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Grand Ward Round 2 nd August 2007. Francine Yang Medical Officer. History. Mdm HS 51 year old Indian female Past medical history: Diabetes mellitus – on Metformin Hypertension – on Nifedipine Hyperlipidemia – on Simvastatin Manic depression – on Lithium, Benil & Haloperidol.

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Grand ward round 2 nd august 2007 l.jpg

Grand Ward Round2nd August 2007

Francine Yang

Medical Officer


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History

Mdm HS

51 year old Indian female

Past medical history:

  • Diabetes mellitus – on Metformin

  • Hypertension – on Nifedipine

  • Hyperlipidemia – on Simvastatin

  • Manic depression – on Lithium, Benil & Haloperidol


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Presented on 5th July 2007:

  • Left eye floaters for 2 weeks

  • Photopsia for past 1 year



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Left Fundus (Superior temporal region): Lesion, vitritis, vascular sheating

Right fundus was normal


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Differential diagnoses vascular sheating

Posterior uveitis: Yellowish-white retinal lesion with surrounding vasculitis

Causes to Consider

  • Infective:

    • Parasitic Uveitis

      • Toxoplasma retinitis

      • Toxocariasis

    • Bacterial

      • Tuberculosis

      • Syphilis

    • Viral Uveitis

  • Non-infective:

    • Sarcoidosis

    • Bechet’s disease


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Investigations vascular sheating

  • FBC

  • ESR, CRP

  • RPR, TPPA

  • Toxoplasma IgM & IgG

  • Mantoux test

  • AC tap for Tetraplex PCR & TB PCR

  • Heptatits B screen

  • LFT


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Results vascular sheating

  • TWC 9.9

  • ESR 19, CRP 2.1

  • RPR & TPPA non-reactive

  • Toxoplasma IgM reactive, IgG >300

  • Mantoux test: negative at 72 hours

  • AC tap:

    CMV DNA – not detected

    HSV PCR – not detected

    VZV DNA – not detected

    T. gondii – detected

    Mycobacterium TB – negative

  • LFT normal

  • Hepatitis B screen negative


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Toxoplasmosis vascular sheating

  • Causative agent: Toxoplasma gondii

    • Obligate intra-cellular protozoan

    • Host: domestic cat

    • Transmission: ingestion, transplacental

    • Life cycle: oocysts, trophozoites, bradyzoites (within cysts)

  • Pathogenesis

    • Ingestion of cysts in undercooked meat or contact with cat faeces

    • Small intestine: cysts rupture, trophozoites rapidly multiply and invade the intestinal wall

    • Spread and enter host cells

    • Develop into cysts in which the parasites multiply slowly (bradyzoites)

    • Cell mediated immunity limits spread and when contained, organisms persist as cysts within tissues

      • No inflammation

      • Asymptomatic unless immunosuppression allows activation of the organisms within the cysts


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Clinical Manifestations vascular sheating

  • Most primary infections in immunocompetent adults are asymptomatic

  • Immunocompromised

    Life-threatening disseminated disease, encephalitis

  • Congenital infection: still birth, neonatal disease with encephalitis and chorioretinitis


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Toxoplasma Retinitis vascular sheating

  • Most frequent cause of infectious retinitis in immunocompetent individuals

  • Majority are acquired postnatally

  • Reactivation: recurrent episodes of inflammation when cysts rupture

  • Symptoms

    • Unilateral, sudden onset of floaters, visual loss and photophobia

  • Clinical features

    • White-yellow retinal lesion: usually solitary, multiple foci uncommon

    • Old pigmented chorioretinal scar

    • Severe vitritis, focal, “headlight in the fog”

    • Optic nerve or macular involvement

    • AC inflammation

    • IOP may be increased in 10-20%

  • Immunocompromised patients: Atypical features

    • Extensive confluent areas of retinitis

    • Absence of pre-existing scar suggesting that the infestation is newly acquired or disseminated from extra-ocular sources

    • Minimal/ No vitritis


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Course vascular sheating

  • Immunocompetent patients: healing occurs within 6-8 weeks

  • Inflammatory focus replaced by a sharply demarcated atrophic scar with a hyperpigmented border

  • Vitreous opacities take longer to resolve

  • Resolution of anterior uveitis is a reliable sign of posterior segment healing

  • Complications: serious visual loss

    • Macula involvement

    • Optic nerve head involvement

    • Occlusion of major blood vessel


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Management vascular sheating

  • Aims

    • Reduce duration and severity of acute inflammation

    • Lessen risk of permanent visual loss

    • Reduce risk of recurrence


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Treatment Regime vascular sheating

  • Pyrimethamine + Folinic acid + Sulfadiazine

  • Prednisolone

  • Clindamycin

  • Alternative therapies: Atovaquone, Trimethroprim/ Sulfamethoxazole

  • Adjuncts: Laser photocoagulation, cryotherapy, vitrectomy

  • Maintenance therapy for immunosuppressed patients


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Progress vascular sheating

  • 5th July 4007

    • G. Pred Forte 2 hourly

    • G. Atropine BD

  • 9th July: improvement in symptoms, decrease in floaters

    • Lab results available

    • Examination findings similar to at presentation

    • IOP: 23 in both eyes

    • Continued on G. Pred Forte and Atropine

    • Started on Clindamycin 300mg QDS

    • Prednisolone 40mg OM x 1 week, then 35mg OM

LE


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  • 12 vascular sheatingth July

    • OS: edges of the lesion more well-defined

    • OD: ? New focus of chorioretinitis, no vitritis, no vasculitis

  • 16th July: decrease in left eye floaters

    • OS: edge of lesion drying up, residual vasculitis

    • OD: no change in size of suspect lesion

  • 23rd July

    • FFA done

    • OS: lesion improving morphologically

    • On third week of oral Clindamycin

    • Weekly review


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23 vascular sheatingrd July 2007


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Literature Review vascular sheating

  • Ocular Toxoplasmosis: Clinical features and prognosis of 154 patients

    Lotje E H, Bosch-Driessen, Tos T J, M Berendschot, J V Ongkosuwito, A Rothova. Ophthalmology 2002; 109: 869-878

    • Observational case series of 154 patients with active lesions of ocular toxoplasma

    • 28% presenting with primary retinal lesions, 72% with a combination of active lesions and old scars

    • Primary ocular toxoplasmosis was noted clinically in 82% of the patients with confirmed serologic characteristics of acute phase infection (IgM +)

    • 2 peaks in presenting age:

      • 15-35 years for active OT during the chronic phase of systemic infection

      • 50-70 years for active OT during the acute stage of systemic infection


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Clinical features vascular sheating

  • Macular lesions were more common in patients with congenital infection

  • Peripheral lesions more common in post-natally acquired toxoplasmosis

  • Retinal lesions adjacent to the optic nerve manifested in 21% of patients in the chronic phase of infection; absent in patient’s in the acute phase

    Prognosis and course

  • Recurrence occurred in 60%

  • Manifested in 49% of previously affected eyes and 3% of initially healthy eyes

  • 24% developed blindness in 1 eye, 1% bilaterally

    • Factors: macular location of retinal lesion, retinal detachment, optic nerve atrophy, corticostoids without anti-parasitic drugs, congenital toxoplasmosis


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  • Effects of reatment on recurrence vascular sheating

    • Belfore et al.

    • Patients treated for 14 months were less likely to have recurrent lesions than untreated patients

  • Effects of treatment on short term changes in visual acuity and acute chorioretinitis

    • Inconsistent

Prospective, randomised trial of pyrimethamine and azithromycin vs pyrimethamine and sulfadiazine for the treatment of ocular toxoplasmosis

Prospective randomized trial of trimethoprim/ sulfamethoxazole versus pyrimethamine and sulfadiazine in the treatment of ocular toxoplasmosis

Atovaquone for the treatment of toxoplasma retinochoroiditis in immunocompetent patients


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Thank you vascular sheating


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