ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Posterior ischemic optic neuropathy

Posterior ischemic optic neuropathy
Literature review current through: May 2024.
This topic last updated: Apr 29, 2024.

INTRODUCTION — Ischemic optic neuropathy is the most common optic nerve disorder in patients over age 50 years [1]. Ischemic optic neuropathy is generally categorized as anterior (affecting the optic disc) versus posterior (retrobulbar) and as arteritic versus nonarteritic. Posterior ischemic optic neuropathy (PION) is less common than anterior ischemic optic neuropathy (AION).

PION is believed to result from an infarction of the retrobulbar optic nerve and is distinguished clinically from AION by a normal-appearing optic nerve head. As such, the diagnosis of PION can be somewhat more challenging than AION; PION must be distinguished from other causes of retrobulbar optic neuropathy as well as other causes of abrupt vision loss.

This topic discusses PION. Other forms of ischemic optic neuropathy and other optic neuropathies are discussed separately. (See "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies" and "Clinical manifestations of giant cell arteritis" and "Optic neuropathies".)

VASCULAR ANATOMY — The vascular supply of the retrobulbar optic nerve is distinct from that of the optic nerve head. (See "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies", section on 'Vascular anatomy'.)

The posterior segment of the optic nerve is supplied by a pial capillary plexus that surrounds the nerve and is derived from collateral branches of the ophthalmic artery (figure 1) [2,3]. Most of the vascular supply is superficial; only a small number of capillaries penetrate the nerve and extend to its central portion, making this area somewhat poorly vascularized in comparison with its anterior portion. Because it is encased in the sphenoid optic canal, the early swelling that occurs after ischemic insult can lead to axonal compression further exacerbating optic nerve damage [4].

The histopathology of PION occurring in the perioperative setting has been reported in at least four cases that showed intraorbital optic nerve infarction extending from the juxtabulbar to intracanalicular portions bilaterally [5-9]. Consistent with its vascular supply, predominant involvement of the central axial portion of the retrobulbar nerve, with relatively sparing of the periphery, was observed in three of these cases [6,10]. Relative sparing of the central portion of the nerve in one case suggests that there may be some variability in the vascular supply; some individuals may have an axial supply stemming in retrograde fashion from the central retinal artery [2,5].

EPIDEMIOLOGY — PION is relatively uncommon as compared with anterior ischemic optic neuropathy (AION).

Two large, published case series describe the epidemiologic features of PION in 42 and 72 patients, respectively [2,11]:

The mean patient age was 62 years in one series (range 18 to 90 years). The mean age varied by etiology; patients with giant cell arteritis (GCA) were older (mean 78 years, range 50 to 82 years), while those with PION in the setting of spine surgery were younger on average.

There is a higher-than-expected prevalence of atherosclerotic risk factors and comorbid vascular disease, especially in patients with nonarteritic (idiopathic) PION, with 87 percent of patients having at least one risk factor for, or one other manifestation of, atherosclerotic vascular disease.

Sex does not appear to be a risk factor.

Over 90 percent of patients are White individuals.

ETIOLOGIES AND PATHOGENESIS — PION is typically categorized etiologically as perioperative (7 to 39 percent), arteritic (8 to 29 percent), and nonarteritic (53 to 67 percent) [2,11]. These wide ranges likely reflect differences in case sampling and referral bias.

Perioperative PION — Both anterior and posterior ischemic optic neuropathy are reported complications of a wide range of surgical procedures [2,4,9-13]. The most common surgical procedures that are associated with perioperative ischemic optic neuropathy are cardiac surgery and spine surgeries [4,10,14-16]. Although anterior ischemic optic neuropathy (AION) appears to be more common than PION after cardiac surgery, PION is relatively more common in cases of spine surgery and radical neck dissection [15,17-25]. The incidence of PION after spine surgery is estimated at 0.03 to 0.11 percent [19,22,23,26], while the incidence of ischemic optic neuropathy (AION and PION) after cardiac surgery was found to be 0.014 percent in a study using the National Inpatient Sample database between 1998 and 2013 [16]. (See "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies", section on 'Perioperative ischemic optic neuropathy'.)

Perioperative factors implicated in the development of PION include intraoperative hypotension, long duration of surgery, intraoperative blood loss and anemia, the type and amount of intraoperative fluid administration, and prone position [4,11,17,19,20,24,27-31]. Vascular risk factors (male sex, diabetes, obesity), prevalent in these patients, may play a causative role [29]. In theory, an atherosclerotic vasculopathy may impair autoregulatory function, particularly in the setting of hypotension [4,10,24]. In a case series of ischemic optic neuropathy after spine surgery, 94 percent of incident cases had an anesthetic duration over six hours and 82 percent had estimated blood loss of one or more liters [24]. Because that report [24] and other reports were based on uncontrolled observations, it is uncertain if these factors truly increase the risk of ischemic optic neuropathy. However, in one multicenter case-control study that included 80 cases of ischemic optic neuropathy occurring after prone spinal surgery and 315 controls, factors independently associated with ischemic optic neuropathy were male sex, obesity, use of the Wilson frame, longer anesthetic duration, greater estimated blood loss, and a lower percentage of colloid replacement [29].

In patients undergoing spine surgery, prolonged use of the prone position is implicated as a risk factor for PION [4,10,11,19,20,27,28,32]. The presumed mechanism is an increase in central venous pressure caused by increased intra-abdominal and intrathoracic pressure. The increase in ocular venous pressure may, in turn, compromise optic nerve perfusion, particularly in the setting of the other factors mentioned previously. The retrobulbar intraorbital segment of the optic nerve may be particularly susceptible to increased venous pressure because the arterial vessels that supply that segment are small end vessels emanating from the surrounding pia. A multicenter case-control study found that the use of the Wilson frame during spinal fusion surgery was associated with an increased odds ratio for ischemic optic neuropathy of 4.3 [29]. This device places the patient in a prone position with the head lower than the heart, potentially raising venous pressure in the orbit. In one case report, markedly dilated superior ophthalmic veins were demonstrated on postoperative brain magnetic resonance imaging (MRI) in a patient who sustained bilateral PION after prolonged prone positioning during lumbar laminectomy [33]. This finding disappeared on follow-up brain MRI five months later. This finding is, however, not universally demonstrated in all patients who sustain a PION.

Patients undergoing radical neck dissection may develop ocular venous hypertension as a result of jugular vein ligation [5,17,18,21,34]. Prolonged use of a steep supine (Trendelenburg) position during surgery may also increase venous pressure and has been suggested to play a role in cases of PION after prostate surgery [35]. PION was reported to occur from vasospasm involving the ophthalmic artery after craniopharyngioma resection [36].

Arteritic PION — PION is a rare complication of giant cell arteritis (GCA). In a study of 85 patients with visual loss due to biopsy-proven GCA, PION was the mechanism in just six patients (7 percent) [37]. In another study, PION was the presentation of visual loss in 1 of 42 patients (2.8 percent) with GCA [38]. In these cases, PION results from inflammatory occlusion of the ophthalmic and/or short posterior ciliary arteries. (See "Pathogenesis of giant cell arteritis".)

Vision loss in arteritic PION is often severe (finger-counting or worse) and is more likely to be bilateral, either at onset or in rapid sequence [11,39]. Prodromal episodes of transient vision loss are more common in GCA than in nonarteritic PION.

The clinical syndrome of GCA-associated PION is similar to GCA-associated AION, with older age at presentation and symptoms of polymyalgia rheumatica, which includes jaw claudication, proximal myalgias and arthralgias, scalp tenderness, headache, and fatigue. Laboratory investigation will typically reveal elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). (See "Clinical manifestations of giant cell arteritis".)

Nonarteritic (idiopathic) PION — Among patients with nonarteritic (idiopathic) PION, vascular risk factors and comorbid vascular disease are prevalent, as they are in nonarteritic anterior ischemic optic neuropathy (NAION) [11,40]. (See "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies", section on 'Atherosclerosis'.)

Among 38 patients with idiopathic PION in one series, 33 had at least one vascular risk factor or comorbid disease, 15 had hypertension, 9 had diabetes, and 15 had a smoking history. Thirty-two patients had comorbid cardiac, cerebral, or peripheral vascular disease [11]. Similar findings were found in another case series [2]. This suggests that in these patients, PION may represent a manifestation of systemic vascular disease, perhaps a microangiopathy, although this has not been identified pathologically.

Others — PION has also been described in the setting of acute volume loss (trauma, gastrointestinal bleeding) [4,8,41,42] and systemic hypotension in association with dialysis [43] and other causes [44].

Vasospasm has been implicated as the mechanism of PION occurring in the setting of migraine and with vasoactive stimulant drugs (eg, methamphetamine) [45-47].

While embolism from carotid disease is not understood to be a common mechanism of PION, acute carotid occlusion in cases of carotid dissection has been implicated as the underlying cause in a few reported cases [48-50]. This presumably leads to an abrupt decrease in arterial perfusion downstream, causing a watershed-type infarction in a vulnerable arterial territory.

There have also been isolated case reports of PION occurring in the setting of other rare conditions such as Takayasu arteritis [51], granulomatosis with polyangiitis (GPA) [52-54], systemic lupus erythematosus [55,56], cavernous sinus fistula [57], herpes zoster [58-60], invasive fungal sinusitis [61], and sickle cell hemoglobinopathy [62]. The exact cause of optic nerve dysfunction is not known and may be either ischemic or inflammatory.

CLINICAL PRESENTATION

Monocular or binocular vision loss – The typical presentation of idiopathic PION is sudden, painless, monocular vision loss [1]. However, in the postoperative setting and with sudden hypotension from other causes, simultaneous binocular involvement occurs in 50 to 67 percent of patients [4,10,11,19,24]. Arteritic PION can also cause binocular involvement, but sequential (mean interval 22 days) rather than simultaneous involvement is more typical in these cases [11].

The severity of vision loss in PION is related to the underlying etiology. In the setting of giant cell arteritis (GCA) or after surgery, 70 to 90 percent of cases have severe acuity loss: finger-counting or worse [2,10,11,19]. By contrast, those with idiopathic nonarteritic PION often have milder degrees of vision loss.

Fundoscopic examination – In the acute setting of PION, the optic disc appears normal, in contrast to nonarteritic anterior ischemic optic neuropathy (NAION), which displays acute swelling of the affected optic disc [2]. Patients with PION develop optic nerve atrophy with disc pallor over four to six weeks.

In contrast to NAION, the contralateral, unaffected eye does not typically demonstrate a small optic disc cup, the so-called disc at risk. Among 72 patients with PION, only 4 percent of patients were found to have a cupless optic disc in either eye [11]. Optic disc cupping may develop later in arteritic but not in other forms of PION [2,10].

Other clinical features – As with other optic neuropathies, patients with PION have an afferent pupillary defect unless there is equivalent vision loss in both eyes [11].

Impaired color vision is observed in most patients (80 percent).

Perimetry, if performed, typically demonstrates a nerve fiber bundle defect, often altitudinal or a central scotoma [2,11].

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of PION includes other retrobulbar optic neuropathies (table 1) [1]. Most compressive and infiltrative optic neuropathies produce vision loss that is more insidious and gradual in onset than with PION. Visual loss in optic neuritis can be abrupt but, unlike PION, typically occurs in younger patients and is accompanied by periocular pain. (See "Optic neuritis: Pathophysiology, clinical features, and diagnosis".)

In the postoperative setting, PION must be distinguished from other causes of perioperative vision loss, including central retinal artery occlusion, cerebral infarction, globe injury, and pituitary apoplexy [9,19,22,24,26,28,32].

There are numerous other causes of optic nerve disease (table 1). Some of the clinical features of the more common disorders are contrasted in the table (table 2); these are discussed in more detail separately. (See "Optic neuropathies".)

DIAGNOSIS

Diagnostic criteria — Diagnostic criteria for PION have been proposed as follows [10,43]:

Acute deficit in visual acuity and/or visual field

Ipsilateral relative afferent pupillary defect unless bilateral

Normal optic disc appearance at onset of visual loss

Exclusion of other causes (retinal vascular occlusion, glaucoma, chorioretinal scars)

Exclusion of other causes of optic neuropathy such as compression, demyelination, or inflammation with neuroimaging, preferably brain MRI with gadolinium

Abnormal visual evoked response, either absent or decreased amplitude

Normal electroretinogram

Development of optic disc pallor within four to eight weeks of onset

Not all of these tests are required, as discussed below.

Diagnostic evaluation — There is no confirmatory diagnostic test for PION, which is a diagnosis of exclusion. In that regard, some diagnostic evaluation is essential to exclude other causes of acute visual loss. The following tests are recommended:

ESR and CRP – It is imperative to exclude the diagnosis of giant cell arteritis (GCA) in patients with PION. This evaluation is urgent in order to institute treatment and prevent vision loss in the second eye. Older patients with PION should be questioned regarding headache, scalp tenderness, and jaw claudication, symptoms that suggest GCA. Regardless of the presence or absence of these other symptoms, if the patient is older than 50 years, an erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels should be obtained. Temporal artery biopsy should be considered if ESR or CRP are abnormal or if there is an otherwise high clinical suspicion for GCA because of suggestive symptoms such as headache or jaw claudication. Empiric corticosteroid therapy should be initiated for high-risk patients pending biopsy results. (See "Diagnosis of giant cell arteritis".)

Both CRP and ESR can be elevated after major surgical procedures and are unreliable tests in the postoperative setting to rule out GCA [10]. However, in the absence of other premorbid symptoms, such as prodromal episodes of transient visual loss or those that suggest polymyalgia rheumatica, GCA would be considered unlikely in a patient with perioperative PION.

Ophthalmologic examination – An ophthalmologic examination is essential in all patients to exclude other causes of acute monocular visual loss, including central retinal artery occlusion or retinal vein occlusion [19]. (See "Approach to the adult with acute persistent visual loss".)

Visual evoked response and electroretinogram are not essential in the diagnosis of PION and are not routinely performed. Fluorescein angiography is usually normal in PION, but this test is also not required for the diagnosis [2].

Neuroimaging – A brain MRI performed with contrast enhancement should be performed to exclude other inflammatory, infiltrative, and compressive causes of a retrobulbar optic neuropathy [11].

In patients with PION due to GCA, enhancement of the optic nerve has been noted on MRI [63,64]. This must be differentiated from other causes of optic neuropathies, such as inflammation or tumor infiltration, by the clinical setting and temporal artery biopsy results.

While the primary role of MRI in this setting is to exclude other diagnoses, some reports have documented restricted diffusion (decreased apparent diffusion coefficient [ADC]) in the optic nerve on diffusion-weighted MRI (DWI) studies in the acute phase of PION [10,39,65-69]. This finding distinguishes PION from retrobulbar demyelinating optic neuritis, which typically shows increased ADC on DWI in the acute stage [70].

PROGNOSIS, TREATMENT, AND PREVENTION

Perioperative PION – Based upon the risk factors identified as noted above, the American Society of Anesthesiologists recommends that patients undertaking spine surgery undergo continuous hemodynamic monitoring and that colloids, along with crystalloids, be administered in patients who have substantial blood loss [71,72]. Additional recommendations include that patients be positioned to keep the head at or above heart level, with the neck in a neutral forward position when possible, and that staged rather than single, long-duration procedures be considered when appropriate. Vision should be assessed when the patient becomes alert.

There is no treatment for perioperative PION; vision loss does not typically improve significantly.

Arteritic PION – The appropriate treatment of arteritic PION is with corticosteroids. Prognosis and treatment of this condition are discussed separately. (See "Treatment of giant cell arteritis".)

Nonarteritic PION – Patients with nonarteritic PION are also occasionally treated with corticosteroids, particularly if giant cell arteritis (GCA) has not been excluded. While some authors believe that steroid therapy may improve prognosis in these patients, the evidence is limited to uncontrolled observations, and corticosteroids are not recommended for nonarteritic PION [2,73].

Case reports of intravenous infusion of prostaglandin E1 (PGE1) describe possible benefit in patients with nonarteritic anterior ischemic optic neuropathy (NAION) and PION [73-75]. PGE1 is a potent vasodilator and, when given as an intravenous infusion at a dose of 1 microgram/kg within 12 hours of symptom onset, appeared to improve vision and visual fields in affected patients. The efficacy of this treatment is considered unproven pending confirmation by other investigators.

Recurrences of PION in the same or fellow eye have been described, but the incidence rate is not well established [11,73]. In one series of patients with nonarteritic PION, PION subsequently developed in the fellow eye in 21 percent of patients with a mean interval of 256 days between occurrences [11].

As with NAION, treatment with daily aspirin and atherosclerosis risk factor management is appropriate for most patients as primary prevention of cardiovascular disease (see "Overview of primary prevention of cardiovascular disease"). However, these measures are not known to improve visual prognosis or to prevent recurrence in patients with PION.

SUMMARY AND RECOMMENDATIONS

Pathogenesis – Posterior ischemic optic neuropathy (PION) is believed to result from an infarction of the retrobulbar optic nerve. While there is much overlap, the vascular anatomy, etiologies, and clinical presentation of PION are distinct from those of anterior ischemic optic neuropathy (AION), which is more common and affects the optic disc.

Etiologic categories – There are three distinct etiologic categories that account for the majority of patients with PION. (See 'Etiologies and pathogenesis' above.)

Perioperative PION – Perioperative PION is most often described in the setting of spinal surgeries and radical neck dissection, although a wide range of operative procedures have been implicated. Hypotension secondary to blood loss is the most universal risk factor for this complication. Localized venous hypertension resulting from prolonged use of the prone position in spine surgery and from internal jugular venous ligation in neck dissections is believed to contribute to PION. (See 'Perioperative PION' above.)

Arteritic PION – PION is an infrequent complication of giant cell arteritis (GCA), a condition occurring exclusively in older adults (>50 years) and associated with a prodrome of polymyalgia rheumatica. (See 'Arteritic PION' above.)

Nonarteritic (idiopathic) PION – More than half of PION cases are classified as idiopathic-nonarteritic. Associated comorbidities in these patients suggest that this form of PION is a manifestation of systemic vascular disease. (See 'Nonarteritic (idiopathic) PION' above.)

Clinical presentation – Most patients with PION present with abrupt, painless, monocular vision loss. Approximately half of patients with perioperative PION will have bilateral vision loss, while patients with arteritic PION may sustain sequential vision loss in both eyes within an interval of days to weeks.

Vision loss is usually severe in patients with perioperative and arteritic PION and more variable in patients with nonarteritic PION. (See 'Clinical presentation' above.)

Evaluation and diagnosis – PION is a diagnosis of exclusion. The most urgent diagnostic imperative is to diagnose or exclude GCA with erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) and/or a temporal artery biopsy.

Patients also require ophthalmologic examination and a contrast-enhanced MRI study that focuses on the optic nerves. (See 'Diagnosis' above.)

Treatment – Patients with PION and GCA are treated with corticosteroids and other disease-modifying therapies. Treatment is aimed at preventing vision loss in the other eye. (See "Treatment of giant cell arteritis".)

There is no treatment for perioperative or nonarteritic PION. (See 'Prognosis, treatment, and prevention' above.)

Prognosis – Patients with arteritic and perioperative PION do not usually experience significant visual recovery, while up to one-third of patients with nonarteritic (idiopathic) PION may improve.

Patients with nonarteritic PION may experience a subsequent episode in the other eye over the next months and years; atherosclerotic risk factor management is not known to be preventive. (See 'Prognosis, treatment, and prevention' above.)

  1. Rucker JC, Biousse V, Newman NJ. Ischemic optic neuropathies. Curr Opin Neurol 2004; 17:27.
  2. Hayreh SS. Posterior ischaemic optic neuropathy: clinical features, pathogenesis, and management. Eye (Lond) 2004; 18:1188.
  3. Olver JM, Spalton DJ, McCartney AC. Microvascular study of the retrolaminar optic nerve in man: the possible significance in anterior ischaemic optic neuropathy. Eye (Lond) 1990; 4 ( Pt 1):7.
  4. Dunker S, Hsu HY, Sebag J, Sadun AA. Perioperative risk factors for posterior ischemic optic neuropathy. J Am Coll Surg 2002; 194:705.
  5. Schobel GA, Schmidbauer M, Millesi W, Undt G. Posterior ischemic optic neuropathy following bilateral radical neck dissection. Int J Oral Maxillofac Surg 1995; 24:283.
  6. Nawa Y, Jaques JD, Miller NR, et al. Bilateral posterior optic neuropathy after bilateral radical neck dissection and hypotension. Graefes Arch Clin Exp Ophthalmol 1992; 230:301.
  7. Marks SC, Jaques DA, Hirata RM, Saunders JR Jr. Blindness following bilateral radical neck dissection. Head Neck 1990; 12:342.
  8. Johnson MW, Kincaid MC, Trobe JD. Bilateral retrobulbar optic nerve infarctions after blood loss and hypotension. A clinicopathologic case study. Ophthalmology 1987; 94:1577.
  9. Williams EL, Hart WM Jr, Tempelhoff R. Postoperative ischemic optic neuropathy. Anesth Analg 1995; 80:1018.
  10. Buono LM, Foroozan R. Perioperative posterior ischemic optic neuropathy: review of the literature. Surv Ophthalmol 2005; 50:15.
  11. Sadda SR, Nee M, Miller NR, et al. Clinical spectrum of posterior ischemic optic neuropathy. Am J Ophthalmol 2001; 132:743.
  12. Luscavage LE, Volpe NJ, Liss R. Posterior ischemic optic neuropathy after uncomplicated cataract extraction. Am J Ophthalmol 2001; 132:408.
  13. Remigio D, Wertenbaker C. Post-operative bilateral vision loss. Surv Ophthalmol 2000; 44:426.
  14. Wessels IF. Posterior ischemic optic neuropathy during general surgery. Am J Ophthalmol 1987; 104:555.
  15. Nuttall GA, Garrity JA, Dearani JA, et al. Risk factors for ischemic optic neuropathy after cardiopulmonary bypass: a matched case/control study. Anesth Analg 2001; 93:1410.
  16. Rubin DS, Matsumoto MM, Moss HE, et al. Ischemic Optic Neuropathy in Cardiac Surgery: Incidence and Risk Factors in the United States from the National Inpatient Sample 1998 to 2013. Anesthesiology 2017; 126:810.
  17. Pazos GA, Leonard DW, Blice J, Thompson DH. Blindness after bilateral neck dissection: case report and review. Am J Otolaryngol 1999; 20:340.
  18. Fenton S, Fenton JE, Browne M, et al. Ischaemic optic neuropathy following bilateral neck dissection. J Laryngol Otol 2001; 115:158.
  19. Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol 2008; 145:604.
  20. Ho VT, Newman NJ, Song S, et al. Ischemic optic neuropathy following spine surgery. J Neurosurg Anesthesiol 2005; 17:38.
  21. Worrell L, Rowe M, Petti G. Amaurosis: a complication of bilateral radical neck dissection. Am J Otolaryngol 2002; 23:56.
  22. Baig MN, Lubow M, Immesoete P, et al. Vision loss after spine surgery: review of the literature and recommendations. Neurosurg Focus 2007; 23:E15.
  23. Chang SH, Miller NR. The incidence of vision loss due to perioperative ischemic optic neuropathy associated with spine surgery: the Johns Hopkins Hospital Experience. Spine (Phila Pa 1976) 2005; 30:1299.
  24. Lee LA, Roth S, Posner KL, et al. The American Society of Anesthesiologists Postoperative Visual Loss Registry: analysis of 93 spine surgery cases with postoperative visual loss. Anesthesiology 2006; 105:652.
  25. Kalyani SD, Miller NR, Dong LM, et al. Incidence of and risk factors for perioperative optic neuropathy after cardiac surgery. Ann Thorac Surg 2004; 78:34.
  26. Stevens WR, Glazer PA, Kelley SD, et al. Ophthalmic complications after spinal surgery. Spine (Phila Pa 1976) 1997; 22:1319.
  27. Alexandrakis G, Lam BL. Bilateral posterior ischemic optic neuropathy after spinal surgery. Am J Ophthalmol 1999; 127:354.
  28. Gill B, Heavner JE. Postoperative visual loss associated with spine surgery. Eur Spine J 2006; 15:479.
  29. Postoperative Visual Loss Study Group. Risk factors associated with ischemic optic neuropathy after spinal fusion surgery. Anesthesiology 2012; 116:15.
  30. Levinson B, Reddy S. Posterior Ischemic Optic Neuropathy After Extensive Spine Surgery: A Case Report and Review of the Literature. AANA J 2019; 87:37.
  31. Wang MY, Brewer R, Sadun AA. Posterior ischemic optic neuropathy: Perioperative risk factors. Taiwan J Ophthalmol 2020; 10:167.
  32. Myers MA, Hamilton SR, Bogosian AJ, et al. Visual loss as a complication of spine surgery. A review of 37 cases. Spine (Phila Pa 1976) 1997; 22:1325.
  33. Reddy A, Foroozan R, Edmond JC, Hinckley LK. Dilated superior ophthalmic veins and posterior ischemic optic neuropathy after prolonged spine surgery. J Neuroophthalmol 2008; 28:327.
  34. Kirkali P, Kansu T. A case of unilateral posterior ischemic optic neuropathy after radical neck dissection. Ann Ophthalmol 1990; 22:297.
  35. Weber ED, Colyer MH, Lesser RL, Subramanian PS. Posterior ischemic optic neuropathy after minimally invasive prostatectomy. J Neuroophthalmol 2007; 27:285.
  36. Tauscher RG, Bison HS, Simon SS, Volpe NJ. Intracranial Posterior Ischemic Optic Neuropathy and Ophthalmic Artery Occlusion. J Neuroophthalmol 2022; 42:e476.
  37. Hayreh SS, Podhajsky PA, Zimmerman B. Ocular manifestations of giant cell arteritis. Am J Ophthalmol 1998; 125:509.
  38. Issa M, Donaldson L, Jeeva-Patel T, Margolin E. Ischemic ocular manifestations of giant cell arteritis: A Canadian case series. J Neurol Sci 2022; 436:120222.
  39. Albarrak AM, Mohammad Y, Hussain S, et al. Simultaneous bilateral posterior ischemic optic neuropathy secondary to giant cell arteritis: a case presentation and review of the literature. BMC Ophthalmol 2018; 18:317.
  40. Inoue M, Tsukahara Y. Vascular optic neuropathy in diabetes mellitus. Jpn J Ophthalmol 1997; 41:328.
  41. Asensio JA, Forno W, Castillo GA, et al. Posterior ischemic optic neuropathy related to profound shock after penetrating thoracoabdominal trauma. South Med J 2002; 95:1053.
  42. Huang TW, Liu CM, Cheng PW, Yang CH. Posterior ischemic optic neuropathy following endoscopic sinus surgery. Otolaryngol Head Neck Surg 2003; 129:448.
  43. Buono LM, Foroozan R, Savino PJ, et al. Posterior ischemic optic neuropathy after hemodialysis. Ophthalmology 2003; 110:1216.
  44. Choi JH, Choi KD, Kim JS, et al. Simultaneous posterior ischemic optic neuropathy, cerebral border zone infarction, and spinal cord infarction after correction of malignant hypertension. J Neuroophthalmol 2008; 28:198.
  45. Lee AG, Brazis PW, Miller NR. Posterior ischemic optic neuropathy associated with migraine. Headache 1996; 36:506.
  46. Foroozan R, Marx DP, Evans RW. Posterior ischemic optic neuropathy associated with migraine. Headache 2008; 48:1135.
  47. Wijaya J, Salu P, Leblanc A, Bervoets S. Acute unilateral visual loss due to a single intranasal methamphetamine abuse. Bull Soc Belge Ophtalmol 1999; 271:19.
  48. Rivkin MJ, Hedges TR 3rd, Logigian EL. Carotid dissection presenting as posterior ischemic optic neuropathy. Neurology 1990; 40:1469.
  49. Biousse V, Touboul PJ, D'Anglejan-Chatillon J, et al. Ophthalmologic manifestations of internal carotid artery dissection. Am J Ophthalmol 1998; 126:565.
  50. Kawabe K, Nagaoka T, Iguchi H, et al. Optic nerve MRI enhancement in posterior ischaemic optic neuropathy due to internal carotid artery dissection. Clin Neurol Neurosurg 2010; 112:350.
  51. Kiyosawa M, Asano T. [A case of posterior ischemic optic neuropathy associated with pulseless disease]. Nippon Ganka Gakkai Zasshi 1982; 86:2050.
  52. Blaise P, Robe-Collignon N, Andris C, Rakic JM. Wegener's granulomatosis and posterior ischemic optic neuropathy: Atypical associated conditions. Eur J Intern Med 2007; 18:326.
  53. Nagashima T, Matsumoto K, Murosaki T, et al. Posterior ischemic optic neuropathy in a patient with granulomatosis with polyangiitis (Wegener's). Rheumatol Int 2013; 33:1915.
  54. Nelson PC, Kunam V, Prospero Ponce C. Atypical painless vision loss in a patient with granulomatosis with polyangiitis. GMS Ophthalmol Cases 2020; 10:Doc46.
  55. Jabs DA, Miller NR, Newman SA, et al. Optic neuropathy in systemic lupus erythematosus. Arch Ophthalmol 1986; 104:564.
  56. Saraux H, Laroche L, Foels A, Martin-Gousset D. [Posterior acute ischemic optic neuropathy (author's transl)]. J Fr Ophtalmol 1982; 5:167.
  57. Hashimoto M, Ohtsuka K, Suzuki Y, Hoyt WF. A case of posterior ischemic optic neuropathy in a posterior-draining dural cavernous sinus fistula. J Neuroophthalmol 2005; 25:176.
  58. Wu CE, Wen KH, Huang CW. Delayed Nonarteritic Posterior Ischemic Optic Neuropathy following Herpes Zoster Ophthalmicus: A Case Report. Case Rep Neurol 2023; 15:69.
  59. Pakravan M, Ahmadieh H, Kaharkaboudi AR. Posterior Ischemic Optic Neuropathy following Herpes Zoster Ophthalmicus. J Ophthalmic Vis Res 2009; 4:59.
  60. Kothe AC, Flanagan J, Trevino RC. True posterior ischemic optic neuropathy associated with herpes zoster ophthalmicus. Optom Vis Sci 1990; 67:845.
  61. Ghabrial R, Ananda A, van Hal SJ, et al. Invasive Fungal Sinusitis Presenting as Acute Posterior Ischemic Optic Neuropathy. Neuroophthalmology 2018; 42:209.
  62. Perlman JI, Forman S, Gonzalez ER. Retrobulbar ischemic optic neuropathy associated with sickle cell disease. J Neuroophthalmol 1994; 14:45.
  63. Lee AG, Eggenberger ER, Kaufman DI, Manrique C. Optic nerve enhancement on magnetic resonance imaging in arteritic ischemic optic neuropathy. J Neuroophthalmol 1999; 19:235.
  64. López JM, Nazabal ER, Muñiz AM, Rey del Corral P. Detection of posterior ischemic optic neuropathy due to giant cell arteritis with magnetic resonance imaging. Eur Neurol 2001; 46:109.
  65. Purvin V, Kuzma B. Intraorbital optic nerve signal hyperintensity on magnetic resonance imaging sequences in perioperative hypotensive ischemic optic neuropathy. J Neuroophthalmol 2005; 25:202.
  66. Bhatt NP, Morales RE, Mathews MK. MRI findings in Post-operative Bilateral Posterior Ischemic Optic Neuropathy. Open J Ophthalmol 2013; 3:51.
  67. Quddus A, Lawlor M, Siddiqui A, et al. Using Diffusion-Weighted Magnetic Resonance Imaging to Confirm a Diagnosis of Posterior Ischaemic Optic Neuropathy: Two Case Reports and Literature Review. Neuroophthalmology 2015; 39:161.
  68. Danyel LA, Miszczuk M, Pietrock C, et al. Utility of standard diffusion-weighted magnetic resonance imaging for the identification of ischemic optic neuropathy in giant cell arteritis. Sci Rep 2022; 12:16553.
  69. Yang TH, Lin MC. Using diffuse weighted image and apparent diffusion coefficient in MRI for diagnosis of posterior ischemic optic neuropathy in a young male: a case report and literature review. BMC Ophthalmol 2022; 22:168.
  70. He M, Cestari D, Cunnane MB, Rizzo JF 3rd. The use of diffusion MRI in ischemic optic neuropathy and optic neuritis. Semin Ophthalmol 2010; 25:225.
  71. American Society of Anesthesiologists Task Force on Perioperative Blindness. Practice advisory for perioperative visual loss associated with spine surgery: a report by the American Society of Anesthesiologists Task Force on Perioperative Blindness. Anesthesiology 2006; 104:1319.
  72. American Society of Anesthesiologists Task Force on Perioperative Visual Loss. Practice advisory for perioperative visual loss associated with spine surgery: an updated report by the American Society of Anesthesiologists Task Force on Perioperative Visual Loss. Anesthesiology 2012; 116:274.
  73. Steigerwalt RD Jr, Pascarella A, De Angelis M, et al. Three episodes of non-arteritic posterior ischemic optic neuropathy in the same patient treated with intravenous prostaglandin E1. Drug Discov Ther 2016; 10:177.
  74. Steigerwalt RDJ, Limoli PG, Nebbioso M. Visual field improvement in non-arteritic posterior ischemic optic neuropathy in a patient treated with intravenous prostaglandin E1 and steroids. Drug Discov Ther 2017; 11:226.
  75. Steigerwalt RD, Cesarone MR, Belcaro G, et al. Non-arteritic Posterior Ischaemic Optic Neuropathy Treated with Intravenous Prostaglandin E1 and Oral Corticosteroids. Neuroophthalmology 2011; 35:81.
Topic 5232 Version 13.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟