Multiple Myeloma Relapse Presenting as Unilateral Blindness

Multiple Myeloma is a chronic disease. While therapy is largely focused for control, relapse is inevitable. Central nervous system relapse of myeloma is less common. Unilateral painless blindness is a rare entity and its occurrence in the setting of multiple myeloma has not been commonly reported. We encountered a case of multiple myeloma on treatment, who developed unilateral blindness and later on confirmed to have relapse of disease.

Sudden Unilateral Blindness and Ophthalmoplegia after Ruptured Anterior Communicating Artery Aneurysm Surgery: Report of 2 Cases / 대한뇌혈관외과학회지

The incidence of unilateral blindness and ophthalmoplegia after aneurysm surgery is very rare, especially in an anterior communicating artery (ACoA) aneurysm, but if it occurs, it is mainly caused by intra-operative nerve injury or retinal ischemia. We experienced 2 cases of unilateral blindness immediately after surgery. Both patients were classified into Hunt-Hess grade 1 and Fisher grade 3. Angiographic findings of these patients revealed that the aneurysms were located at the left ACoA. The aneurysms were clipped easily with minimal brain retraction via standard pterional craniotomy. In both cases, injury of the optic nerve during surgery was unlikely. Both patients complained of visual loss with ophthalmoplegia ipsilateral to the site of surgery on the 1st postoperative day and showed evidence of retinal ischemia with central retinal artery occlusion on fundoscopic examination. In our patients, we hypothesize that the complications were most likely related to the intra-orbital ischemia initiated by the collapse of the arterial and venous channels in the orbit and/or to the direct or indirect contusion on the intra-orbital structures. These situations could be produced by inadvertent pressure placed on the eyeball with a bulky retracted frontal skin flap. Visual acuity in both patients ranged from no light perception to finger-counting. Their external ophthalmoplegia had completely disappeared 2 weeks after surgery and visual acuity in one patient began to improve. But in the other patient, the condition was irreversible. The degree of visual recovery seems to be dependent on the duration and severity of retinal ischemia by orbital compression. Unfortunately, there is no satisfactory treatment. We recommend careful surgical manipulation, including the use of an eye shield just before aneurysm surgery to protect the ipsilateral eyeball.

Five Cases of Orbital Infarction Syndrome Caused by Compression of Surgical Scalp Flap / 대한뇌혈관외과학회지

Orbital infarction syndrome is a rare disorder resulting from ischemia of the intraocular and intraorbital structures due to hypoperfusion of the ophthalmic artery and its branches. The syndrome can occur with common carotid artery occlusion, orbital mucormycosis, giant cell arteritis and complications of surgery and manifests proptosis, ophthalmoplegia, and unilateral blindness. We recently experienced 5 cases of proptosis, ophthalmoplegia and unilateral blindness immediately after operation for 2 years. The cause of orbital infarction syndrome in these cases appeared to be the direct compression of orbit by the tightly retracted frontal scalp flap. We report and discuss possible mechanism with literature review.

Sudden Unilateral Blindness after Intracranial Aneurysm Surgery

The incidence of unilateral blindness and ophthalmoplegia after aneurysm surgery is very rare, but if there is, it is mainly caused by intraoperative nerve injury. We experienced 6 cases of unilateral blindness immediately after surgery for 5 recent years. These patients were classified from Hunt-Hess grade I to II except for one patient with III. All patients complained of visual loss with varying degree of lid edema and ophthalmoplegia ipsilateral to the surgery site. Angiographic examination of these patients revealed that the aneurysm site was located at the internal carotid artery bifurcation in one case and the middle cerebral artery bifurcation in five cases. All of them were relatively far from the optic nerve. The aneurysm was clipped easily with minimal brain retraction via standard pterional craniotomy since the brain was slack in all cases. In all cases, injuring the optic nerve during surgery was remote. All patients showed evidence of retinal ischemia of fundoscopy with or without fluorescein an giography. The pathophysiology of this ischemic event is unknown. In our patients, we could exclude possible etiologic factors such as abnormal systemic and ocular conditions, causing ischemia in intraorbital structures, increased intracranial pressure, intraoperative hypotension, carotid atherosclerosis, and vasculitis. Accordingly we believe that the complications ween in our cases were most likely related to intraorbital ischemia initiated by a collapse of the arterial and venous channels in the orbit and/or to direct or indirect contusion on the intraorbital structures. These situations could be produced by inadvertent pressure placed on the eyeball with a bulky retracted frontal skin flap. Visual acuity in these patients ranged from no light perception to the ability to see objects and detect color. Their conditions were irreversible. Unfortunately a satisfactory treatment is lacking. Neurosurgeons should be aware that this complication may follow intracranial aneurysm surgery and should ensure that the retracted flap is not compressive to the eye-ball, especially in patients with risk factors.