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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Giant cell arteritis is a rare systemic vasculitis affecting large- and medium-sized arteries. Focal arteries lesions, include mononuclear cells infiltration of the vessel wall with giant cell formation. It is a disease of elderly persons and can result in a wide variety of systemic, neurological and ophthalmic complications, due to ischemia. The incidence of visual loss and ocular involvement varies between 14-88%, but one of the most common and severe complications is anterior ischemic optic neuropathy. The other ocular ischemic lesions include: central retinal artery occlusion, choroidal ischemia, diplopia, ocular motor paresis, anterior uveitis, cataract, ocular hypotony, corneal oedema and ulcerations, episcleritis and anterior scleritis, orbital cellulitis and pseudotumor. Because giant cell arteritis is potentially blinding disease, early diagnosis and immediate treatment with high dose corticosteroids may prevent further damage to the affected eye and prevent visual loss in the opposite eye. The purpose of this review is to revise established knowledge and to highlight the recent developments in diagnosis and management of giant cell arteritis.
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PMID:[A new approach towards giant cell arteritis]. 1702 3

We report a case of a 48-year-old pseudophakic woman who presented 3 weeks after Heidelberg retinal angiography using intravenous sodium fluorescein 2%. Bilateral retinal vasculitis with severe retinal ischemia and extensive capillary dropouts had been diagnosed. Anterior segment examination revealed green staining on the silicone optic of the 3-piece SI-30NB intraocular lens (IOL) (AMO), with no cell or flare in the aqueous humor. The anterior and posterior capsules were not stained. The patient did not report dark vision, double vision, or altered color vision. The anterior and posterior IOL surfaces demonstrated an autofluorescence at the time of fundus photography, which persisted to the 6-week examination although there were no symptoms. This is suggestive of deposits of sodium fluorescein on the IOL surface following angiography.
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PMID:In vivo fluorescein staining of SI-30NB silicone intraocular lens. 1718 15

Myasthenia gravis (MG) is a rare, autoimmune neuromuscular junction disorder. Contemporary prevalence rates approach 1/5,000. MG presents with painless, fluctuating, fatigable weakness involving specific muscle groups. Ocular weakness with asymmetric ptosis and binocular diplopia is the most typical initial presentation, while early or isolated oropharyngeal or limb weakness is less common. The course is variable, and most patients with initial ocular weakness develop bulbar or limb weakness within three years of initial symptom onset. MG results from antibody-mediated, T cell-dependent immunologic attack on the endplate region of the postsynaptic membrane. In patients with fatigable muscle weakness, the diagnosis of MG is supported by: 1. pharmacologic testing with edrophonium chloride that elicits unequivocal improvement in strength; 2. electrophysiologic testing with repetitive nerve stimulation (RNS) studies and/or single-fiber electromyography (SFEMG) that demonstrates a primary postsynaptic neuromuscular junctional disorder; and 3. serologic demonstration of acetylcholine receptor (AChR) or muscle-specific tyrosine kinase (MuSK) antibodies. Differential diagnosis includes congenital myasthenic syndromes, Lambert Eaton syndrome, botulism, organophosphate intoxication, mitochondrial disorders involving progressive external ophthalmoplegia, acute inflammatory demyelinating polyradiculoneuropathy (AIDP), motor neuron disease, and brainstem ischemia. Treatment must be individualized, and may include symptomatic treatment with cholinesterase inhibitors and immune modulation with corticosteroids, azathioprine, cyclosporine, and mycophenolate mofetil. Rapid, temporary improvement may be achieved for myasthenic crises and exacerbations with plasma exchange (PEX) or intravenous immunoglobulin (IVIg). Owing to improved diagnostic testing, immunotherapy, and intensive care, the contemporary prognosis is favorable with less than five percent mortality and nearly normal life expectancy.
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PMID:Myasthenia gravis. 1798 28

Orbital infarction syndrome is defined as ischemia of global intraorbital structures such as extraocular muscles, optic nerves, and retina. The most common cause of this syndrome is carotid arterial occlusion. Other causes include vasculitis, vasospasm, and compression of intraorbital circulation. There has never been reported a case of orbital infarction syndrome in nephrotic syndrome patient. We present a case of 42-year-old Thai man with underlying disease nephrotic syndrome presented with abrupt onset of headache at left temporal area, horizontal diplopia, limitation of eye movement in all directions, ptosis, and blurred vision on the left eye. He was treated with pulse methylprednisolone intravenously for 3 days. Leg edema was improved however, the eye symptoms persisted. There was no evidence of hypercoagulable state. Magnetic resonance imaging (MRI), magnetic resonance angiography (MRA) revealed loss of signal intensity at left internal carotid artery from base of skull to intracavernous part. Cerebral angiography demonstrated complete occlusion of left common carotid artery. After the anticoagulant treatment, his symptoms were gradually improved. The cause of extensive carotid arterial occlusion in this patient is most likely from hypercoagulable state. Although it was negative for hypercoagulable state evidence, the authors assume that the high dose steroid treatment could lead to remission of nephrotic syndrome and resulting in the resolution of hypercoagulable state.
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PMID:Orbital infarction syndrome in nephrotic syndrome patient with extensive carotid arteries occlusion. 1818 41

A visual impairment occurs in about 50% of patients with giant cell arteritis (GCA), an amaurosis fugax (AF) in about 30%, and diplopia in about 10%. An arteritic anterior ischemic optic neuropathy was found in about 80%-90% of patients with visual loss and an arteritic central retinal artery occlusion in about 10%-20%. Without therapy, involvement of the fellow eye may occur within hours or days in a patient with unilateral blindness. Involvement of the anterior segment of the eye (iris ischemia, episcleritis) is rare. Ocular ischemic syndrome is defined by visual loss with hypotony, ischemia of the iris, and cotton wool spots (CWS). CWS may already occur with AF episodes. In the case of strong suspicion of GCA, immediate therapy with steroids is indicated. Duplex sonography and a gadolinium MRI examination are of diagnostic importance. A biopsy of the temporal artery may be carried out after the initiation of therapy.
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PMID:[Ocular findings and differential diagnoses in giant cell arteritis (Arteriitis cranialis)]. 1922 26

Diplopia is frequently encountered in neurological practice and may occur as part of the clinical spectrum of 3rd cranial nerve palsy. Correct localization of the underlying problem is the first step in making an accurate diagnosis. Pathologies affecting the supranuclear structures, cranial nerves and nuclei, extraocular muscles and the neuromuscular junction may cause or simulate 3rd nerve palsy. We report a case of a patient with longstanding quiescent SLE who presented with sudden onset of diplopia and discuss possible aetiologies including ischemia, demyelination, neuromuscular conditions and medication-induced.
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PMID:Third cranial nerve palsy or pseudo 3rd nerve palsy of myasthenia gravis? A challenging diagnosis in systemic lupus erythematosus. 1957 9

We report a 28-year-old male who presented with severe vertigo, vomiting, diplopia, clumsiness of right extremities. Physical examination revealed low reading of blood pressure in the left upper limb and evidence of mild left upper limb ischemia. On neurological examination he had right cerebellar ataxia. Computed tomography and magnetic resonance imaging, revealed an acute right cerebellar infarction in the anterior inferior cerebellar artery territory. Doppler ultrasono-graphy revealed an aneurysm of the left subclavian artery. The patient was tested positive for serology of syphilis.
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PMID:Left subclavian artery aneurysm secondary to syphilitic arteritis presenting with a right ischemic cerebellar infarction. 2013 37

A 68-year-old man presented with sudden onset of left hemiparesis, diplopia and numbness of the left side of the body and was admitted to our hospital. MRI of the brain revealed no abnormality. However, neurological examination on admission strongly suggested ischemia of the brainstem. Under anticoagulation therapy his symptoms gradually disappeared by the fourth hospital day. He had a past history of bouts of unconsciousness caused by right rotation of the head. Dynamic plain roentgenograms of the cervical spine showed spondylotic changes and lateral osteophyte formation at C5/6 without instability. Computed tomography (CT)-angiography demonstrated narrowing of the right vertebral artery due to compression of the lateral osteophyte at C5/6. Vertebral angiography revealed complete occlusion of the right vertebral artery induced by right rotation of the head. The artery-to-artery embolism caused by repeated occlusion of the right vertebral artery due to the neck motion was suggested as the mechanism of ischemic attack in this patient. Osteophytectomy at C5/6 via the anterior approach successfully treated dynamic occlusion of the right vertebral artery. Occlusion of the vertebral artery at C1/2 by the head rotation is well known as Bow-Hunter's syndrome. However, dynamic occlusion due to spondylotic changes at C5/6 is rare. In case of ischemic attack of the posterior circulation with lateral osteophyte formation of the cervical spine, dynamic occlusion mechanisms of the vertebral artery at the lower cervical level should be considered.
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PMID:[Cerebral ischemia originating from rotational vertebral artery occlusion caused by C5/6 spondylotic changes: a case report]. 1966 39

In the author's department, 5 patients developed retrobulbar hemorrhage from the 199 patients with midface fractures, between August 2007 and March 2010 (2.5%). 4 of these patients became irreversibly blind on the affected eye. With timely treatment, one patient avoided blindness. The author presents a retrospective analysis of the patients from different departments with midface/orbital fractures and blindness. Bleeding and oedema behind the eyeball due to midface/orbital fractures in the relatively non-expandable orbit results a quick elevation of orbital pressure and consequently diminished circulation, ischemia, and later necrosis of the optic nerve (orbital compartment syndrome) with irreversible blindness. Immediate medical (high dose of intravenous steroids, mannitol, acetazolamide) and surgical intervention (lateral canthotomy, cantholysis, orbitotomy) on noticing the signs (proptosis, ecchymosis, ophthalmoplegia, mydriasis) and symptoms (pain, diplopia, decreased visual acuity, blindness), of a retrobulbar hemorrhage could theoretically give a chance to save the affected eye. Treatment started beyond 20 minutes of onset of blindness, might not revert the vision. Unfortunately, the description and treatment of the retrobulbar hemorrhage and the orbital compartment syndrome is not within the curriculum of the medical university, thus young colleagues could have vague idea about the diagnosis, the urgency and the treatment - as shown in these cases. With the introduction of these cases the author would like to highlight the signs, symptoms and necessary treatment. Knowledge of the disease could also increase the detected number of retrobulbar hemorrhages, which might be less rare than we think. Including the disease into the medical curriculum and postgraduate trainings could help to reduce the number of sad cases in the future.
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PMID:[Blindness caused by retrobulbar hemorrhage (orbital compartment syndrome)]. 2082 78

Preoperatively, strabismus surgeons need to obtain informed consent, identify any ocular or systemic risk factors, decide on the preferred method of anesthesia, and determine whether the patient is an appropriate candidate for an adjustable suture technique. Three major categories of complications should be listed on the consent form: Loss of vision, double vison, and need for reoperation. If a patient is at particulary high risk to have one of these complications, then the surgeon should emphasize this point during the preoperative discussion. The incidence of visual loss after strabismus surgery due to anterior segment ischemia, retinal detachment, or endophthalmitis is approximately 1 in 7,400 cases. The preferred method of anesthesia depends on the procedure planned, the age and general health status of the patient, and whether or not an adjustable suture technique is to be utilized. At the conclusion of the preoperative discussion, the patient should be well informed and comfortable with the choice or procedure, have reasonable postoperative expectations in terms of diplopia, and be prepared for any unexpected complications.
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PMID:Preoperative issues in adult strabismus. 2114 41


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