Neodymium:yttrium-aluminum-garnet laser arteriotomy with embolectomy for central retinal artery occlusion

Reynard, Michael; Hanscom, Thomas A.

doi:10.1016/s0002-9394(03)00817-1

Cited by 30 publications

(11 citation statements)

References 3 publications

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“…Therapies aimed at physically dislodging the embolus include ocular massage, which increases retinal artery perfusion pressure via retinal arteriolar dilatation and decreased IOP (17,22,73), and the use of an Nd:YAG laser to physically dislodge a visible embolus (74,75). The use of ocular massage, either alone or in combination with IOP lowering medications, has not been shown to significantly improve visual function following acute retinal ischemia (17,22,76).…”

Section: Treatment Of Acute Retinal Ischemia (Crao or Brao)mentioning

confidence: 99%

“…The use of ocular massage, either alone or in combination with IOP lowering medications, has not been shown to significantly improve visual function following acute retinal ischemia (17,22,76). Nd:YAG embolysis for the treatment of acute retinal ischemia is controversial and is not considered the standard of care; it is associated with significant side effects, such as vitreous hemorrhage and creation of false aneurysms in the CRA (74,75). …”

Section: Treatment Of Acute Retinal Ischemia (Crao or Brao)mentioning

confidence: 99%

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Acute retinal arterial ischemia

Dattilo¹,

Newman²,

Biousse³

2018

Ann. Eye Sci

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Acute retinal arterial ischemia, which includes transient monocular vision loss (TMVL), branch retinal artery occlusion (BRAO), central retinal artery occlusion (CRAO) and ophthalmic artery occlusion (OAO), is most commonly the consequence of an embolic phenomenon from the ipsilateral carotid artery, heart or aortic arch, leading to partial or complete occlusion of the central retinal artery (CRA) or its branches. Acute retinal arterial ischemia is the ocular equivalent of acute cerebral ischemia and is an ophthalmic and medical emergency. Patients with acute retinal arterial ischemia are at a high risk of having further vascular events, such as subsequent strokes and myocardial infarctions (MIs). Therefore, prompt diagnosis and urgent referral to appropriate specialists and centers is necessary for further work-up (such as brain magnetic resonance imaging with diffusion weighted imaging, vascular imaging, and cardiac monitoring and imaging) and potential treatment of an urgent etiology (e.g., carotid dissection or critical carotid artery stenosis). Since there are no proven, effective treatments to improve visual outcome following permanent retinal arterial ischemia (central or branch retinal artery occlusion), treatment must focus on secondary prevention measures to decrease the likelihood of subsequent ischemic events.

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Section: Treatment Of Acute Retinal Ischemia (Crao or Brao)mentioning

confidence: 99%

Section: Treatment Of Acute Retinal Ischemia (Crao or Brao)mentioning

confidence: 99%

Acute retinal arterial ischemia

Dattilo¹,

Newman²,

Biousse³

2018

Ann. Eye Sci

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“…The laser, using 0.8–1.1 mJ intensity, was focused slightly posterior to the visible arterial wall at the site of the embolus [68, 69]. The laser tends to dislodge the embolus, which dissolves later.…”

Section: Treatmentmentioning

confidence: 99%

Treatment Options for Central Retinal Artery Occlusion

Cugati

Varma

Chen

et al. 2012

Curr Treat Options Neurol

137

121

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Opinion statementCentral retinal artery occlusion (CRAO) is an ocular emergency and is the ocular analogue of cerebral stroke. It results in profound, usually monocular vision loss, and is associated with significant functional morbidity. The risk factors for CRAO are the same atherosclerotic risk factors as for stroke and heart disease. As such, individuals with CRAO may be at risk of ischemic end organ damage such as a cerebral stroke. Therefore, the management of CRAO is not only to restore vision, but at the same time to manage risk factors that may lead to other vascular conditions. There are a number of therapies that has been used in the treatment of CRAO in the past. These include carbogen inhalation, acetazolamide infusion, ocular massage and paracentesis, as well as various vasodilators such as intravenous glyceryl trinitrate. None of these “standard agents” have been shown to alter the natural history of disease definitively. There has been recent interest shown in the use of thrombolytic therapy, delivered either intravenously or intra-arterially by direct catheterisation of the ophthalmic artery. Whilst a number of observational series have shown that the recovery of vision can be quite dramatic, two recent randomised controlled trials have not demonstrated efficacy. On the contrary, intra-arterial delivery of thrombolytic may result in an increased risk of intracranial and systemic haemorrhage, while the intravenous use of tissue plasminogen activator (tPA) was not shown to be efficacious within 24 h of symptom onset. Nevertheless, both of these studies have shown one thing in common, and that is for treatment to be effective in CRAO, it must be deployed within a short time window, probably within 6 h of symptom onset. Therefore, while CRAO is a disease that does not have a treatment, nevertheless it needs to follow the same principles of treatment as any other vascular end organ ischaemic disease. That is, to attempt to reperfuse ischemic tissue as quickly as possible and to institute secondary prevention early.

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“…Similarly, a meta-analysis by Biousse et al [34] noted that intraarterial thrombolytic therapy yielded a complication rate of 10% (25/249), with 12 TIAs, six minor cerebral infarctions, two serious cerebral infarctions, two cerebral hemorrhages, and two groin hematomas. There are several absolute contraindications to the use of thrombolytic therapy in acute ischemic stroke [1-3, 11,20,[28][29][30]32 ]:…”

Section: Complications and Disadvantages Of Thrombolytic Therapymentioning

confidence: 99%