoperatively, most surgeons prescribe central retinal artery occlusion. Clin Experiment Ophthalmol. Jul
a broad-spectrum antibiotic, such as cephalexin, for the 2010;38(5):496-501.
patient. Wound care includes topical ophthalmic antibiotic
ointment 4 times per day and ophthalmic antibiotic solution 2. Hodge C, Lawless M. Ocular emergencies. Aust Fam Physician. Jul
4 times per day. Acute microscopic repair with either an 2008;37(7):506-9.
operating microscope or surgical loupes is required to
reanastomose the severed ends of the canaliculi. In most 3. Harlan JB Jr, Pieramici DJ. Evaluation of patients with ocular trauma.
injuries, this repair can be accomplished within 48 hours of Ophthalmol Clin North Am 2002; 15:153.
the trauma. Animal bites should be addressed immediately
because of the significant contamination present in the 4. Ang LP, Ang LP. Current understanding of the treatment and outcome
wound. of acute primary angle-closure glaucoma: an Asian perspective. Ann
Repairs on children are best performed under general Acad Med Singapore. Mar 2008;37(3):210-5.
anesthesia. For most adults, repairs can be performed with
monitored anesthesia with intravenous sedation or if an 5. Bergin DJ, Wright JE. Orbital cellulitis. Br J Ophthalmol. Mar
isolated laceration even local anesthesia. In those patients 1986;70(3):174-8.
with extensive ocular adnexal trauma or more extensive
injuries, general anesthesia may be the preferred anesthetic 6. Salz JJ, Reader AL, Schwartz LJ, Van Le K. Treatment of corneal
approach. Because of the difficulty in finding the severed abrasions with soft contact lenses and topical diclofenac. J Refract
ends if one is not experienced with these injuries, a wide Corneal Surg. Nov-Dec 1994;10(6):640-6.

7. Read JE, Goldberg MF. Traumatic hyphema: Comparison of medical
treatment. Trans Am Acad Ophthalmol Otolaryngol. 1974;78:799.

8. Hawes M, Dortzbach R. Trauma of the lacrimal drainage system.
In: Linberg J, ed. Lacrimal Surgery. New York: Churchill Livingstone;
1988:241-262.

www. dosonline.org l 71

MonthlyMoMntheleytMineegtinCgoCronrneerr

Acute Proptosis in Childhood: A
Rare Case of Rhabdomyosarcoma Shaifali Chahar

MBBS, DNB

Shaifali Chahar MBBS, DNB, A.K Grover MD, Shaloo Bageja DNB
Sir Ganga Ram Hospital, New Delhi

Four year old female child was brought by her parents -18 mm). Rest of the ocular examination was grossly within
to the hospital with painless, progressive bulging of normal limits.
the left eye present for the last 4 days (Figure 1). It was Lab Investigation: Her complete blood count was normal.
associated with diplopia on third day of presentation, as the LDH was grossly elevated – 227 IU/ml (normal range – 91
bulging progressed. There was no associated diminution of to 180 IU/ml).Peripheral smear was normal.
vision. No history of recent febrile illness, upper respiratory CT SCAN of the orbit (Figure 2) showed proptosis of left
tract infection, nausea, vomiting, headache, trauma, ENT eyeball with 2.3 X 2.2 X1.5 cm size peripherally enhancing
complaints / sinusitis, neck swelling, abdominal swelling lesion in superolateral aspect of left orbit. No calcification
or intake of systemic medication or bone destruction was seen. Optic nerve was deviated
On Examination: Her vitals were stable, no
lymphadenopathy was present, systemic examination was
grossly normal.
Ocular examination – Visual acuity was 6/36 (both eyes)
improving to 6/9 (with -1.50 DC @ 180 deg). Color
vision was normal, intraocular pressure was normal.
Left hypoglobus was seen (~10 PD) with restriction in
supraduction. Apparent unilateral eccentric proptosis with
fullness in superolateral area of left orbit. Proptosis was non-
compressible, firm on retropulsion and orbital tension was
raised. It was non pulsatile with no change in head posture
or Valsalva maneuver or coughing. Exophthalmometry
revealed proptosis of 5 mm on left side (Right-13mm, left

Figure 1: Clinical Picture Figure 2: CT Scan of Orbit
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Monthly Meeting Corner

Figure 3: Histopathology • Myeloid (Granulocytic) sarcoma
• Burkitt’s lymphoma
inferomedially. USG abdomen was normal. Whole • Eosinophilic granuloma
body PET scan showed a FDG avid enhancing lesion • Sickle cell disease
in superolateral aspect of left orbit, rest of the body no • Capillary hemangioma (rapid growth phase)
abnormality was detected. • Lymphangioma (h’gic cyst)
Management: Left lateral orbitotomy with debulking • Traumatic hematoma
was planned. Per operative findings – necrotic tumor • Dermoid cyst (rupture and inflammation)
mass which came out as piece meal. Mass was sent for • NSOID
histopathological examination. • Cellulitis /abscess
Histopathology report (Figure 3) suggested of typical Rhabdomyosarcoma is the most common soft tissue
tumor cell population with anisomorphic nuclei, scanty sarcoma in age group < 15 years. It is the most common
cytoplasm, and brisk mitotic activity and raised Nuclear: pediatric primary orbital malignancy. It is particulary
cytoplasm ratio. Cell was positive for Vimentin, Desmin alarming due to its abrupt onset and explosive course.HPE
and myogenin. Ki 67 proliferation was 20-25%. Final types include – Embryonal variety – most common with
diagnosis – Left orbital rhabdomyosarcoma good prognosis. Pleomorphic form – Least common with
In view of HPE report, Hemato-oncology consult was best prognosis, Alveolar form – Most malignant with worst
requested. Chemotherapy was planned. PICC line was prognosis and Botryoid form – rare1.
inserted in basilic vein and VAC protocol was started – According to Lawrence and Gehan pretreatment staging
Vincristine, Actinomycin D, Cyclophosphamide along with and post surgical Grouping they are divided into –
Mesna and peg-GCSF. Further cycles were planned for the 1) Low risk – VA / VAC protocol – > 90 % survival
next visit. 2) Intermediate risk – VAC + radiotherapy +/- Topotecan
Discussion
Acute proptosis in childhood is a separate entity, and - 55-70 % survival
efforts made towards – narrowing the differential diagnosis, 3) High risk – VAC + Irinotecan + Radiation – 30%
prompt diagnosis and early treatment – can be life saving!
Sudden Rapidly Progressive proptosis – D/Ds survival
• Rhabdomyosarcoma Chemotherapy is given for 1-2 days in a row  once per
• Other primary sarcoma week  till 6 months – a year. Radiotherapy is given for
• Neuroblastoma mets 5-6 weeks. In case of treatment failure salvage therapy
• Other metastatic lesions in the form of exenteration / excision of residual tumor
with brachytherapy can be done. As trends have changed
over the years and benefits of multimodal management
(surgery+ chemotherapy + radiotherapy) has come into
picture survival rates has drastically improved in children2,3.
Importance of clinical suspicion when dealing with acute
childhood proptosis is a must. PROMPT referral to a
tertiary centre after imaging is the responsibility of primary
ophthalmologist, family practitioner or a pediatrician.
References

1. Rao AA, Naheedy JH, Chen JY, Robbins SL, Ramkumar HL. A clinical
update and radiologic review of pediatric orbital and ocular tumors.
J Oncol. 2013;2013:975908.

2. Punyko JA, Mertens AC, Baker KS, et al. Long-term survival
probabilities for childhood rhabdomyosarcoma. A population-based
evaluation. Cancer. 1 2005;103(7):1475-83.

3. Pappo AS, Shapiro DN, Crist WM, Maurer HM. Biology and therapy
of pediatric rhabdomyosarcoma. J Clin Oncol. 1995;13(8):2123-39.

74 l DOS Times - Vol. 19, No. 9 March, 2014

Forthcoming Events

MAY 2014 (Friday - Sunday) 26th – 28th September, 2014
(Friday - Saturday ) 9th May – 10th May, 2014 6th National CME on Eye Banking (organised by Eye
Two day Topical Seminar On “Emerging Trends in Bank Association of India)
Hospital Administration”
Venue: Hyderabad
Venue: Sri. V.D. Swami Auditorium, Sri. T.S. Santhanam Contact: Dr. Samar Basak, Eye Bank Association of India,
floor,KNBIRVO Block,Sankara Nethralaya Main Campus Plot No.12, BNR Colony, Road No. 14, Banjara Hills,
No 18, College Road, Nungambakkam,Chennai – 600 006 Hyderabad-500034
Organizing Secretary: A. Mahalingam, Assistant Registrar Email: [email protected], [email protected]
The Sankara Nethralaya Academy (TSNA) Website: www.ebai.org
Email: [email protected] Phone: +91-40-23545454, 4504
Website: www.thesnacademy.ac.in
Mobile: +91-(0) 97104 85295 OCTOBER 2014
(Friday - Sunday) 3rd – 5th October, 2014
JULY 2014 Uttara Eyecon 2014 (XI Annual Conference of
(Saturday - Sunday) 5th – 6th July, 2014 Uttarakhand State Ophthalmological Society)
IIRSI (Indian Intraocular Implant and Refractive Society)
Conference 2014 Venue: Golden Palm Hotel & Spa****, The Mall, Musssoorie
Contact: Dr. Vinod Arora,, Navjyoti Eye Hospital & Dehradun
Venue: Hotel Le Royal Meridien, Chennai Wave Lasik Centre, Nehru Nagar Colony, Haridwar Road ,
Contact: Amar Agarwal, Dr. Agarwal’s Eye Hospita, L-19 Dehradun -248001
Cathedral Road, Chennai - 600086 Email: [email protected]
Email: [email protected] Website: www.uksos.org
Website: http://www.iirsi.com Phone: +91-0135- 3272525, 0999-7171-888
Phone: +91-44-2811 6233 , +91-44-2811 2959
NOVEMBER 2014
SEPTEMBER 2014 (Saturday - Sunday) 22nd – 23rd November, 2014
(Thursday - Sunday) 11th – 14th September, 2014 14th Annual Meeting of the Uveitis Society of India
EYE FEST 2014: 24th Annual Conference of Glaucoma
Society of India Venue: India Habitat Centre, New Delhi
Contact: Dr. Shishir Narain Organizing Secretary, 14th USI
Venue: Bhubaneswar, Odisha Meeting, New Delhi
Contact: Dr. Ashok Kumar Nanda Email: [email protected]
Email: [email protected]
DECEMBER 2014
(Friday - Sunday) 26th – 28th September, 2014 (Saturday- Sunday) 20th and 21st December 2014
7th Beinnal meeting of Asia Pacific Society of 49th Annual Conference of UP State Ophthalmological
Oculoplasty & Reconstructive Surgery (APSOPRS) and Society
Silver Jubilee Meeting of the Oculoplastics Association of
India (OPAI) Venue: Hotel Radisson Blue, Sector 18, Noida, Uttar Pradesh
Contact: Dr. Mohita Sharma, Organizing Secretary, Tirupati Eye
Venue: India Habibt Centre, Lodhi Road,New Delhi (India) Centre, C-8, Sector 19, Noida-201301, U.P.
Contact: Dr. A.K. Grover, Chairman Organizing Committee Mobile : 09560889495,
Email: [email protected] Email: [email protected], [email protected]
Website: www.apsoprs2014delhi.com Website: www.upsosonline.org
Phone: +91-011-26267611

76 l DOS Times - Vol. 19, No. 9 March, 2014

DOS Times Quiz Delhi
Ophthalmological
Society

Instructions:

1. Please return your answers to [email protected] or mail them to “The Quizmaster, DOS Times Quiz, Dr. Rajesh Sinha,

Room No. 479, Dr. R.P. Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, Ansari Nagar, New Delhi -

110029”. Please write your DOS membership number along with your answers.

2. The answers should reach not later than 30th June, 2014.

The quiz can also be viewed and directly answered on our website www.dosonline.org

3. The results will be announced at the DOS monthly clinical meeting on July 2014. The correct entry will be given a prize of

Rs. 2,500. If there are more than one correct entries, the winner of the prize will be decided by draw of lots.



Quiz compiled by Dr. Digvijay Singh Quiz Prizes Sponsored by

M/s. Syntho Pharmaceuticals Ltd.

OCULAR EMERGENCIES: Organisms R Us Answer for February issue of DOS Times

1. Common Organism responsible for Preseptal and Orbital 1. Waardenberg
Cellulitis in India: 2. Axenfeld-Rieger
3. Alport
a oo u 4. Aicardi

2. Endophthalmitis developing after YAG capsulotomy is most
likely to be caused by:

o io i a e iu

3. Contact Lens Wearer Keratitis

aa a oe a

4. Common Fungus in Post traumatic endophthalmitis

aei u

## ##

Membership No. __________ Name : _______________________Mobile No. _____________Email: _________________

Answer to DOS Times Quiz January 2014 B. ___________________________________________
A. __________________________________________ D. ___________________________________________
C. __________________________________________

TearsheetDiagnosis Pain Hyperemia Foreign Dis-Itch- Pho- Onset Vision Threat Cornea Pupil Col-
to vision oured
Differential Diagnosis of body charge ing topho- halos
Acute Red Eye
sensa- bia
www. dosonline.org l 79
tion

Episcleritis No Focal/Dif- No Tearing No No Rapid Not af- No Clear Not af- No
fuse fected fected

Scleritis Yes Focal/ Dif- No No No Yes Progressive Not af- Yes Occa- Not af- No
fuse fected sional fected
periph-
eral
opacity

Uveitis Yes Diffuse, No Watery, No Yes Sudden Blurred Yes May be Con- Yes
minimal
perilimbal hazy stricted,

sluggish

reaction

Allergic No Diffuse, Yes Watery Yes No Progressive Not af- No Clear Not af- Yes/ no
conjuncti- No towards Yes to mu- No fected fected
vitis fornices coid

Viral con- Diffuse, Watery No Sudden Not af- No Clear Not af- Yes/ no
junctivitis towards and clear fected
fornices with rapid fected

progression

Bacterial No Diffuse, Yes Mucopu- No No Sudden Not af- No Clear Not af- Yes/ no
conjuncti- Yes towards Yes rulent fected fected
vitis fornices
Mucopu- No Yes Sudden Blurred Yes Hazy Not af- Yes/no
Corneal Diffuse, rulent Clear fected No
ulcer perilimbal
No No No Acute Not af-
Subcon- No Focal No Not af- No fected
junctival Yes No fected
haemor- Diffuse,
rhage perilimbal Tearing No Yes Sudden, Blurred Yes Hazy Mid- Yes
usually in
Acute evening dilated,
angle
closure vertically
glaucoma
oval, Non

reactive

Tearsheet

Antibiotic Therapy of Bacterial Keratitis

Organism Antibiotic Topical Subconjunctival
Concentration Dose
No organism\ identified or Cefazolin 50 mg/ml 100 mg in 0.5 ml
multiple types of organisms with 9–14 mg/ml 20 mg in 0.5 ml
Gram-positive Cocci Tobramycin/Gentamicin Various†
Gram-negative Rods or 100 mg in 0.5 ml
Gram-negative Cocci§ Fluoroquinolones* 50 mg/ml 25 mg in 0.5 ml
Non-tuberculous Cefazolin 15–50 mg/ml
Mycobacteria Vancomycin‡ 10,000 IU 20 mg in 0.5 ml
Bacitracin‡ Various† 100 mg in 0.5 ml
Fluoroquinolones* 9–14 mg/ml 100 mg in 0.5 ml
Tobramycin/Gentamicin 50 mg/ml 100 mg in 0.5 ml
Ceftazidime Various† 20 mg in 0.5 ml
Fluoroquinolones 50 mg/ml
Ceftriaxone 50 mg/ml
Ceftazidime Various†
Fluoroquinolones 20–40 mg/ml
Amikacin 10 mg/ml
Clarithromycin 10 mg/ml
Azithromycin: Various†
Fluoroquinolones

Nocardia Sulfacetamide 100 mg/ml 20 mg in 0.5 ml
Amikacin 20–40 mg/ml
Trimethoprim/ 16 mg/ml
Sulfamethoxazole: 80mg/ml
Trimethoprim
Sulfamethoxazole

* Fewer gram-positive cocci are resistant to gatifloxacin and moxifloxacin than other fluoroquinolones.
† Besifloxacin 6 mg/ml; ciprofloxacin 3 mg/ml; gatifloxacin 3 mg/ml; levofloxacin 15 mg/ml; moxifloxacin 5 mg/ml; ofloxacin 3 mg/ml, all
commercially available at these concentrations.
‡ For resistant Enterococcus and Staphylococcus species and penicillin allergy. Vancomycin and bacitracin have no gram-negative activity and
should not be used as a single agent empirically in treating bacterial keratitis.
§ Systemic therapy is necessary for suspected gonococcal infection.

Vijay Kumar Sharma MS

Vijay Kumar Sharma MS
Rajendra Prasad Centre for Ophthalmic Sciences,
All India Institute of Medical Sciences, New Delhi

80 l DOS Times - Vol. 19, No. 9 March, 2014