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急性発症の視力障害

著者: 須網和也 名古屋掖済会病院 救急科

監修: 箕輪良行 みさと健和病院 救急総合診療研修顧問

著者校正/監修レビュー済:2021/06/30
患者向け説明資料

概要・推奨   

  1. 急性視力障害の鑑別のためには問診が重要である。特に重要なことは、発症までの時間経過・痛みの有無・片側性が両側性か、一過性か持続性かを聴取することである。身体所見では、対座法での視野検査に併せて対光反射を確認することが大切である。特に、相対性求心性瞳孔障害を認める患者では、視神経障害、広範な網膜の障害が考えられるため、眼科コンサルトが必要となる症例が多く、適切な介入が必要となる。また患者の目が赤く見えるいわゆる赤目をきたしていた場合、鑑別疾患を絞ることができる。特殊な状況として、眼科手術後・外傷に伴う急性視力障害は眼科コンサルトが必要になることが多い。
薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
須網和也 : 未申告[2021年]
監修:箕輪良行 : 特に申告事項無し[2021年]

改訂のポイント:
  1. 急性視力障害の鑑別は多岐にわたるが、緊急眼科コンサルトが必要な疾患や、膠原病や血管炎に関連する全身精査が必要な疾患を、フローチャートを用いて体系的に診断できるように改訂した。

病態・疫学・診察

疫学情報・病態・注意事項  
  1. 急性の視力障害は眼のぼやけ程度の症状も含めると多くの人が訴える症状であり、鑑別疾患は多岐にわたる。
  1. 眼科専門医への早急なコンサルトが必要な疾患も多く、タイミングを逃さないように心がける。
  1. 緊急に治療を開始すべき疾患を見逃さない。
問診・診察のポイント  
 
  1. 視力障害の原因として大きく以下の4つに分けて考える。
    ①透光体の異常、②網膜の異常、③視神経~視交叉の異常、④視交叉~脳の異常
  1. 患者が急性発症と訴えていても、本当に急性発症なのか、徐々に進行していた病態を急に自覚しただけなのかを問診にて区別することが必要である。

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文献 

著者: Prabhat K Pokhrel, Sanaz A Loftus
雑誌名: Am Fam Physician. 2007 Sep 15;76(6):829-36.
Abstract/Text Prompt recognition and appropriate treatment of ocular emergencies are essential in the primary care setting when the outcome may depend on timely management. All ocular emergencies, including a penetrating globe injury, retinal detachment, central retinal artery occlusion, acute angle-closure glaucoma, and chemical burns, should be referred immediately to the emergency department or an ophthalmologist. Careful eye examination and simple tests can help primary care physicians make decisions about appropriate treatment and referral. All patients with eye problems should be tested for visual acuity and ocular movements. Confrontation visual field examination, pupillary examination, and direct ophthalmoscopy of both eyes also should be performed. Ocular injury from high-velocity trauma or from chemicals may be easily misdiagnosed. After a chemical burn, thorough eye washing for at least 30 minutes or until the pH of the eye is within physiologic range is critical to prevent further damage. Use of an eye shield is required in patients with a ruptured globe to protect the injured eye and preserve the patient's vision.

PMID 17910297  Am Fam Physician. 2007 Sep 15;76(6):829-36.
著者: Jane W Chan
雑誌名: Neurologist. 2012 Jan;18(1):23-31. doi: 10.1097/NRL.0b013e31823d7acd.
Abstract/Text BACKGROUND: About half of multiple sclerosis patients present with optic neuritis (ON) as a clinically isolated syndrome (CIS). In the Optic Neuritis Treatment Trial study, 28% of patients with ON and an abnormal brain magnetic resonance imaging (MRI) did not have a relapse at the end of 15 years. It is still difficult to predict which CIS patients will go on to develop clinically definite multiple sclerosis and which will have a benign course.
REVIEW SUMMARY: This review focuses on more advanced methods of detecting and quantifying ON in multiple sclerosis that have been developed in the past 15 years, especially on recent developments in optical coherence tomography measurement of the retinal nerve fiber layer and its role in monitoring axonal loss in the course of the disease. New clinical trial methods of measuring visual acuity include high-contrast visual acuity testing with the Early Treatment Diabetic Retinopathy Study charts, low-contrast letter acuity, and contrast sensitivity testing. More advanced neuroimaging techniques include magnetization transfer imaging and diffusion tensor imaging to quantify visual pathway lesions. Other tests of visual function, such as multifocal visual-evoked potentials and functional MRI, have been shown to be more sensitive than conventional visual-evoked potentials or MRI in detecting early, subtle visual impairment in ON and early recovery of visual function related to cortical plasticity. Newer agents are currently being investigated for CIS in ongoing clinical trials.
CONCLUSIONS: Better methods are being developed for the earlier diagnosis, monitoring, and treatment of ON. In the future, CIS patients may be stratified according to their risk of development of clinically definite multiple sclerosis and therefore, receive the appropriate treatment.

PMID 22217611  Neurologist. 2012 Jan;18(1):23-31. doi: 10.1097/NRL.0b0・・・
著者: R W Beck, P A Cleary, M M Anderson, J L Keltner, W T Shults, D I Kaufman, E G Buckley, J J Corbett, M J Kupersmith, N R Miller
雑誌名: N Engl J Med. 1992 Feb 27;326(9):581-8. doi: 10.1056/NEJM199202273260901.
Abstract/Text BACKGROUND AND METHODS: The use of corticosteroids to treat optic neuritis is controversial. At 15 clinical centers, we randomly assigned 457 patients with acute optic neuritis to receive oral prednisone (1 mg per kilogram of body weight per day) for 14 days; intravenous methylprednisolone (1 g per day) for 3 days, followed by oral prednisone (1 mg per kilogram per day) for 11 days; or oral placebo for 14 days. Visual function was assessed over a six-month follow-up period.
RESULTS: Visual function recovered faster in the group receiving intravenous methylprednisolone than in the placebo group; this was particularly true for the reversal of visual-field defects (P = 0.0001). Although the differences between the groups decreased with time, at six months the group that received intravenous methylprednisolone still had slightly better visual fields (P = 0.054), contrast sensitivity (P = 0.026), and color vision (P = 0.033) but not better visual acuity (P = 0.66). The outcome in the oral-prednisone group did not differ from that in the placebo group. In addition, the rate of new episodes of optic neuritis in either eye was higher in the group receiving oral prednisone, but not the group receiving intravenous methylprednisolone, than in the placebo group (relative risk for oral prednisone vs. placebo, 1.79; 95 percent confidence interval, 1.08 to 2.95).
CONCLUSIONS: Intravenous methylprednisolone followed by oral prednisone speeds the recovery of visual loss due to optic neuritis and results in slightly better vision at six months. Oral prednisone alone, as prescribed in this study, is an ineffective treatment and increases the risk of new episodes of optic neuritis.

PMID 1734247  N Engl J Med. 1992 Feb 27;326(9):581-8. doi: 10.1056/NE・・・
著者: Lucy Goold, Shane Durkin, John Crompton
雑誌名: Aust Fam Physician. 2009 Oct;38(10):764-7.
Abstract/Text BACKGROUND: Sudden loss of vision requires careful history and examination to identify the underlying cause.
OBJECTIVE: This article discusses the various causes of sudden loss of vision and provides the general practitioner with a guide to examination.
DISCUSSION: Rapidity of onset, duration and associated symptoms provide vital clues to the nature of the disease process. Simple examination techniques such as visual acuity measurement, confrontational visual field testing, pupil assessment and fundoscopy are integral to the appropriate assessment, treatment and referral of patients presenting with sudden loss of vision.

PMID 19893813  Aust Fam Physician. 2009 Oct;38(10):764-7.
著者: Lucy Goold, Shane Durkin, John Crompton
雑誌名: Aust Fam Physician. 2009 Oct;38(10):770-2.
Abstract/Text BACKGROUND: Sudden vision loss usually requires urgent ophthalmic assessment. Diagnosis and management requires the judicious use of a wide range of serological and imaging investigations to guide appropriate treatment and referral.
OBJECTIVE: This article follows on from the previous discussion of the role of history and examination to discuss the appropriate investigation and management of common causes of sudden visual loss.
DISCUSSION: The key historical and examination findings have now been extracted and synthesised and these inform the next step. The general practitioner must now decide upon the most appropriate and timely investigation pathway or the need for, and urgency of, referral.

PMID 19893814  Aust Fam Physician. 2009 Oct;38(10):770-2.
著者: Syed S Azhar, Rosa A Tang, E Ulysses Dorotheo
雑誌名: Geriatrics. 2005 Aug;60(8):26-30.
Abstract/Text Giant cell arteritis (GCA), also known as temporal arteritis, cranial arteritis, or granulomatous arteritis, is a systemic necrotizing vasculitis seen in patients typically over age 50. If untreated, GCA can cause permanent visual loss in one or both eyes in 13% to 50% of patients. Primary care physicians routinely see elderly patients with headaches and fatigue; these may be potential symptoms of GCA. C-reactive protein (CRP) in conjunction with erythrocyte sedimentation rate (ESR) has 97% specificity in diagnosing GCA. Temporal artery biopsy confirms the diagnosis in many cases. Early recognition and treatment of this potentially blinding condition is thus essential. Systemic steroids are the standard therapy for patients with a positive diagnosis of GCA, and in a high percentage of patients the treatment may extend for more than one year.

PMID 16092890  Geriatrics. 2005 Aug;60(8):26-30.
著者: Aikaterini Arida, Miltiades Kyprianou, Meletios Kanakis, Petros P Sfikakis
雑誌名: BMC Musculoskelet Disord. 2010 Mar 8;11:44. doi: 10.1186/1471-2474-11-44. Epub 2010 Mar 8.
Abstract/Text BACKGROUND: Ultrasonography of temporal arteries is not commonly used in the approach of patients with suspected giant cell arteritis (GCA) in clinical practice. A meta-analysis of primary studies available through April 2004 concluded that ultrasonography could indeed be helpful in diagnosing GCA. We specifically re-examined the diagnostic value of the ultrasonography-derived halo sign, a dark hypoechoic circumferential thickening around the artery lumen, indicating vasculitic wall edema, in GCA.
METHODS: Original, prospective studies in patients with suspected GCA that examined ultrasonography findings of temporal arteries using the ACR 1990 classification criteria for GCA as reference standard, published through 2009, were identified. Only eight studies involving 575 patients, 204 of whom received the final diagnosis of GCA, fulfilled technical quality criteria for ultrasound. Weighted sensitivity and specificity estimates of the halo sign were assessed, their possible heterogeneity was investigated and pooled diagnostic odds ratio was determined.
RESULTS: Unilateral halo sign achieved an overall sensitivity of 68% (95% CI, 0.61-0.74) and specificity of 91% (95% CI, 0.88-0.94) for GCA. The values of inconsistency coefficient (I2) of both sensitivity and specificity of the halo sign, showed significant heterogeneity concerning the results between studies. Pooled diagnostic odds ratio, expressing how much greater the odds of having GCA are for patients with halo sign than for those without, was 34 (95% CI, 8.21-138.23). Diagnostic odds ratio was further increased to 65 (95% CI, 17.86-236.82) when bilateral halo signs were present (sensitivity/specificity of 43% and 100%, respectively). In both cases, it was found that DOR was constant across studies.
CONCLUSION: Temporal artery edema demonstrated as halo sign should be always looked for in ultrasonography when GCA is suspected. Providing that currently accepted technical quality criteria are fulfilled, halo sign's sensitivity and specificity are comparable to those of autoantibodies used as diagnostic tests in rheumatology. Validation of revised GCA classification criteria which will include the halo sign may be warranted.

PMID 20210989  BMC Musculoskelet Disord. 2010 Mar 8;11:44. doi: 10.118・・・
著者: T A Bley, M Uhl, J Carew, M Markl, D Schmidt, H-H Peter, M Langer, O Wieben
雑誌名: AJNR Am J Neuroradiol. 2007 Oct;28(9):1722-7. doi: 10.3174/ajnr.A0638. Epub 2007 Sep 20.
Abstract/Text BACKGROUND AND PURPOSE: Clinical indications of giant cell arteritis may be unspecific, and noninvasive diagnosis is often difficult. This study investigated the hypothesis that high-resolution MR imaging of the superficial cranial arteries is a noninvasive imaging technique that can detect the occurrence of giant cell arteritis.
MATERIALS AND METHODS: Contrast-enhanced, high-resolution MR imaging was performed on 64 consecutive patients with suspected giant cell arteritis. Mural thickness, lumen diameter, and a mural contrast enhancement score were assessed with T1-weighted spin-echo images with submillimeter in-plane spatial resolution. The final rheumatologist's diagnosis according to the clinical criteria of the American College of Rheumatology including laboratory tests and results of temporal artery biopsies from 32 patients was used as a "gold standard" for the evaluation of the MR imaging findings.
RESULTS: All of the examinations provided diagnostic image quality. Evaluation of the mural inflammatory MR imaging signs for diagnosing vasculitis resulted in a sensitivity of 80.6% and a specificity of 97.0%. In comparison, histology results alone showed a sensitivity of 77.8% and specificity of 100%. The mean wall thickness increased significantly from 0.39 mm (+/-0.18 mm) to 0.74 mm (+/-0.32 mm; P < .001), and the lumen diameter decreased significantly from 0.84 mm (+/-0.29 mm) to 0.65 mm (+/-0.38 mm; P < .05) for patients with giant cell arteritis.
CONCLUSION: Contrast-enhanced, high-resolution MR imaging allows noninvasive assessment of mural inflammation in giant cell arteritis with good diagnostic certainty. Measures of mural thickening and contrast enhancement can be obtained in these small vessels and provide valuable vasculitic MR imaging findings.

PMID 17885247  AJNR Am J Neuroradiol. 2007 Oct;28(9):1722-7. doi: 10.3・・・
著者: Shyamanga Borooah, Arjun Dhillon, Baljean Dhillon
雑誌名: BMJ. 2015 Jun 8;350:h2093. doi: 10.1136/bmj.h2093. Epub 2015 Jun 8.
Abstract/Text
PMID 26055964  BMJ. 2015 Jun 8;350:h2093. doi: 10.1136/bmj.h2093. Epub・・・
著者: Nika Bagheri, Sonia Mehta
雑誌名: Prim Care. 2015 Sep;42(3):347-61. doi: 10.1016/j.pop.2015.05.010.
Abstract/Text Acute vision loss can be transient (lasting <24 hours) or persistent (lasting >24 hours). When patients present with acute vision loss, it is important to ascertain the duration of vision loss and whether it is a unilateral process affecting one eye or a bilateral process affecting both eyes. This article focuses on causes of acute vision loss in the nontraumatic setting and provides management pearls to help health care providers better triage these patients.

Copyright © 2015 Elsevier Inc. All rights reserved.
PMID 26319342  Prim Care. 2015 Sep;42(3):347-61. doi: 10.1016/j.pop.20・・・
著者: Nancy Newman, Valérie Biousse
雑誌名: Continuum (Minneap Minn). 2014 Aug;20(4 Neuro-ophthalmology):785-815. doi: 10.1212/01.CON.0000453317.67637.46.
Abstract/Text PURPOSE OF REVIEW: This review emphasizes the differential diagnosis of visual loss for the neurologist.
RECENT FINDINGS: As an expert on the CNS, of which the eye is a part, the neurologist is expected to be able to evaluate a patient's report of visual loss and provide at least a cursory examination of the ocular apparatus and visual pathways. To appropriately localize the lesion within the eye and to generate a diagnosis, the neurologist must at least be aware of the other clinical entities that can cause visual loss, especially sudden visual loss, other than optic nerve damage. Once the problem has been localized to the optic nerve, a complete differential diagnosis will include all the pathophysiologic processes that can affect any tissue, specifically any piece of brain tissue. Intracerebral visual loss from damage to the chiasm or retrochiasmal pathways or to the downstream centers of higher visual processing is also common, given that the visual pathways constitute more than one-third of the supratentorial brain mass and are frequently affected by structural lesions and a wide range of neurologic disorders. The paucity of neuro-ophthalmologists makes it essential for neurologists to feel comfortable evaluating and managing patients with visual loss from presumed optic neuropathies or lesions of the intracranial visual pathways.
SUMMARY: The diagnosis of visual loss is not always easy, even for ophthalmologists. Good collaboration between neurologists and ophthalmologists is the key to a correct diagnosis and appropriate management when a neuro-ophthalmologist is not readily available.

PMID 25099095  Continuum (Minneap Minn). 2014 Aug;20(4 Neuro-ophthalmo・・・
著者: Ana Miguel, Filipe Henriques, Luís Filipe Azevedo, Altamiro Costa Pereira
雑誌名: Pharmacoepidemiol Drug Saf. 2014 Mar;23(3):221-33. doi: 10.1002/pds.3566. Epub 2014 Jan 27.
Abstract/Text PURPOSE: To perform a comprehensive and systematic review regarding ophthalmic adverse drug reactions (ADRs) to systemic drugs to: (i) systematically summarize existing evidence, (ii) identify areas, ophthalmic ADRs or drugs that lacked systematization or assessment (namely drugs with original studies characterizing specific ophthalmic ADRs but without causality assessment nor without meta-analysis).
METHODS: Systematic review of several electronic databases (last search 1/7/2012): Medline, SCOPUS, ISI web of knowledge, ISI Conference Proceedings, International Pharmaceutical Abstracts and Google scholar. Search query included: eye, ocular, ophthalmic, ophthalmology, adverse and reaction. Inclusion criteria were: (i) Primary purpose was to assess an ophthalmic ADR to a systemic medication; (ii) Patient evaluation performed by an ophthalmologist; (iii) Studies that specified diagnostic criteria for an ocular ADR. Different types of studies were included and analyzed separately. Two independent reviewers assessed eligibility criteria, extracted data and evaluated risk of bias.
RESULTS: From 562 studies found, 32 were included (1 systematic review to sildenafil, 11 narrative reviews, 1 trial, 1 prospective study, 6 transversal studies, 6 spontaneous reports and 6 case series). Drugs frequently involved included amiodarone, sildenafil, hydroxychloroquine and biphosphonates. Frequent ophthalmic ADRs included: keratopathy, dry eye and retinopathy.
CONCLUSIONS: To increase evidence about ophthalmic ADRs, there is a need for performing specific systematic reviews, applying strictly the World Health Organization's (WHO) definition of ADR and WHO causality assessment of ADRs. Some ophthalmic ADRs may be frequent, but require ophthalmological examination; therefore, ophthalmologists' education and protocols of collaboration between other specialties whenever they prescribe high-risk drugs are suggestions for the future.

Copyright © 2014 John Wiley & Sons, Ltd.
PMID 24464938  Pharmacoepidemiol Drug Saf. 2014 Mar;23(3):221-33. doi:・・・
著者: Ahmed T Toosy, Deborah F Mason, David H Miller
雑誌名: Lancet Neurol. 2014 Jan;13(1):83-99. doi: 10.1016/S1474-4422(13)70259-X.
Abstract/Text Acute optic neuritis is the most common optic neuropathy affecting young adults. Exciting developments have occurred over the past decade in understanding of optic neuritis pathophysiology, and these developments have been translated into treatment trials. In its typical form, optic neuritis presents as an inflammatory demyelinating disorder of the optic nerve, which can be associated with multiple sclerosis. Atypical forms of optic neuritis can occur, either in association with other inflammatory disorders or in isolation. Differential diagnosis includes various optic nerve and retinal disorders. Diagnostic investigations include MRI, visual evoked potentials, and CSF examination. Optical coherence tomography can show retinal axonal loss, which correlates with measures of persistent visual dysfunction. Treatment of typical forms with high-dose corticosteroids shortens the period of acute visual dysfunction but does not affect the final visual outcome. Atypical forms can necessitate prolonged immunosuppressive regimens. Optical coherence tomography and visual evoked potential measures are suitable for detection of neuroaxonal loss and myelin repair after optic neuritis. Clinical trials are underway to identify potential neuroprotective or remyelinating treatments for acutely symptomatic inflammatory demyelinating CNS lesions.

Copyright © 2014 Elsevier Ltd. All rights reserved.
PMID 24331795  Lancet Neurol. 2014 Jan;13(1):83-99. doi: 10.1016/S1474・・・
著者: Sohan Singh Hayreh
雑誌名: Indian J Ophthalmol. 2011 Mar-Apr;59(2):123-36. doi: 10.4103/0301-4738.77024.
Abstract/Text 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.

PMID 21350282  Indian J Ophthalmol. 2011 Mar-Apr;59(2):123-36. doi: 10・・・
著者: Priya Sharma, Jayanth Sridhar, Sonia Mehta
雑誌名: Prim Care. 2015 Sep;42(3):425-35. doi: 10.1016/j.pop.2015.05.011.
Abstract/Text Flashes and floaters are common ocular complaints. Flashes refer to aberrations of light that are seen in a patient's field of gaze. The flashes can be of varying sizes, colors, frequency, and durations, depending on the cause. Floaters are another common visual phenomenon caused by particles or debris in the vitreous gel of the eye that cause shadows and thus visual changes, especially against bright backgrounds and in brightly lit environments. Flashes and floaters can occur individually or together. This article discusses common causes of flashes and floaters to help with the triaging and management of these patients.

Copyright © 2015 Elsevier Inc. All rights reserved.
PMID 26319347  Prim Care. 2015 Sep;42(3):425-35. doi: 10.1016/j.pop.20・・・

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