scholarly journals Postoperative Visual Loss Following Spine Surgery: A Case Report

2019 ◽  
Vol 57 (218) ◽  
Author(s):  
Sabin Bhandari ◽  
Krishna Pokharel ◽  
Birendra Prasad Sah

Postoperative visual loss is a rare but devastating complication of non-ophthalmic surgery. Its aetiology is poorly understood and multiple associated factors have been proposed. We present a report of a 33-year-old female who developed irreversible diminution of vision on the right eye (non-arteritic-posterior-ischemic-optic-neuropathy) following general anaesthesia for pedicle screw fixation and plating for fracture vertebrae and hip in prone position and then screw placement for fracture calcaneum in supine position. The vision loss, limited to finger count close to face on the right eye, did not improve till follow-up at one-year. The combination of mild intraoperative hypotension, anaemia, prone positioning, prolonged surgery and anaesthesia may have contributed to postoperative visual loss in our patient.  

2020 ◽  
pp. 112067212096206
Author(s):  
Kaveh Abri Aghdam ◽  
Ali Sadeghi ◽  
Mostafa Soltan Sanjari ◽  
Ali Aghajani ◽  
Saba Gholamalizadeh

A previously healthy 28-year-old female developed bilateral painless vision loss, more prominent in the right eye than in the left, following abdominoplasty and liposuction surgery. Laboratory studies showed severe peri- and post-operative anemia. Over a 5-month follow-up, visual function remained decreased but stable in the right eye and improved in the left eye. This is the second reported case of anterior ischemic optic neuropathy in one eye and posterior ischemic optic neuropathy in the other eye after liposuction. Level of evidence: Level VI, case report study.


Cephalalgia ◽  
2021 ◽  
pp. 033310242110562
Author(s):  
Nikita Chhabra ◽  
Chia-Chun Chiang ◽  
Marie A Di Nome ◽  
Odette Houghton ◽  
Rachel E Carlin ◽  
...  

Background Retinal migraine is defined by fully reversible monocular visual phenomena. We present two cases that were complicated by permanent monocular vision deficits. Cases A 57-year-old man with history of retinal migraine experienced persistent monocular vision loss after one stereotypical retinal migraine, progressing to finger-count vision over 4 days. He developed paracentral acute middle maculopathy that progressed to central retinal artery occlusion. A 27-year-old man with history of retinal migraine presented with persistent right eye superotemporal scotoma after a retinal migraine. Relative afferent pupillary defect and superotemporal visual field defect were noted, consistent with ischemic optic neuropathy. Conclusion Retinal migraine can complicate with permanent monocular visual loss, suggesting potential migrainous infarction of the retina or optic nerve. A thorough cerebrovascular evaluation must be completed, which was unrevealing in our cases. Acute and preventive migraine therapy may be considered in retinal migraine patients, to mitigate rare but potentially permanent visual loss.


2007 ◽  
Vol 48 (4) ◽  
pp. 808-811 ◽  
Author(s):  
Meyeon Park ◽  
Grant T. Liu ◽  
Jody Piltz-Seymour ◽  
Catherine L. Wisda ◽  
Alain H. Rook ◽  
...  

2017 ◽  
Vol 9 (1) ◽  
pp. 31-35
Author(s):  
Karim Hammamji ◽  
Ehud Reich ◽  
Amit Arora ◽  
Victoria M.L. Cohen ◽  
Mandeep S. Sagoo

Melanoma of the eye is rare, but can mimic a range of disorders. This report highlights 2 cases of choroidal melanoma with vision loss mimicking neurological diagnoses. The first patient is a 41-year-old white male with a known history of multiple sclerosis and a previous episode of optic neuritis in the right eye, who presented with a 6-month history of decreased vision in the same eye, and occasional photopsiae. He was treated with 2 courses of oral steroids for presumed recurrent optic neuritis. After a temporary improvement in his symptoms, his vision worsened, following which he had a head MRI, which revealed a solid intraocular mass. He was subsequently diagnosed with a choroidal melanoma for which he was treated successfully with ruthenium-106 plaque brachytherapy. The second patient is a 57-year-old female, who presented with a progressive cerebellar syndrome under investigation by the neurology service, as well as decreased vision in the right eye. Her visual acuity gradually deteriorated and her neurological assessment, which included a PET-CT, revealed uptake in the right eye. The diagnosis of a choroidal melanoma was made, and following conservative treatment with proton beam radiotherapy, she had an enucleation of the eye. Intraocular tumours can masquerade as many different entities. Unexplained unilateral visual loss, especially if it is atypical for a neurological syndrome, should prompt dilated fundoscopy and referral to an ophthalmologist.


2019 ◽  
Author(s):  
Xia Yuan ◽  
Yuliang Feng ◽  
Dan Li ◽  
Mei Li

Abstract Abstract Background: Visual impairment occurred as an infrequent form of chemotherapeutic toxicity and was often underestimated despite of several reports. We described a case of acute unilateral visual impairment after one cycle of intravenous chemotherapy of a normal dose, aiming at raising attention to chemotherapy-induced ocular toxicity. Case presentation: The patient developed a progressive vision loss in the right eye during the chemotherapy. After one cycle of intravenous chemotherapy, her visual acuity decreased by 0.6 in the right eye (VOD=0.4) compared to the previous value of 1.0 (VOD=1.0). No evidence of ocular infiltration was observed from the cerebral magnetic resonance imaging (MRI). During her follow-up period, we documented the ophthalmologic examinations including visual acuity, visual field (VF), visual evoked potential (VEP), electroretinogram (ERG), fundus photograph (FP), fundus fluorescein angiography (FFA) and optical coherence tomography (OCT). Ophthalmoscope examination and fundus photograph showed optic disc edema, fuzzy boundary and linear hemorrhages in her right eye. Fundus fluorescein angiography (FFA) revealed capillary underdevelopment at the nasal and superior temporal area of the optic disc in the early phase and capillary fluorescein leakage in the late phase. The result of VEP test suggested the impaired function of the optic nerve. Thus, a diagnosis of nonarteritic anterior ischemic optic neuropathy (NAION) was made by the ophthalmologist according to these results. The patient was prescribed prednisone combined with neuroprotective drugs, which did not work. After the cessation of chemotherapy, her impaired vision gradually recovered. Conclusions: This is the first reported case of acute visual impairment in a patient who underwent chemotherapy of a normal dose. It is indicated that while receiving benefits from chemotherapy, cancer patients simultaneously suffer from the risk of vision loss. Key words: Vision loss, Chemotherapy, Nonarteritic anterior ischemic optic neuropathy


2016 ◽  
Vol 64 (4) ◽  
pp. 975.2-976
Author(s):  
Z Asad ◽  
A Chaudhary ◽  
A Awab

IntroductionA wide spectrum of ocular diseases is associated with diabetes mellitus (DM) and most of them lead to gradual loss of vision that is almost always irreversible. Sudden vision loss in severe diabetic ketoacidosis (DKA) that is reversible with treatment of the metabolic abnormality is a very rare complication that has been reported three times previously.Case PresentationA 59 year-old male with Type 1 DM presented with altered consciousness, epigastric pain, hypothermia and sudden complete bilateral vision loss for three days. He was not complaint with insulin. There was no history or laboratory evidence of ethanol, methanol, ethylene glycol ingestion, head trauma, baseline vision problem, cold or intense bright light exposure.Physical examination revealed rapid shallow breathing at 55/min, blood pressure 90/60 mm Hg, heart rate 102/min and temperature 90.2F. He was oriented only to place,pupils were dilated and non-reactive to light. No light perception in both eyes. Fundoscopy was normal without any evidence of retinal pallor, retinal detachment, retinal hemorrhages, papilledema or cataract.Labs revealed blood glucose 1100 mg/dl, pH 6.95,positive serum and urine ketones, pCO2 11 mm Hg and anion gap 36. He received aggressive warm fluid resuscitation, electrolyte replacements and intravenous insulin infusion with close monitoring. 18 hrs later his blood glucose, pH,anion gap and body temperature normalized and vision spontaneously returned to normal. A repeat fundoscopy exam by ophthalmologist and magnetic resonance image (MRI) brain was completely normal; ruling out posterior ischemic optic neuropathy and occipital stroke. He recovered very well, resumed diet, was ambulatory and had an uneventful rest of hospital course.DiscussionSudden painless vision loss has a wide differential diagnosis and it is usually caused by ischemia at retinal, ocular or cortical level. No history of methanol ingestion or trauma, normal fundoscopy, normal MRI and rapid return of vision after correction of diabetic ketoacidosis strongly suggests that blindness was related to acidosis.Alcoholic ketoacidosis has been reported to cause transient reversible blindness in other case reports and correction of acidosis lead to reversal of blindness. Other rare causes of reversible blindness include posterior reversible encephalopathy syndrome, brain tumors, anterior ischemic optic neuropathy and valsalva retinopathy.The mechanism of acidosis causing blindness is believed to be uncoupling of horizontal cells at pH <7.0 inhibiting photoreceptor transmission as suggested by studies on fish and salamander. Other possible mechanisms include hyperosmolarity causing ischemia or transient lens opacification but in none of the reported cases this was proven. Also lens opacification would have been seen at fundoscopy. Posterior ischemic optic neuropathy is another possibility but it is irreversible. The exact mechanism of blindness remains poorly understood. However irrespective of mechanism of acidosis, its rapid correction to pH >7.0 leads to rapid recovery suggesting a common pathogenesis.


Author(s):  
David E. Traul

Postoperative visual loss (POVL) is a rare but devastating condition associated with many types of nonocular surgery. In spine surgery, the most common causes of POVL are ischemic optic neuropathy (ION), central retinal artery occlusion (CRAO), and cortical blindness. Although the association of POVL with spine surgery has long been recognized, the low incidence of this complication hinders the identification of patient and perioperative risk factors and limits our understanding of the causes of POVL. In adult spine surgery, POVL is most frequently attributed to ION whereas CRAO is more commonly seen in cardiac procedures. POVL due to cortical blindness has the highest incidence in pediatric spine surgery. While several risk factors for POVL have been identified in spine surgery, there are currently no standardized practice guidelines to eliminate the risk for POVL. Currently, there are no effective treatments for POVL, and recovery from ION and CRAO is limited.


1995 ◽  
Vol 83 (2) ◽  
pp. 348-349 ◽  
Author(s):  
Andrew G. LEE

✓ This 48-year-old hypertensive man, a cigarette smoker, awoke in the recovery room with visual loss in the right eye after uncomplicated lumbar spine surgery. His intraoperative blood pressure had been maintained at relatively low levels to reduce bleeding; a loss of 1500 cc of blood was reported. Postoperative hemoglobin was 4.2 g/dl less than the preoperative hemoglobin; however, the patient did not receive a blood transfusion. A postoperative ophthalmological examination revealed decreased visual acuity, color vision, and visual field in the right eye. The right optic nerve and retina were initially normal but the patient eventually developed optic nerve atrophy consistent with the clinical diagnosis of ischemic optic neuropathy. Neurosurgeons should be aware that this condition may follow uncomplicated lumbar spine surgery and should obtain prompt ophthalmological consultation when patients develop postoperative visual loss. Aggressive and rapid correction of blood pressure and hematocrit may be helpful in individuals who develop ischemic optic neuropathy after lumbar spine surgery.


2008 ◽  
Vol 49 (2) ◽  
pp. 370-371 ◽  
Author(s):  
Martin Lubow ◽  
Deborah M. Grzybowski ◽  
Hamdy Awad

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