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CASE REPORT OF RARE CASE IF GOLDENHAR SYNDROME IN A 3 YEARS OLD MAKE CHILD TITLE PROF TITLE PROFILE CASE REPORT AFFILIATION AUTHOURS NAME DR GOWHAR AHMAD SR CON OPHTHALMOLOGIST FLORENCE HOSPITAL CHANAPORA SRINAGAR KASHMIR UNIVERSITY OF J AND K COUNTRY INDIA EMAIL ADDRESS gowhar.ahmad1948@gmail.com KEY WORDS CONG LIMBAL DERMIOD PREAURICULAR SKIN TAG PREAURICULAR APPENDAGE SQUINT ANOPHTHALMOS COLOBOMAS OF LID IRIS RETINA ASTIGMATISM MICROPHTHALMOS BLEPHROPHMOSIS SYNDTOME FACIAL ASYMETRY HIGH ARCHED PALATE HARE KIO CLEFT PALATE DEFECTS IN KIDNEY DOUBLE URETERS HYDRONEPHROSIS DEFECTS IN LIMBS SPINE CING HEART UNDERLYING ORBITAL INVOLEMENT DENTAL ANAMOLIES HEARING DEFECT IMPAIRMENT OF MEMORY MENTAL FACALITY 7TH N INVOLVEMENT TRIGEMINAL ANASTHESIA ABASTRACT IT WAS MAURICCE GOLDENHAR AN AUSTRIAN OPHTHALMOLOGIST IN THE YEAR 1850 WAS THE FIRST TO DESCRIBE THE SYNDROME COMPLEX CHARETERISED BY CONG PRESENCE OF LIMBAL DERMIID WITH CONG ASSOCIATED ORESENCE OF PREAURICULAR SKIN TAG OR APPENDAGE SOMETIMES PRESENCE OF SQUINT ANOPHTHALMOS COLOBOMAS OF THE U LID IRIS RETINA ASTIGMATISM MICROPHTHALMOS BLEPHROPHMOSIS SYNDROME MAY ALSO BE SEEN HOWEVER IT IS VERY RARE G H S IS ALSO TERMED AS OCULO AURICULO VERTEBRAL SYNDROME AND CRANIIFACIAL SYNDROME INVOLVIMG HEAD FACE EAR NOSE SOFT PALATE AND MANDIBLE 80 TO 85 CASES OF G H S ARE NORMAL from.visual AND MENTAL FACALITY POINT OF VIEW IT IS OMLY IN 10 TO 15 PERECENT CASES OF G H S THEIR SRE ADDITIONAL CONG ANAMOLIES WHICH ARE DUE TO INCOMPLETE DEVOLPMENT OF 1ST AND SECOND BRANCHIAL ARCH DUE TO DEFECTS IN GENES NOT INHERETED AUTOSOMAL DOMINANT AND RECESSIVE ALSO DUE TO MATERNAL GESTATIONAL D M IR EXPOSURE TO RUBELLA HEAMOPHILUS CYTOMEGALIC INC VIRUS OR INTAKE OF THALIDOMIDE COCAINE AND RETINIOC ACID IN THE FIRST TRIMESTER OF PREGNANCY ONE HAS TO WORK UP FOR THESE ANAMOLIES IN THE FIRM OF USG ABDOMEN XRAY LIMBS SPINE ECHOCARDIOGRAPHY MRI ORBITS OPHTHALMIC EXAMINATION DENTAL EXAMINATION HEARING TESTS E E G CONG DERMIODS ARE USUALLY UNILATERAL CAN BE BILTERAL THOUGH RARE CAN INVOLVE ENTIRE CORNEA BUT MAY BE CONFINED TI CONJUCTIVA ONLY INCIDENCE 1 IN 10 000 INFEROTEMPORAL SITE IS TGE COMMONEST 70 PERCENT MALE FEMALE RATIO 3 TO 2 GRADED ACCORDING TO CONEAL INVOLVEMENT GRADE 1 EPETHELIAL INVOLVEMENT GRADE 2 DESMETS MEMBRANE INVOLEMENT GRADE 3 INVOLVEMENT OF ENTIRE ANT SEGMENT CASE REPORT 3 YEARS OLD MALE CHILD WAS SEEN BY ME SOME TIME AGO WITH PARENTS HAVING NOTICED SMALL PALISH WHITE LESION IN THE INFEROTEMPRAL SITE IF LIMBUS R EYE WITH ASSOCIATED CONG PRESENCE OF L SIDED PREAURICULAR SKIN TAG SYNDROMECOMPKEX DIAGNOSTIC OF G H S FT DELIVERED CHILD FROM NON COUSIN. MARRIED COUPLE FOLLOWING LSCS NO.HISTORY OF EXPOSURE TO OXYGEN JAUNDICE BREAST FED NORMAL MIKE STONES VISION MYDRIATIC REFRACTION AND FUNDII NORMAL NO OTHER ASSOCIATED CONG ANAMOLIES THIS CHILD HAD LIMBAL DERMIOD NOT INVOLVING VISUAL AXIS NEEDED ONLY REASSURANCE FOR THE PARENTS AND OBSERVATION HOWEVER IF THE LIMBAL DERMIOD INVOLVES VISUAL TREATMENT IS SURGICAL WHICH IS BOTH VISUAL AND COSMOTIC SURGICAL MODALITIES ARE LAMELLAR KERATAPLASTY AUTOGRAFT STEM CELL GRAFT SMILE LENTICULE TATOOINING FIBRIN GLUE HERE AFTER EXCITON OF DERMIOD.ITNIS TATTOED TO GET ORIGINAL COLOUR THEN CORNEAL LENTICULE IS OUT IN SITU HELD IN POSITION WITH FIBRIN GLUE SINCE NO STICHES ARE APPLIED SO PIST OPERATIVE PAIN AND ASTIGMATISM IS LESS DISCUSSION G H S IS A GENETIC DISORDER CHARETERISED BY CONG PRESENCE OF CONG LIMBAL DERMIOD WITH CIG ASSOCIATED PRESENCE OF PREAURICULAR SKIN TAG OR APPENDAGE WAS DESCRIBED FIRST BY AN AUSTRIAN OPHTHALMOLOGIST MAURICCE GOLDENHAR IN THE YEAR 1850 80 TO 85 PERCENT CASES OF G H S ARE NORMAL FROM VISUAL AND MENTAL FACALITY POINT OF VIEW ONLY 10 TO.15 PERCENT CASES OF ADDITIONAL CONG ANAMOLIES REFENCES WE GAVE G H S SUPPORT GROUPS THEIR ARE FAMILIES OF G H S 17 DUCH FAMILIES IG G H S ARE SEEN IN GREECE CHILDREN BORN IN MIDDLE EAST IN GULF WAR BORN IN DIFFERENT MILIATRY HOSPITALS HAD HIGH INCEDENCE OF G H S MITTAL ETAL IN YEAR 1968 IN INDIAN JOURNAL OF OPHTHALMOLOGY REPORTED 3 CASES OF OPTIC NERVE DRUSENS ASSOCIATED WITH G H S
MINI REVIEW ON BIL CONG CORNEAL DYSTROPHY AND ITS RARE CONG ANAMOLIES AUTHOURS NAME DR GOWHAR AHMAD SR CON OPHTHALMOLOGIST FLORENCE HOSPITAL CHANAPORA SRINAGAR KASHMIR INDIA EMAIL ADDRESS GOWHAR.AHMAD1948@GMAIL.COM CONG CORNEAL DYSTROPHY IS A RARE CONG DISORDER WHOSE EXACT CSUSE IS NOT KNOWN IT IS A KIND OF CONDITION CHARETERISED ZBY DEPISITION OF SOME UNKNOWN SUBSTANACE IN TGE CORNEAL STROMA EXACT CAUSE NIR KNOWN HOWEVER HEREDOFAMALIAL TENDENCY PLAYS AN IMPORTANT FACTOR CONG COR DYSTOPHY IS USUALKY BILTERAL WHERAS CONG CORNEAL DEGENERATION IS UNILATERAL AND OF NON HERDETERY EXISTENCE CLINICAL CLASSEFECATION OF CONG CORNEAL DYSTROPHY IS LESIONS IN TGE CORNEA OF AN UNKNOWN ATEOLOGY WHICH MAY MANIFEST EITHER AT BIRTH OR AT 1ST IR 2ND DECADE OF LIFE MAY REMAIN STATIONERY OR PROGRESSIVE HAS GOT STRONG HERODOFAMALIAL TENDENCY BIL CENTRAL SYMETRICAL CORNEAL OPACITY WITH ABSENCE OF DEEP VASCULARISATION AND IMPAIRED CORNEAL SENSATIONS IS CONG CORNEAL DYSTROOHY UNLESS PROVED OTGERWISE DOME OF RARE ASSOCIATED CONG ANAMOLIES ARE CONG GLAUCOMA KERATACONUS ANT STAPHYLOMA CONG ABSENCE OF DEDT MEMBRANE DEAFNESS C H E D K C SICCA MEDULLATED OPTIC NERVE FIBERS PTOSIS U KID CONJUCTIVAL XEROSIS
RECENT ADVANCES IN THE BLOOD SUPPLY OF OPTIC NERVE HEAD AUTHOURS NAME DR GOWHAR AHMAD SR CON OPHTHALMOLOGIST FLORENCE HOSPITAL CHANAPORA SRINAGAR KASHMIR INDIA E-MAIL ADDRESS gowhar.ahmad1948@gmail.com WE KNOW OPTIC NERVE IS SUPPLIED BY POST CILIARY ARTERY BRACH OF OPHTHALMIC ARTERY WHICH ARISES FROM IST DIV OF INTERNAL CAROTID ARTERY DISTAL TO CAVERNOUS SINUS S S HARRY A WIRLD FAMOUS ANATOMIST WHO HAS WRITTEN LOT OF ARTIVLES IN B J O IN RECENT ADVANCES OF BLOOD SUPPLY OF OPTIC NERVE HEAD SAYS THAT P C A AFTER SUPPLYING THE DISC HAS GOT SEGMENTAL DISTRIBUTION IN CHORIOD AND CHORIODAL VESSELS ARE END ARTERIES IT FOLLOWS THEIR FORE THAT ANY CONDITION WHICH INTERFERES WITH BLOOD SUPLY OF PC A NOT ONLY PRODUCES CHANGES IN OPTIC NERVE HEAD BUT IN EPI PAPILLARY CHORIOD CHATRERISED BY CAVERNOUS DEGENERATION OF OPTIC NERVE HEAD FILLING OF BLOOD IN OPTIC N HEAD AND EPIPAPILLARY CHIRIOD DEPEND UOP DIFFERENCE OF PERFUSION PRESDURE AT OPTIC N HEAD AND EPIPAPILLARY CHIRIOD GREATER THE THAT PERFUSION PRESSURE BETTER IS THE FILLING IN A WAY IF IOP IS LOW PERFUSION PRESSURE IS HIGH SO BETTER FILLING AND VISE VERSA IF IOP IS HIGH PERFUSION PRESSURE IS LOW SO NOT BETTER FILLING HARRY'S CONCEPT OF RECENT ADVANCES IN BLOOD SUPPLY OF OPTIC NERVE HEAD GIVES USCAN IDEA OF ATEOPATHOGENESIS OF ANT ISCHEMIC OPTIC NEUROPATHY BITH ARTERITIC AND NON ARTERITIC
MEDECAL TREAMENT OF MYOPIA AUTHORS NAME DR GOWHAR AHMAD SR CON OPHTHALMOLOGIST FLORENCE HOSPITAL CHANAPORA SRINAGAR KASHMIR INDIA EMAIL ADDRESS GOWHAR.AHMAD1948@GMAIL.COM ARTICLE NAME ORTHOKERATALOGY ORTHOKERATALOGY IS A KIND OF MODALITY FOR M3DICAL TREAMENT IF MYOPIA IN CHILDREN OF 6 NTO 8 YEARS OF AGE BY SPECIAL TYPES OF CONTACT LENSES KNOWN AS ARTHO L CONTACT LENSES WHEN PUT AT NIGHT BY CHILDREN OF 6 TO 8 YEARS OF AGE THEY CAUSE CORNEAL RESHAPING AND UN TGE MORNING MYOPIA GETS CORRECTED FIR COUPLE OF DAYS ALSO VERY GOOD FIR CHILDREN WHO WANT TI GI FOR SPORTS THESES SPECIAL C LENSES ARE ALSO KNOWN TO REGRESS PROGRESSION OF MYOPIA BY 40 PERCENT ALSI HAS BEEN TRIED FOR HYPERMETROPIA PRESBYOPIA ADTIGMATISM
MINIREVIEW AUTHOURS NAME DR GOWHAR AHMAD SR CON OPHTHALMOLOGIST FLORENCE HOSPITAL CHANAPORA SRINAGAR KASHMIR INDIA NAME OF THE ARTICLE SOME OF THE CONG ANAMOLIES ASSOCIATED WITH OPTIC DISC 1 CONG PUT OF DISC 2 CONG COLOBOMA OF DISC 3 CONG TILTED DISC SYNDTOME 4 HYPOPLASIA OF DISC 5 DRUSEN OF DISC 6 MEDULLATED OPTIC NERVE FIBERS 7 MORNING GLORY DISC SYNDROME 8 PERI PAPILLARY POST STAPHYLOMA
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A coloboma describes conditions where normal tissue in or around the eye is missing from birth. Coloboma comes from the Greek word that means “curtailed.” The eye develops quickly during a fetus’ first three months of growth. A gap, known as the choroidal fissure, appears at the bottom of the stalks that eventually form the eye. This fissure generally closes by the seventh week of gestation. If it does not close, a coloboma or space forms. A coloboma can affect one or both eyes. If both eyes are involved, it can affect them the same way or differently. There are different types of coloboma, depending on the part of the eye affected: Eyelid coloboma- A piece of the upper or lower eyelid is missing. Lens coloboma- A piece of the lens, the part of the eye that focuses light onto the retina, is missing. Macular coloboma- The macula is the central part of the retina responsible for daylight, fine and color vision. In this coloboma, the macula fails to develop normally. Optic nerve coloboma- In this coloboma, the optic nerve, the bundle of fibers that relay light signals to the brain, is hollowed out, reducing vision. Uveal coloboma- The uvea is the middle layer of the eye. This coloboma can affect the iris, the colored part of the eye, giving it a distinct keyhole or cat-eye appearance. Chorio-retinal coloboma- In this coloboma, part of the retina (the light-sensitive tissue lining the back of the eye) is missing.
Dr. Dinesh Choudhary2 Likes12 Answers - Login to View the image
Goldenhar syndrome Corneo limbal dermoid Pre auricular tags .(b/l).+hypoplasia of mandible. Maxilla ..Sen neural deafness were present
Dr. Kunal Verma4 Likes10 Answers - Login to View the image
SPOTTER- 6yr old girl, presented with following findings- B/L. Diagnosis, associated syndromes/ conditions and management. What is the embryologic significance
Dr. Murari M5 Likes19 Answers - Login to View the image
Female 2kg delivered normally at term without any significant maternal history.mother age is 40 years having 4 children all r normal. This baby is tachypnic and maintaining saturation at minimal oxygen.neonate has micrognathia rounded eyes left microtia grade 2 almost and right sided is grade 3.there is murmur which is pansystolic. Other systemic review is unremarkable Ur opinion Plz
Dr. Anirudha Kulkarni10 Likes19 Answers - Login to View the image
OCULAR MANIFESTATIONS OF SLE. SLE is a chronic auto immune disease with multisystem involvement.SLE is multifactorial . Possible factors are genetic susceptibility, environmental factors and disturbances in both innate and adaptive immunity. Early detection and prompt referral to ophthalmologist can prevent permanent visual loss in some instances. OCULAR MANIFESTATIONS. SLE can affect any part of the eye and visual pathway.Eyelids ,orbit, lacrimal system , conjunctiva ,cornea ,sclera ,episclera ,retina , choroid ,uvea ,cataract ,glaucoma and cranial nerve are all involved. EXTERNAL EYE DISEASES : 1.EYELID DISEASE:Discoid lupus rash over the eyelids present as discrete raised scaly lesions. HPE shows hyperkeratotic epithelium with liquefactive degeneration of the basal layer and dense perivascular lymphocytic infiltration. ANA titre,ESR,C reactive protein,CBC,LFT,RFT Complement factors C3 &C4,anti phospholipid antibodies ,immunoglobulins,rheumatoid factor TSH,VDRL,GFR,24 hour urinary protein etc are the investigations necessary. 2.LACRIMAL SYSTEM DISEASE : Dry eye syndrome is the most common ocular presentation. 3.ORBITAL DISEASE. It can present as orbital mass,periorbital oedema ,orbital myositis,panniculitis,acute orbital ischemia and infarction. Clinical presentation can be ptosis,proptosis, orbital pain,limitation of extra ocular movements and enophthalmos. Treatment is by immunosupression. ANTERIOR EYE SEGMENT MANIFESTATIONS 4.CONJUNCTIVA : Chronic conjunctivitis is infrequent.Conjunctiva is inflammed in SLE associated keratitis and scleritis. Treatment NSAID or anti malarial therapy given. 5.CORNEAL DISEASE: Breakdown of corneal epithelium can cause recurrent corneal erosions.The inflammatory process in SLE causes PERIPHERAL ULCERATIVE KERATITIS. Treatment is with systemic corticosteroids and cytotoxic agent during acute phase of the disease and lubrication of corneal surface concommitantly.TOPICAL STEROIDS ARE NOT ADVOCATED AS THEY INHIBIT NEW COLLAGEN PRODUCTION AND THEREBY INCREASE THE RISK OF PERFORATION. 6.EPISCLERA : Episcleritis is benign inflammation of the episclera. 7.SCLERAL DISEASE : Scleritis is a painful and potentially sight threatening disorder.b ANTERIOR SCLERITIS presents as diffuse nodular or necrotising scleritis resulting in significant destruction and scleral thinning. Redness is caused by injection of deep episcleral vessels. POSTERIOR SCLERITIS :Affects the sclera posterior to the equator of the globe. presenting symptoms are pain and blurry vision caused by exudative retinal detachment papillitis and cystoid macular edema. Immunosupression is essential. 8.ANTERIOR UVEITIS Rare presentation.Prompt immunosuppressive therapy is considered. 9.CATARACT : Iatrogenic steroid use in SLE is associated with cataract formation. 10.GLAUCOMA : Open angle glaucoma and angle closure glaucoma are seen in SLE. POSTERIOR EYE SEGMENT MANIFESTATIONS 11.SLE RETINOPATHY. The earliest findings are small intra retinal hemorrhages and cotton wool spots,multiple areas of polygonal retinal whitening between the retinal arterioles and venules. Systemic therapy with steroids, Immunosupression ,laser therapy,intra vitreal anti-vascular endothelial growth factor agents (anti-VEGF) and vitrectomy are all treatments offered. 12.RETINAL VEIN OCCLUSION / RETINAL ARTERY OCCLUSION. Pathogenesis of vaso occlusive retinopathy is due to thrombosis associated with anti- phospholipid syndrome. 13.RETINAL VASCULITIS : This is a rare potentially blinding complication of SLE. 14 CHOROIDOPATHY : Choroidopathy with exudative retinal detachment is a rare ocular manifestation of SLE.It is manifested as multi focal serous detachments of the retinal pigment epithelium (RPE) and the neural retina ,with the transduction of the accumulated fluid through bruch's membrane and RPE affected by the choroidal ischemia and inflammation. The presenting feature is visual loss ,which depends on the extent of the macular involvement. 15. OPTIC NEURVE DISEASE: SLE can cause optic neuritis and ischemic optic neuropathy.The optic nerve damage is believed to be secondary to an occlusive vasculitis of the small arterioles of the nerve , which leads to demyelination and /or axonal necrosis. Signs of optic nerve disease. *Reduced visual acuity. *Impairment of color vision. *Diminished light brightness sensitivity. *Decreased contrast sensitivity. *Afferant pupillary defect. *Visual field defects. 16.CRANIAL NERVE INVOLVEMENT. Ocular motor nerve palsy can occur. MANY OCULAR COMPLICATIONS ARE PREVENTABLE,TREATABLE OR EVEN CURABLE.PROMPT TREATMENT WITH HIGH DOSE SYSTEMIC CORTICOSTEROIDS AND IMMUNOSUPPRESSIVE THERAPY ARE NECESSARY.
Dr. Suvarchala Pratap11 Likes18 Answers
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