Chiombon chua corpuz cua david de vera detera diaz din dizon eugenio evangelista
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Chiombon. Chua. Corpuz. Cua. David. De Vera. Detera. Diaz. Din. Dizon. Eugenio. Evangelista. Interesting case. General Data. CT 29/Female DOA: 03 August 2010. Chief Complaint. Blurring of Vision. History of Present Illness. History of Present Illness. History of Present Illness.

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Chiombon chua corpuz cua david de vera detera diaz din dizon eugenio evangelista

Chiombon. Chua. Corpuz. Cua. David. De Vera.

Detera. Diaz. Din. Dizon. Eugenio. Evangelista.

Interesting case


General data
General Data

  • CT

  • 29/Female

  • DOA: 03 August 2010


Chief complaint
Chief Complaint

  • Blurring of Vision






Past medical history
Past Medical History

  • Allergies: none

  • No previous illnesses, hospitalizations and blood transfusions

  • TB exposure: (-)

  • Injuries: Burn 2nd and 3rd degree burns (1992)

  • Medications: none


Personal and social history
Personal and Social History

  • Diet: Mixed

  • Smoking: 3.5 pack years

  • Alcohol: 2 bottles of beer/day from 23-27 years

  • Substance abuse: Denies illicit drug use


Family history
Family History

  • Diabetes Mellitus- Grandmother

  • Glaucoma- (-)

  • Hypertension – (-)

  • Cancer – (-)


Review of systems
Review of Systems

  • (-) Weight change , (-) fever & chills

  • (-) rashes; (-)pruritus;(-) bruising

  • (-) dizziness; syncope

  • (-) blurring of vision, eye discharge

  • (-) hearing changes; pain; discharge; vertigo;

  • (-) epistaxis; obstruction; nasal discharge, gum bleeding; oral ulcers

  • (-) cough, (-) dyspnea, (-) night sweats

  • (-) chest pain; (-)dyspnea on exertion; (-)PND; (-)palpitations

  • (-) abdominal pain; (-)dysphagia, (-)nausea, (-)vomiting,(-) Dyspepsia

  • (-)diarrhea, (-) constipation (-) indigestion, (- flatulence

  • (-) frequency; urgency; dysuria; nocturia; dribbling

  • (-) arthralgia/arthritis (-) trauma; (-)back pain


Physical examination
Physical Examination

  • Conscious, Coherent, Ambulatory, not in Cardiorespiratory distress

  • Vital signs: 110/80, PR 74 Regular, RR: 20, Temp 36.6 C

  • Warm, moist skin, no active dermatoses (+) Scars, both upper extremeties

  • Pink palpebral conjunctiva, anicteric sclerae, pupils L= 3-4mm, RTL, R= 2-3 mm RTL anisocoric, slightly hyperemic conjunctiva

  • Septum midline, turbinates not congested, no nasoaural discharge, impacted cerumen

  • Moist buccal mucosa, no oral and palatal lesions, nonhyperemic posterior pharyngeal wall, tonsils not enlarged

  • No limitation of neck movement, no palpable cervical lymphadenopathy

  • (-) thyroid gland enlargement

  • No breast mass palpated, no discharge

  • Thorax: no deformities, no intercostal and subcostal retractions, symmetrical chest expansion, equal tactile fremiti, resonant, clear and equal breath sounds


Physical examination1
Physical Examination

  • Adynamic precordium, AB at the 5th LICS MCL, no LV heave, thrills, no lifts, s1 louder than s2 at the apex, s2 louder than s1 at the base, no murmurs


Physical examination2
Physical Examination

  • Globular abdomen, Normoactive bowel sounds, (-) bruits, (-) tenderness, guarding, masses, (-) Murphy’s sign, Nonpalpable gallbladder, Traube’s space not obliterated

  • Pulses full and equal, (-) cyanosis, edema, clubbing


Eye examination
Eye Examination

Amsler Grid

(+) Scotoma on OU

(+) Metamorphopsia


Eye examination1
Eye Examination

External eye examination:

  • Eyelids: non tender

  • Lashes: not matted

  • Conjunctiva: Hyperemic

  • Sclera: anicteric

  • Cornea: Clear

  • Anterior Chamber: deep

  • Lens: Clear

  • Pupils: Anisocoric L= 3-4mm, RTL, R= 2-3 mm RTL

  • Iris: Pigmented


Eye examination2
Eye Examination

  • EOM: Full and equal

  • Fundoscopy:

    • (+) ROR

    • (+) Blurred disc Margins , OU

    • (+) Serous Retinal Detachment, OU

    • (+) Hyperemia of choroid

  • Tonometry: 18mmHg OU

  • Fluorescein angiography: hyperfluoresence of optic disc


Neuroexam
NeuroExam

  • Conscious, coherent, oriented to 3 spheres, able to follow commands, GCS 15 E4V5M6

  • (-) Anosmia, anisocoric pupils L= 3-4mm, RTL, R= 2-3 mm RTL; Can smile, frown, raise eyebrows, uvula midline, can shrug shoulders, turn head from side to side against resistance tongue deviated to right. Motor exam: RUE: 5/5, RLE:5/5, LUE and LLE 5/5.

  • Reflexes: ++

  • Cerebellar- can do APST, FTNT with ease, No tremors

  • No sensory deficit

  • (-) Babinski, Nuchal rigidity, Brudzinski, Kernig’s sign


Initial assessment
Initial Assessment

  • Incomplete Vogt-Koyanagi-Harada Disease, Acute uveitic stage

  • r/o TB Uveitis


Uveitis
Uveitis

  • is inflammation of the Uvea Tract, middle section of the eye.

  • Uvea Tract has three parts:

    • the Iris (the colored part of the eye)

    • Ciliary body (behind the iris, accomodation, aqueous humor)

    • Choroid (the vascular lining tissue underneath the Retina).



Incomplete vogt koyanagi harada disease acute uveitic stage r o tb uveitis
Incomplete Vogt-Koyanagi-Harada Disease, Acute uveitic stager/o TB uveitis



Laboratories
Laboratories

  • CBC

  • Chest X-ray

  • AFB smear

  • PPD



Chest x ray
Chest X-ray

  • Lung fields are clear

  • The heart is not enlarged

  • Both hemidiaphragm and costophrenic sulci are intact

  • Impression: No significant chest findings


Afb stain
AFB Stain

  • No Acid Fast Bacilli seen in 300 oil immersion fields on both routine and concentration methods


Therapeutics
Therapeutics

  • Methylprednisolone 1mg/kg/day per IV for 3 days

  • Ranitidine 150mg/tab, 1 tab OD

  • Tropicamide eyedrops 1gtt BID

  • CaC03 + Vit D 1 tab OD


Course in the wards
Course in the wards

  • On admission:

    • CBC with Platelet, PPD, Chest X-ray, and ESR were requested.

    • Tropicamide eyedrops OU was also started.

  • On the 2nd hospital day

    • Referred to Rheumatology

      • Plans for induction of high-dose steroids


Course in the wards1
Course in the Wards

  • On the 3rd Hospital day:

    • PPD test was started

  • On the 4th Hospital day

    • Methylprednisolone 1g/kg to run for 1 hour for 3 days.


Course in the wards2
Course in the wards

  • On the 5th hospital day, visual acuity of the patient improved:

  • (-) Hyperemia of the Conjunctiva

  • (-) PPD test

  • Patient was given 2nd dosage of Methylprednisolone 1mg/kg/IV to run for 1 hour

  • CaC03 + Vit D 1 tab OD was started


Course in the wards3
Course in the wards

  • On the 6th hospital day

  • Patient received last dose of Methylprednisolone 1mg/kg/IV to run for 1 hour.


Course in the wards4
Course in the wards

  • 7th hospital day

  • Prednisone 20mg/tab 1 tab OD was started


Course in the wards5
Course in the wards

  • 8th hospital day

  • Indirect Fundoscopy: Decrease in macular edema, decrease in vitreous cell and optic nerve hyperemia

  • Patient was discharged


Discussion
DISCUSSION

VOGT-KOYANAGI-HARADA DISEASE


Vogt koyanagi harada disease
Vogt-Koyanagi-Harada disease

  • Inflammatory condition of autoimmune nature in which cytotoxic T cell target melanocytes (eyes, inner ears, skin)

  • Described by Persian Physician (Ali-ibn-Isa 940-1010 AD) –Poliosis + eye inflammation

  • 1932- Combined disorders described by Vogt, Koyanagi and Harada manifestations were under the same disease process

New insights into Vogt-Koyanagi-Harada disease. Arq Bras Oftalmol. 2009;72(3):413-20


Epidemiology
Epidemiology

  • Predilection for more darkly pigmented races: Asians, Hispanics, American Indians

  • 6.8-9.2% of all Uveitis referrals in Japan


Vogt koyanagi harada disease classification
Vogt-Koyanagi-Harada diseaseClassification

  • International Nomenclature Committee Revised Diagnostic Criteria

  • Classification:

    • Complete VKH disease

    • Incomplete VKH disease

    • Probable VKH disease

New insights into Vogt-Koyanagi-Harada disease. Arq Bras Oftalmol. 2009;72(3):413-20


Applicability of the 2001 revised diagnostic criteria in Brazilian Vogt-Koyanagi-Harada disease patients

Arq Bras Oftalmol. 2008;71(1):67-70


Vogt koyanagi harada disease stages
Vogt- Brazilian Vogt-Koyanagi-Harada disease patients Koyanagi-Harada diseaseStages

  • Prodromal stage

  • Acute uveitic stage

  • Convalescent stage

  • Chronic recurrent stage


Stages
Stages Brazilian Vogt-Koyanagi-Harada disease patients


Pathophysiology
Pathophysiology Brazilian Vogt-Koyanagi-Harada disease patients

Vogt-Koyonagi-Harada Disease


Vogt koyanagi harada disease autoimmunity against melanocytes
Vogt- Brazilian Vogt-Koyanagi-Harada disease patients Koyanagi-Harada diseaseAutoimmunity Against Melanocytes

  • Clinical features of choroidal and skin depigmentation

  • Transmission electron microscopy (early stage): close contact between melanocytes and lymphocytes in the uvea

  • Histopathology (end stage): disappearance of choroidal melanocytes, and

  • Immunohistochemistry (end stage): T and B lymphocytes in the choroid

New insights into Vogt-Koyanagi-Harada disease. Arq Bras Oftalmol. 2009;72(3):413-20


Vogt koyanagi harada disease autoimmunity against melanocytes1
Vogt- Brazilian Vogt-Koyanagi-Harada disease patients Koyanagi-Harada diseaseAutoimmunity Against Melanocytes

  • Role of CD4+ T cells

    • Cytotoxic leukocytes against melanoma cells in peripheral blood and CSF

    • Cytotoxic CD4 and CD8 T lymphocytes against human melanocytes are present in the peripheral blood.

    • Activated CD4+ T cells in depigmented skin and melanin-laden macrophages d in CSF

New insights into Vogt-Koyanagi-Harada disease. Arq Bras Oftalmol. 2009;72(3):413-20


Vogt koyanagi harada disease autoimmunity against melanocytes2
Vogt- Brazilian Vogt-Koyanagi-Harada disease patients Koyanagi-Harada diseaseAutoimmunity Against Melanocytes

  • Immunogenetics

    • HLA-DR4/DR53

    • secondary association with HLA-DR1 involving a shared sequence linked to susceptibility to rheumatoid arthritis.

    • HLA-DRB1*0405

New insights into Vogt-Koyanagi-Harada disease. Arq Bras Oftalmol. 2009;72(3):413-20


Pathophysiology1
Pathophysiology Brazilian Vogt-Koyanagi-Harada disease patients


Clinical findings in acute phase of vkh
Clinical findings in acute phase of VKH Brazilian Vogt-Koyanagi-Harada disease patients

Figure 1 - A & B: Fundus pictures of both eyes show disc hyperemia, white-yellowish choroidal lesions,

and localized exudative retinal detachments; C & D: Fluorescein angiographies of both eyes show pin-point hyperfluorescence and dye pooling corresponding to areas of retinal detachments; E & F: Indocyanine green angiographies show areas of diffuse hyperfluorescence, dark spot, and “hot-spots”

New insights into Vogt-Koyanagi-Harada disease. Arq Bras Oftalmol. 2009;72(3):413-20


Clinical findings in chronic phase of vkh
Clinical findings in chronic phase of VKH Brazilian Vogt-Koyanagi-Harada disease patients

Figure 2 – A & B: Fundus pictures of both eyes show diffuse retinal depigmentation and peripapillary fibrosis;

C & D: Fluorescein angiographies of both eyes show diffuse window retinal pigment epithelium defects; E & F: Indocyanine green angiographies

show dark spots and diffuse late hyperfluorescence suggestive of disease activity

New insights into Vogt-Koyanagi-Harada disease. Arq Bras Oftalmol. 2009;72(3):413-20


Treatment corticosteroids
Treatment- Corticosteroids Brazilian Vogt-Koyanagi-Harada disease patients

For most patients with bilateral serous detachments and severe visual loss, begin therapy with systemic prednisone

Severe Cases

  • use intravenous methylprednisolone (up to 1 g/d) for several days before beginning oral prednisone (1 mg/kg/d)

    Corticosteroids

    • anti-inflammatory properties and modify the body's immune response to diverse stimuli

    • the length of treatment and subsequent taper must be individualized for each patient


Treatment systemic corticosteroids
Treatment- Systemic Corticosteroids Brazilian Vogt-Koyanagi-Harada disease patients

Prednisone

  • Decrease inflammation

    • reversing increased capillary permeability and suppressing PMN activity

  • DOSE

    • 1-1.5 mg/kg/d PO qd initially

    • Severe cases with profound loss of vision and bilateral serous detachments may require up to 2 mg/kg/d

    • length of treatment and tapering individualized for each patient

      • not be less than 3 mo to avoid recurrence

  • CI: hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease


Treatment topical corticosteroids
Treatment- Topical Corticosteroids Brazilian Vogt-Koyanagi-Harada disease patients

Prednisone Acetate

  • For the treatment of associated anterior uveitis

  • Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability

    DOSE:

  • Instill1 gtt into conjunctival sac

  • dosing frequency is based upon severity of inflammation

    • Severe inflammation may require dosing every hour

    • moderate-to-mild anterior uveitis, dosing at 4-6 times daily may be sufficient

    • taper over an appropriate period to avoid rebound inflammation

      Precaution: hypertension, cataract formation with long-term use, decrease frequency to avoid adrenal insufficiency

      CI: Documented hypersensitivity; viral, fungal, or tubercular infections; cataract and glaucoma


Treatment cycloplegics
Treatment- Cycloplegics Brazilian Vogt-Koyanagi-Harada disease patients

Tropicamide

  • parasympatholytic that produces short acting mydriasis and cycloplegia

  • Instillation of a long-acting cycloplegic agent can relax any ciliary muscle spasm that can cause a deep aching pain and photophobia

  • used to treat anterior uveitis, decreasing risk of posterior synechiae and decreasing inflammation in the anterior chamber of the eye

    Side Effects

  • transient stinging and a slight and transient rise in intraocular pressure

  • cause redness or conjunctivitis (inflammation) and also blurs vision for a short while after instillation

    Tropicamide is preferred over Atropine

    • Atropine has a longer half-life, causing prolonged dilation and blurry vision for up to a week


Treatment homatropine
Treatment- Homatropine Brazilian Vogt-Koyanagi-Harada disease patients

Homatropine

  • Blocks responses of sphincter muscle of iris and muscle of ciliary body to cholinergic stimulation, inducing mydriasis in 10-30 min and cycloplegia in 30-90 min

  • last up to 48 h

  • Individuals with heavily pigmented irides may require larger doses

    DOSE: 1-2 gtt of 2% or 1 gtt of 5% solution up to qid to induce cycloplegia and relieve ciliary spasm

    CI: Documented hypersensitivity; narrow-angle glaucoma

    Precaution: elderly persons w/ increased intraocular pressure; toxic anticholinergic systemic adverse effects can occur but are rare when used sparingly


Treatment immunosuppressives
Treatment- Immunosuppressives Brazilian Vogt-Koyanagi-Harada disease patients

For those patients who fail to respond to high-dose systemic corticosteroids or develop intolerable adverse effects, immunodulatory therapy

  • Cyclosporine

  • Mycophenolate mofetil

  • Azathioprine

  • Tacrolimus

  • Cyclophosphamide


THANK YOU! Brazilian Vogt-Koyanagi-Harada disease patients


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