Supplement To AUSTRALIAN Pharma SEPTEMBER 2012
Supplement toAUSTRALIANpharmaSEPTEMBER 2012z Ultra-widefield imaging technologyz Crocodile tears syndrome z Asymmetric dry eye z Nutritionz Laser vision correction z Optic disc oedema z Fuchs heterochromic iridocyclitis
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AUSTRALIANpharmaPublished by2Perplexing puzzle of asymmetric dry eyeDr William D Townsend5The dry eye and systemic disease connectionDr Ernie Bowling6Optic disc oedema: a diagnosis of exclusionDr Kwang Cham and Dr Neil Shuey8Analysis of retinal pathologies in the context of theentire retinaMary Travis11Clinical quizDr Robert Holloway12Combined refractive and corneal parameters whenplanning laser vision correctionDr Noel Alpins and George Stamatelatos17Nutrition in primary eye careDr Jeffrey Anshel18AbstractsDr Laura Downie20Fuchs heterochromic iridocyclitis is often underdiagnosedDr William Trinh22Crocodile tears syndromeJoel P Causey and Dr Leonid Skorin Jr24PBS list of medicines for optometristsEditor: JEFF MEGAHANNational Publications Manager:SANDRA SHAWJournalist: JENNY KELLETTAdvertising: SANDRA SHAWClinical Editor:Associate Professor MARK ROTHDepartment of Optometry andVision Sciences, The University ofMelbourneOptometrists Association AustraliaABN 17 004 622 431204 Drummond StreetCarlton VIC 3053Tel (03) 9668 8500Fax (03) 9663 asn.auCopyright 2012COVERPhoto: Optomap image of melanomacaptured by ultra-widefield imagingtechnology from Optos.Comments made in PHARMA are of a generalnature and intended for guidance only. Optometrists Association Australia and the individualcontributors expressly disclaim all liability andresponsibility to any person in respect of, andfor the consequences of, anything done oromitted to be done in reliance wholly or partlyon anything in this publication.Pharma is distributed in Australia and New Zealand.All references to pharmaceutical preparations inPharma are applicable within Australia.SEPTEMBER 2012
2Perplexing puzzle ofenough, but when it affects only one eyeor is significantly asymmetric, the underlying cause may be a serious neurologic orsystemic condition. Ferreting out the cause ofasymmetric dry eye necessitates a detailedcase history of previous trauma, as wellas systemic disease and medications, andrequires an understanding of neurologicand hormonal control of tear production.Stern described the lacrimal functionalunit, which is composed of the ocularsurface (cornea, conjunctiva, accessorylacrimal glands and meibomian glands),the main lacrimal gland and afferent/efferent innervation that interconnectsthese structures.4 Damage to these neuralcircuits interrupts normal regulation of tearproduction and causes dry eye disease.5Herpes simplex keratitis is an example of aeyes, published in 1995, increased ourawareness of aqueous deficient versusevaporative dry eye, and provided clinicians with strategies for determining thecauses of dry eye.2 The 2007 report of theInternational Dry Eye Workshop expandedon the 1995 workshop and provided newinformation and a better understanding ofdry eye states.3In 2011, the report of the MeibomianGland Dysfunction Study provided us witha much better understanding of what maybe the most common cause of DES.4 All ofthese studies, plus a plethora of other dryeye related research and publications, havevastly improved our ability to identify andtreat DES.Diagnosing and managing DES presenting as a bilateral condition is challengingDr William D TownsendOD FAAOAdvanced Eye CareCanyon TX, USAThe term dry eye syndrome (DES) isused for a collection of ocular surfaceconditions that share common signs andsymptoms, but may result from a varietyof underlying causes. It is a very commoncondition, especially in older individuals.1During the past two decades, a large bodyof research has expanded our understanding of the underlying pathophysiology ofvarious forms of dry eye.The report of the National Eye Institute/Industry workshop on clinical trials in dryLGFOld pathwayRevised nDPIOFGPGPFOFONPCONPCPOPCN VII parasympathetic innervation of the lacrimal glandDashed line: preganglionic pathway. Dotted line: postganglionic pathway.A: anastomosing branchDP: deep petrosal nerveF: frontal nerveFO: foramen ovaleFR: foramen rotundumGP: greater petrosal nerveIOF: inferior orbital fissureL: lacrimal nerveLG: lacrimal glandMn: mandibular nerveMx: maxillary nerveNPC: nerve of pterygoid canalNC: nasociliary nerveO: ophthalmic nerveP: pterygopalatine ganglionRL: ramus lacrimaleROP: retro-orbital plexusSOF: superior orbital fissureT: trigeminal ganglionZ: zygomatic nervePublished with permission from Jan Bergmanson: Clinical Ocular Anatomy and Physiology, 19th Edition. Published by Texas Eye Research and Technology Center, Houston Texas, 2012OPTOMETRY PHARMA SEPTEMBER 2012
3asymmetric dry eyeDetermining the underlying causes of dry eye requires more than a detailedknowledge of the patient’s case history. You also need an understanding ofneurologic and hormonal control of tear production.condition that damages corneal nerves andmarkedly alters the function of the lacrimalfunctional unit.6The afferent portion of the ‘unit’ beginswith corneal sensory nerves derived fromthe ophthalmic branch of the trigeminalnerve (cranial nerve V); corneal sensation iscritical in preventing injury through the blinkreflex and reflex tearing. It is also crucialto the maintenance of the corneal surface.Loss of sensory innervation (neurotrophickeratitis) leads to punctate keratitis and epithelial loss.5 Lacrimation is innervated by thefacial nerve. Parasympathetic fibres exit thepons and then travel to the pterygopalatineganglion where they synapse. Post-synapticfibres travel to the acini of the main andaccessory lacrimal glands.7 Loss of efferentinnervation to lacrimal glands dramaticallyaffects the ocular surface.Toshida and colleagues reported thatpreganglionic parasympathetic denervationin rabbits resulted in rose bengal staining ofthe conjunctiva, corneal fluorescein staining,increased blink rate, decreased tear filmbreak-up time, decreased goblet cell densityand a 26 per cent reduction in tear flow.8Bell’s palsyBell’s palsy is an idiopathic acute peripheral-nerve palsy affecting the facial nerve(cranial nerve VII), which innervates themuscles of facial expression as well as thelacrimal glands. Bell’s palsy presents asunilateral weakness or complete paralysisof all the facial muscles, including paresis ofthe orbicularis, which results in incompleteclosure of the lids with exposure keratitis.Because the facial nerve also suppliesparasympathetic fibres to stimulate secretion by the lacrimal and salivary glands,Bell’s palsy can produce unilateral dryness.This may be obscured by excessive tearingresulting from lid laxity and subsequent lossof apposition to the puncta to the globe.9The neurologic evaluation of facial nervepalsy should include the ability to blink, thepresence of Bell’s phenomenon and cornealsensation.10The pathophysiology of Bell’s palsy isunknown. The herpes viruses includingherpes simplex 1, herpes zoster and theEpstein-Barr virus have been targetedas potential triggers, and clinicians haveused anti-herpetic medications to treat newcases. Recent studies call this practice intoquestion.In a large clinical trial, Sullivan and colleagues treated subjects with recent onset(less than 72 hours) Bell’s palsy using one ofthree systemic regimens: prednisolone, acyclovir or a combination of the two. At threemonths, 83 per cent of the prednisolonegroup recovered facial function comparedwith 71.2 per cent in the acyclovir group.After nine months, 94.4 per cent of the prednisolone group had recovered comparedwith a recovery rate of only 85.4 per centfor the acyclovir group. There was no significant difference in recovery rate betweenpatients with no treatment compared withthe acyclovir group.11Because of the ocular manifestations ofBell’s palsy, the patient may present to theoptometrist’s practice before seeing anyother health-care provider. It is crucial to triage these individuals immediately, becausea Swedish study showed that elderly individuals with Bell’s palsy who were treatedwith steroids within 48 hours of onset had amuch better prognosis than those for whomtreatment was delayed.12Treatment of the ocular disease focuseson prevention of corneal damage until thecondition resolves and includes therapy withartificial tears and bland ointment to preventdrying of the cornea, and in severe cases,use of a moisture chamber. It is essential thatthe eye is closed during sleep, so patchingmay be necessary. In severe cases, tarsorrhaphy may be helpful and can be reversedonce the condition resolves.13,14Reduced sensationDiminished corneal sensation, a commoncause of unilateral dry eye, can be causedby a wide variety of conditions.15 Reducedsensation can be confirmed with aesthesiometry. The Cochet-Bonnet Aesthesiometeruses mechanical pressure to evaluate andquantify corneal sensitivity.16 A nylonmonofilament enclosed in a tubular housingcan be adjusted from 5 mm to 60 mm inlength. Increasing the length of the filamentdecreases mechanical pressure transmittedto the cornea. In clinical practice we canscreen for reduced corneal sensitivity bytouching the apex of the cornea with acotton wisp or non-flavoured dental floss.16Neurotrophic keratopathyNeurotrophic keratopathy (NK) is a degenerative corneal condition caused byimpaired corneal sensation. The basicunderlying pathophysiology is denervationof the trigeminal nerve (cranial nerve V)resulting in unilateral dry eye and accompanying deterioration of the ocular surface.17Conditions associated with NK includeherpes simplex, herpes zoster, leprosy, lattice and granular corneal dystrophies andContinued page 4OPTOMETRY PHARMA SEPTEMBER 2012
4Perplexing puzzle of asymmetric dry eyeFrom page 3Stage 1. Corneal irregularity, dry spots, punctate keratopathy, superficial vascularisation,stromal scarring and epithelial hyperplasia9,10Stage 2. Epithelial defect, usually located in superior cornea, an area of loose epithelium,stromal oedemaStage 3. Corneal ulceration, stromal melting and perforationTable 1. The Mackie classification system for neurotrophic keratopathyrefractive/penetrating ocular surgery.Any neurosurgical procedure that impinges on and/or damages the trigeminalnerve has the potential to cause cornealanaesthesia.18 The Mackie classification ofneurotropic keratopathy is used to delineatethe severity of the condition (Table 1).Several studies have demonstrated thevital role innervation plays in maintainingthe health of epithelial cells. Araki and colleagues reported alterations in the epithelialsurface and adherence between cells afterdenervation of rabbit corneas. Spontaneousepithelial breakdown was widespread; 83per cent of the corneas showed persistentepithelial defects.19 Epithelial breakdown inneurotrophic keratopathy is believed to besecondary to the loss of neurotransmitterssuch as acetylcholine, catecholamines andsubstance.20Management andtreatmentManagement of the monocular dry eyesecondary to corneal denervation can bevery challenging. Conventional therapiesfor milder cases include non-preservedartificial tears, bland ointments and gels.For more severe presentations, lateraltarsorophy and amniotic membrane transplantation may be indicated.18 Lambiaseand colleagues reported good results intreating refractory neurotrophic ulcers withnerve growth factor.17Reynolds and Kabat reported the caseof a 46-year-old female who suffered fromNK secondary to herpes simplex keratitis.Previous treatment with a bandage contactlens, topical antibiotic and artificial tearswas unsatisfactory. After four weeks of treatment with of BID Restasisa (0.05 per centcyclosporine ophthalmic emulsion; Allergan,Irvine, California), the patient was able toOPTOMETRY PHARMA SEPTEMBER 2012zzzzzzzStructural lesions in the ear or parotidgland, for example, cholesteatoma,salivary tumoursGuillain-Barré syndromeLyme diseaseOtitis mediaRamsay Hunt syndrome (herpes zosterin the facial nerve distribution)SarcoidosisSome influenza vaccinesTable 2. Causes of peripheralneuropathydiscontinue the bandage contact lensesand antibiotic.18Unilateral dry eye can result from a broadrange of conditions, many of which we arenot able to address in this short article. Someare relatively benign, while others have thepotential for vision loss. Optometric education encompasses ocular and neurologicalanatomy and physiology and serves asexcellent preparation for appreciating thefundamental processes that maintain theocular surface and facilitate tear production. Optometrists are well prepared to meetthe challenge of the unravelling the causeof unilateral dry eye.z William D Townsend OD FAAO is a graduateof the University of Houston College of Optometry and practises in a multi-location setting. Heserved for 11 years as a consultant at the VAMedical Centre in Amarillo, Texas. He is an adjunct professor and preceptor for senior Universityof Houston College of Optometry externs whorotate through his practice. He conducts researchin pharmaceutical agents and contact lens materials and solutions and ocular surface disease. DrTownsend is a fellow of the American Academyof Optometry and president of the Ocular SurfaceSociety of Optometry.a. Restasis is commercially unavailable in Australia buttopical Cyclosporin eye-drops can be prescribedthrough a compounding pharmacy.1. Moss SE, Klein R, Klein BE. Incidence of dry eye inan older population. Arch Ophthalmol 2004; 122:369–373.2. Lemp MA. Report of the National Eye Institute/Industry workshop on clinical trials in dry eye. CLAOJ 1995; 21: 221–232.3. 2007 Report of the International Dry Eye Workshop(DEWS) Research in dry eye: report of theResearch Subcommittee of the International Dry EyeWorkShop (2007). Ocul Surf 2007; 5; 2: 179-193.4. Asbell PA, Stapleton FJ, Wickström K, Akpek EK,Aragona P, Dana R, Lemp MA, Nichols KK. Theinternational workshop on meibomian glanddysfunction: report of the clinical trials subcommittee.Invest Ophthalmol Vis Sci 2011; 52: 4: 2065-2085.5. Dastjerdi MH, Dana R. Corneal nerve alterationsin dry eye-associated ocular surface disease. IntOphthalmol Clin 2009; 49: 1: 11-20. Review.6. Hamrah P et al. Corneal sensation and subbasalnerve alterations in patients with herpes simplexkeratitis: an in vivo confocal microscopy study.Ophthalmology 2010; 117: 10: 1930-1936.7. Bergmanson JP. Clinical ocular anatomy andPhysiology, 13th ed. 2006; pp 337-341.8. Toshida H, Nguyen DH, Beuerman RW, MurakamiA. Evaluation of novel dry eye model: preganglionicparasympathetic denervation in rabbit. InvestOphthalmol Vis Sci 2007; 48: 10: 4468-4475.9. Tiemstra JD, Khatkhate N. Bell’s palsy: diagnosisand management. Am Fam Physician 2007; 76: 7:997-1002.10. Bhatti MT, Schiffman JS, Pass AF, Tang RA. Neuroophthalmologic complications and manifestations ofupper and lower motor neuron facial paresis. CurrNeurol Neurosci Rep 2010; 10; 6: 448-458.11. Sullivan FM, Swan IR, Donnan PT, Morrison JM,Smith BH, McKinstry B, Davenport RJ, Vale LD,Clarkson JE, Hammersley V, Hayavi S, McAteer A,Stewart K, Daly F. Early treatment with prednisoloneor acyclovir in Bell’s palsy. N Engl J Med 2007;357: 16: 1598-1607.12. Axelsson S, Berg T, Jonsson L, Engström M, KanervaM, Pitkäranta A, Stjernquist-Desatnik A. Prednisolonein Bell’s palsy related to treatment start and age.Otol Neurotol 2011; 32: 1: 141-146.13. Benítez-Del-Castillo JM et al. Relation betweencorneal innervation with confocal microscopy andcorneal sensitivity with noncontact esthesiometryin patients with dry eye. Invest Ophthalmol Vis Sci2007; 48: 1: 173-181.14. Toker E, Asfuroğlu E. Corneal and conjunctivalsensitivity in patients with dry eye: the effect oftopical cyclosporine therapy. Cornea 2010; 29: 2:133-140.15. Benítez-Del-Castillo JM, Acosta MC, Wassfi MA,Díaz-Valle D, Gegúndez JA, Fernandez C, GarcíaSánchez J. Relation between corneal innervationwith confocal microscopy and corneal sensitivity withnoncontact esthesiometry in patients with dry eye.Invest Ophthalmol Vis Sci 2007; 48: 1: 173-181.16. Martin XY, Safran AB. Corneal hypoesthesia. SurvOphthalmol 1988; 33: 1: 28-40.17. Lambiase A, Rama P, Aloe L, Bonini S. Managementof neurotrophic keratopathy. Curr Opin Ophthalmol1999; 10: 4: 270-276.18. Reynolds SA, Kabat AG. Therapeutic options for themanagement of early neurotrophic keratopathy: Acase report and review. Optometry 2006; 77: 10:503-507.19. Araki K, Ohashi Y, Kinoshita S, Hayashi K,Kuwayama Y, Tano Y. Epithelial wound healing inthe denervated cornea. Curr Eye Res 1994; 13: 3:203-211.20. Dastjerdi MH, Dana R. Corneal nerve alterationsin dry eye-associated ocular surface disease. IntOphthalmol Clin 2009; 49: 1: 11-20.
5The dry eye and systemicdisease connectionWhen managing dry eye, keep in mind all the systemic disorders andmedications that have ocular side-effects.Dr Ernie BowlingOD MS FAAO DiplGadsden AL, USAPart of every ophthalmic work-up includesa comprehensive history that incorporates a review of systems and noting all themedications prescribed.There are many systemic diseases thatcan lead to dry eye. Although some individuals may have ocular surface diseaseintrinsically, numerous systemic diseasesinclude an ocular component that manifestsas dry eye. Knowing the systemic cause ofthe ocular surface disease can aid us in themanagement of dry eye disease.The most common associations betweensystemic diseases and dry eye are autoimmune disorders such as Sjögren’s syndromeand rheumatoid arthritis.1 Skin disorderssuch as rosacea are also likely to have adry eye component, that is, evaporativedry eye or meibomian gland dysfunction.2Finally, some systemic medications can leadto dry eye.Systemic diseasesassociated with dry eyeRheumatoid arthritis is a chronic inflammatory disease that affects about 384,000Australians. Roughly two per cent of thepopulation have been diagnosed withrheumatoid arthritis by a doctor.3 Morethan 90 per cent of people with rheumatoidarthritis have dry eye.4 Up to 31 per centof patients with rheumatoid arthritis havea co-existing Sjögren’s syndrome with dryeye.4 Sjögren’s syndrome is one of the mostprevalent autoimmune disorders affecting asmany as 0.5 per cent of Australians.5Sjögren’s syndrome has its own complexities: its pathogenesis is obscure, it presentswith both dry eyes and dry mouth, and it canpresent as primary or secondary Sjögren’ssyndrome. Dry eye syndrome is the mostcommon ocular feature of systemic lupuserythematosus and is often associated withsecondary Sjögren’s syndrome.6 Thyroideye disease is a common systemic diseaseassociated with dry eye due to thyroid hormone imbalance and exophthalmos-relatedcorneal exposure.7One of the most common ocular manifestations of diabetes is dry eye disease.8 Morethan half
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