Abstract
Purpose
To describe variations in the presentation of monocular visual loss associated with intracranial aneurysm rupture. The clinical course, possible etiologies and management of visual loss in three patients are described.
Clinical features
The first patient developed Terson’s syndrome (vitreal hemorrhage associated with raised intracranial pressure secondary to subarachnoid hemorrhage). Following aneursymal clipping, her postoperative management was conservative and there was no improvement in visual acuity. The second patient underwent surgical clipping of internal carotid aneursysms and sustained visual loss subsequent to surgical dissection and temporary clipping around the optic nerve and anterior choroidal artery. The vessel subsequently thrombosed. Potential contributing factors to visual loss in this case included intraoperative hypotension and anemia. This patient received anti-platelet medications, and experienced subsequent improvement in visual acuity to 6/9. A third patient underwent a right orbito-frontal keyhole craniotomy with the cranial flap retracted across the orbit. Elevated intraocular pressure secondary to external orbital compression may have compromised retinal and choroidal perfusion. This patient also developed vasospasm of both anterior cerebral arteries which resolved partially with papaverine therapy. Hypertensionhypervolemia therapy was instituted, with subsequent partial recovery of visual acuity in her right eye.
Conclusion
Perioperative monocular visual loss associated with intracranial aneurysm repair is an infrequent occurrence, and clinical presentations may be quite variable. The primary pathophysiological mechanisms are intraocular hemorrhage and ischemia of ocular structures, including the optic nerve. Early detection, via regular fundoscopic examination and treatment aimed at decreasing intraocular pressure and augmenting ocular perfusion may improve outcomes.
Objectif
La perte visuelle monoculaire associée à la rupture anévrysmale intracrânienne peut se présenter de diverses façons. Le cas de trois patients est décrit selon le tableau clinique, les causes possibles et le traitement de la perte visuelle.
Éléments cliniques
Chez la première patiente un syndrome de Terson s’est développé (hémorragie vitréenne associée à une hypertension intracrânienne secondaire à une hémorragie sous-arachnoïdienne). Après la ligature anévrysmale, le traitement postopératoire conservateur administré n’a pas amélioré l’acuité visuelle. Le second patient a subi une ligature chirurgicale d’anévrysmes de la carotide interne et une perte visuelle permanente consécutive à la dissection chirurgicale et au clip temporaire autour du nerf optique et de l’artère choroïdienne antérieure. Une thrombose est survenue ensuite dans ce vaisseau. Dans ce cas, les facteurs potentiels de la perte visuelle comprennent l’hypotension et l’anémie peropératoires. Le patient a reçu des anti-plaquettaires qui ont amélioré l’acuité visuelle à 6/9. Un troisième patient a subi une craniotomie orbito-frontale à incision minimale où le lambeau crânien a été rabattu sur l’orbite. Ľélévation intra-oculaire de la pression, secondaire à la compression orbitale externe, peut avoir compromis la perfusion rétinienne et choroïdienne. Un vasospasme des deux artères cérébrales antérieures s’est aussi développé, résorbé partiellement avec la papavérine. Un traitement de l’hypertension-hypervolémie a été institué, suivi d’une récupération partielle de l’acuité visuelle de l’œil droit.
Conclusion
La perte visuelle monoculaire périopératoire associée à la réparation d’un anévrysme intracrânien survient rarement et son tableau clinique peut varier. Les mécanismes physiopathologiques principaux en sont l’hémorragie intra-oculaire et l’ischémie des structures oculaires, dont le nerf optique. La détection précoce, par l’examen régulier du fond de l’œil, et le traitement visant à réduire la pression intra-oculaire et à augmenter la perfusion oculaire peuvent améliorer la situation.
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Chong, C.T., Chin, K.J., Yip, L.W. et al. Case series: Monocular visual loss associated with subarachnoid hemorrhage secondary to ruptured intracranial aneurysms. Can J Anesth 53, 684–689 (2006). https://doi.org/10.1007/BF03021627
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DOI: https://doi.org/10.1007/BF03021627