Hemorragia coroidea expulsiva espontánea. Caso clínico / Spontaneous expulsive choroidal hemorrhage. Case report

CASO CLÍNICO: Se presenta el caso de una paciente de 85 años de edad, procedente de un centro geriátrico, que acudió a urgencias con un cuadro de hemorragia ocular masiva aparentemente de forma espontánea en ojo izquierdo (OI). No había constancia de antecedentes oftalmológicos en su historial clínico. La paciente refería haber sido operada de catarata en ambos ojos hacía más de 25 años y llevar varios años sin visión por el OI. DISCUSIÓN: La hemorragia coroidea expulsiva espontánea (HCEE) no quirúrgica es una entidad clínica devastadora muy rara. Los factores predisponentes implicados en su desarrollo incluyen: edad avanzada, enfermedades vasculares (arterioesclerosis sobre todo), glaucoma y daño corneal severo

CLINICAL CASE: A case is presented of an 85-year-old woman living in a geriatric residence, who was admitted to the emergency department of our hospital with a spontaneous expulsive choroidal hemorrhage in her left eye. There was no a history of ophthalmic disease, and the patient only reported having intracapsular cataract surgery in both eyes 25 years ago, and that she also became blind in her left eye in the past few years. DISCUSSION: Non-surgical spontaneous expulsive choroidal hemorrhage is a very rare and disastrous clinical event. The predisposing factors involved are: advancing age, vascular illness (especially atherosclerosis), glaucoma, and severe corneal damage

Ocular involvement in hemolytic uremic syndrome due to factor H deficiency--are there therapeutic consequences?

Factor H deficiency is responsible for thrombotic microangiopathy (TMA) via uncontrolled activation of the alternative pathway of the complement system. Ocular TMA has never been reported in patients with factor H abnormalities. A male patient with congenital homozygote factor H deficiency reached end-stage renal disease at the age of 10 years. Hemodialysis was uneventful for 3 years, when, suddenly, unilateral ocular pain and blurred vision occurred while he had febrile pharyngitis. Ophthalmologic examination found vitreous bleeding, elevated ocular pressure, choroidal hemorrhage (ultrasound biomicroscopy) and retinal ischemia (fluorescein angiography). C-reactive protein concentration was increased, while haptoglobin levels remained normal. We suspected that TMA due to factor H deficiency was responsible for the ocular manifestations and immediately initiated daily plasma exchanges (PEs) with fresh frozen plasma (FFP) for 10 days followed by three sessions per week. Factor H serum level increased from 6% to 82%, and C3 level normalized. Progressively, ocular pain decreased, and visual acuity and ophthalmologic findings showed improvement. When there is permanent activation of the alternative pathway in patients with end-stage renal disease (ESRD), the search for secondary targets might be of interest. In nephrectomized patients, no biological parameter can predict isolated ocular TMA. Early ophthalmologic investigation and substitution of factor H via FFP may avoid irreversible damage.

Treatment of suprachoroidal hemorrhage with tissue plasminogen activator.

We evaluated the efficacy of tissue plasminogen activator in treating experimental suprachoroidal hemorrhage. Suprachoroidal hemorrhage was created in 30 white rabbit eyes by implanting four pieces of small, exogenously formed blood coagula into the suprachoroidal space. Animals were randomized for treatment with a surgical sponge soaked in 25, 50, or 75 microg of tissue plasminogen activator (tPA) or balanced salt solution (BSS) as a control. The time when initiation and completion of clot dissolution occurred was established, and histological examination was performed to assess damage. Clot dissolution started within 30 min in the 50- and 75-microg tPA group, whereas it took 2.75 days in the control group; complete dissolution of blood clots took 4.5 h in the 75-microg tPA group and 14 days in the control group. Histological examination revealed a minimal change in photoreceptors within 6 h after treatment with 75 microg tPA. Treatment of suprachoroidal hemorrhage with tPA seems to be effective, but further investigations for determining the effective and nontoxic dose are required.