Pathology of Ischemic Optic Neuropathy.

Ischemic optic neuropathy (ION) describes a state of hypoxic injury of the optic nerve. Clinically, ION is divided into anterior and posterior forms defined by the presence or absence of optic disc swelling, respectively. It is further classified as arteritic when secondary to vasculitis, and nonarteritic when not. The site of vascular occlusion for anterior ION from giant cell arteritis is the short posterior ciliary arteries, but mechanical vascular obstruction does not play a role in most nonarteritic cases. Histologically, ION is characterized by axon and glial necrosis, edema, and a sparse mononuclear response. Like other ischemic injuries, the morphologic alternations in the nerve are time dependent. A variant of ION called cavernous degeneration (of Schnabel) features large cystic spaces filled with mucin. Several conditions can histologically mimic cavernous degeneration of the optic nerve. The scarcity of cases of ION examined histologically has contributed to an incomplete understanding of its pathogenesis.

Management of ischemic optic neuropathies.

Ischemic optic neuropathies (IONs) consist primarily of two types: anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). AION comprises arteritic AION (A-AION: due to giant cell arteritis) and non-arteritic AION (NA-AION: due to other causes). PION consists of arteritic PION (A-PION: due to giant cell arteritis), non-arteritic PION (NA-PION: due to other causes), and surgical PION (a complication of several systemic surgical procedures). These five types of ION are distinct clinical entities etiologically, pathogenetically, clinically and from the management point of view. In the management of AION, the first crucial step with patients aged 50 and over is to identify immediately whether it is arteritic or not because A-AION is an ophthalmic emergency and requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. Patients with NA-AION, when treated with systemic corticosteroid therapy within first 2 weeks of onset, had significantly better visual outcome than untreated ones. Systemic risk factors, particularly nocturnal arterial hypotension, play major roles in the development of NA-AION; management of them is essential in its prevention and management. NA-PION patients, when treated with high-dose systemic steroid therapy during the very early stages of the disease, showed significant improvement in visual acuity and visual fields, compared to untreated eyes. A-PION, like A-AION, requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. There is no satisfactory treatment for surgical PION, except to take prophylactic measures to prevent its development.

[Anterior ischemic optic neuropathy: Etiology, pathogenetic mechanisms and therapy]. / Anteriore ischämische Optikusneuropathie : Atiologie, Pathogenese und Therapie.

Ischemic optic neuropathy is caused by ischemia of the optic nerve head in the region of the lamina cribrosa. Differentiation is made between arteritic (AION) and nonarteritic (NAION) forms. AION is the most common ophthalmological manifestation of giant cell arteritis and is usually well controlled with systemic steroid therapy. Temporal artery biopsy for confirmation of the diagnosis is mandatory. NAION is not a disease entity but rather the common pathogenetic pathway of a large variety of diseases and conditions and is often the result of several interacting factors. For this reason, there is no "standard therapy" for NAION. Careful interdisciplinary work up in NAION frequently reveals previously unrecognized diseases requiring treatment according to internal medicine standards. Adequate treatment frequently results in improvement of the affected eye and reduced risk of NAION in the other eye or of brain infarction.

Neuropatía óptica isquémica en el paciente politraumatizado / Ischemic optic neuropathy in the multiple trauma victim

neuropatía óptica isquémica es una causapoco conocida de ceguera en el paciente crítico yespecialmente en el politraumatizado sin daño directodel globo ocular. Presentamos el caso de unpaciente joven que desarrolla una ceguera bilateralcompleta tras sufrir un profundo shock hemorrágicosecundario a un traumatismo toracoabdominalcerrado por aplastamiento. Se ha realizado una revisión de la literatura relacionada y se han identificado como factores de riesgo más importantes la hipotensión arterial prolongada y el descenso brusco del hematocrito

Ischemic optic neuropathy is an uncommon ofblindness in the critically ill patient that occurs especially in multiple trauma victims with no directinjury of the eyeball. We present the case of ayoung male patient with total bilateral blindnessafter profound hemorrhagic shock secondary tothoracoabdominal non-penetrating traumatismcaused by crushing. A search of the literature wasconducted, identifying prolonged arterial hypotensionand sudden drop in hematocrit value as the most important risk factors (AU)

Clinical spectrum of posterior ischemic optic neuropathy.

PURPOSE: To describe the systemic and visual characteristics and prognosis in patients with posterior ischemic optic neuropathy (PION). DESIGN: Observational case series. METHODS: Retrospective chart review in a multicenter setting. Seventy-two patients (98 eyes) with a clinical diagnosis of PION. Co-morbid systemic diseases and visual function were recorded at both initial presentation and after mean visual follow-up of 4.1 years and systemic follow-up of 5.4 years. RESULTS: PION occurred in three main settings: in the perioperative period following a variety of surgical procedures (28 patients), associated with giant cell (temporal) arteritis (6 patients), and associated with nonarteritic systemic vascular disease (38 patients). Patients with perioperative and arteritic PION were more likely to have severe, bilateral visual loss that did not improve. Among eyes with nonarteritic PION, 34% experienced improvement in vision, 28% remained stable, and 38% worsened. Among patients with nonarteritic PION, carotid artery disease and a history of stroke (with or without carotid artery disease) were both associated with a statistically significant increased risk of poor final visual outcome. CONCLUSIONS: There are three distinct subtypes of PION: perioperative, arteritic, and nonarteritic. Patients with PION that is unassociated with surgery should undergo an evaluation for systemic vascular diseases, including giant cell arteritis, that may or may not be apparent at the time of vision loss. The visual prognosis for patients with perioperative or arteritic PION is poor, whereas that for nonarteritic PION is similar to that for patients with nonarteritic AION.