charla de catarata. copia cd - pdf[1]
TRANSCRIPT
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Dra. Michelle Freundt CoelloPráctica Clínica en Oftalmología Veterinaria
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PATOLOGIAS
Liberación de células dentro del ojo.
Cambios en la posición.
Pérdida de transparencia.
Esclerosis.
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CAUSAS
Hereditaria
Traumática (electricidad, golpes, úlceras)
Tóxica: Diazóxido, Fenilpiperazina, penfloxacina, fluconazol, DMSO
Metabólica (uveítis, diabetes, T4, Cushing)
Radiaciones
Senil
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FISIOPATOGENIA
Modificación de las células endoteliales.
Fibras del lente.
Acumulo de líquido.
Coagulación proteica y cambios en el citoplasma
Opacidad
Factores: luz del día, dieta, diabetes.
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CLASIFICACION
Por localización
Nuclear
Laminar
Cortical (Centr)
Coronaria (Per)
Subcapsular
Polar Ant y Post
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CLASIFICACION
EVOLUCION EDAD
Estacionaria
Progresiva
Congénita
Juvenil
Senil
-Inmadura-Madura-Hipermadura
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UNA VEZ HECHO EL DIAGNÓSTICO, EL SIGUIENTE PASO ES REMITIRLO PARA UN ESTUDIO MAS COMPLETO Y ESCOGER LA
TÉCNICA NECESARIA.
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TRATAMIENTO MEDICO
Médico
Solucionar enfermedad precedente
Aminoácidos, Vitaminas
Lutrax (Azapentaceno)
Vitreolent, Catalín.
Ocluvet . N-acetyl Carnosina 2% + glutation+ rivoflavina + l-taurina.
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TRATAMIENTO QUIRURGICO
Enfermedades precedentes. ARP
Indicación a partir de la aparición de ceguera
Premedicación 24 horas antes.
Midriasis pupilar
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FACOEMULSIFICACION
Emulsifica, I/A.
Incisión de 3.2 mm.
Estabilidad de cámara anterior.
Rápida recuperación.
1993 Faco Chop
90%
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Por incumbencias profesionales, diferencias anatómicas y fisiológicas, reacciones a
ciertas drogas, derivaciones éticas y judiciales, los oftalmólogos humanos, no
deben asumir este compromiso.
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