Sudden decrease in visual acuity

DROP VISUAL ACUITY SPIKE:

Amaurosis fugax or transient monocular blindness:

In a subject or older with known vascular field is the amaurosis fugax or transient monocular blindness (CMT). The patient describes well the total loss of vision in that eye or the feeling of being “as in cotton.”

Occlusion of the other eye would make him unable to move. Recovery is complete, usually in about ten minutes, at least within 24 hours. But this should not reassure. This is a real transient ischemic attack and it shares the prognosis.It may be the harbinger of stroke or myocardial infarction with known morbidity and mortality. An embolic heart disease and vascular risk factors will be sought through a clinical examination with echocardiography and Doppler ultrasound of the neck vessels. Anticoagulation and / or antiplatelet may be considered. It is especially essential to eliminate a disease Horton (functional and physical signs, but especially ESR and CRP, see Box 1). In these circumstances, ophthalmologic consultation should not delay the initiation of urgent therapeutic measures.

Box 1. Horton’s disease
After 65 years, any visual symptoms (sudden visual loss, binocular diplopia or single fl or binocular …) is a disease of Horton until proven otherwise.
Search loss of appetite with or without weight loss, pain in the shoulders, headache, tenderness or pain in the scalp wet combing, intermittent claudication of the jaws. On examination, the temporal arteries are thickened, indurated, sensitive. If the pulse is abolished, the artery remains palpable as a thick indurated cord.
ESR and CRP are required urgently and treatment started without delay (IV bolus) due to the risk eye (blindness of the second eye can follow that of the first eye in a few hours!). The temporal artery biopsy is not negated by corticosteroids few weeks.

Transient deficit in hemifield namesake lateral arrangement:

Such a deficit is indicative of a transient ischemic cerebral vascular accident in the territory later, behind the chiasm, and lead to the same attitude as supra. The fundus is normal except the stigma of arteriosclerotic vascular field.

Note that very few patients think separately study the vision of each eye (alternately hiding one eye and then with the other hand) and mistakenly think that only the affected eye in temporal worries about the deficit.

In this circumstance, the interview can be misleading.

Horizontal transitional deficit that stops on the horizontal line of an eye:

The diagnosis is evoked with acute anterior ischemic optic neuropathy (NOIAA) (in reality often final). GCA should always be the first pressing concern.

TRANSIENT DECREASE OF VISUAL ACUITY PERCEPTION WITH LIGHTS IN A SUBJECTSCINTILLANTES YOUNG:

The positive visual phenomena are perceived colored lights that sparkle and extend “fortifications” to the periphery of the visual field ( “migraine aura”), about twenty minutes. A minimum of 4 minutes of progression between the All-Start and the maximum visual manifestations of migraine qualify for walking. A scintillating scotoma can reach central vision.Again, the visual symptoms are often seen as unilateral by patients because they only pay attention to the eye with the temporal part is concerned. In reality the other eye was a violation of its namesake nasal hemifield, obvious to some that search.

Thus warned, the patient will recognize the next crisis. Migraine headaches in hémicrânie can follow, but are fickle.

The diagnosis is that of ophthalmic migraine.

There are usually no exploration to practice, except atypia or recent onset and frequent repetition of migraine.

DROP VISUAL ACUITY UNILATERAL PERMANENT – EYE IS NOT RED:

Central retinal artery occlusion:

If there is an elderly, the most likely diagnosis is a central retinal artery occlusion (OACR) with decrease in visual acuity brutal, immediately maximal, often seen after waking up (probably in connection with the early morning blood pressure).

Visual acuity is not measurable and fundus shows ischemia beaches (edema of the nerve fibers) with cherry red macula by contrast, as the nerve fiber layer is absent. In the rare cases where it took less than six hours from the occlusion, it may be worth hypotoniser the globe by the Diamox® and massage it in the hope of improving the retinal blood circulation and / or to migrate the circulatory obstacle farther beyond vascular fork. Turning on anticoagulants or support in interventional neuroradiology environment can be discussed. Risk factors are arteriosclerosis, more rarely emboligenic heart disease or, again, GCA. The functional prognosis is unfortunately gloomy with poor or no visual recovery. But there’s usually no neovascular retinal ischemic complications in the long term.

Besides, the few cases where there may be a macular savings by presence of cilioretinal artery (anatomic variant) remains infused with tunnel vision.

Central retinal vein occlusion:

If this decline sudden unilateral visual acuity occurred is less deep or even moderate, it can be a central retinal vein occlusion (CRVO) with risk factors for, again, arteriosclerosis, the high blood pressure, certain blood disorders, antiphospholipid syndrome and also poorly controlled glaucoma. The visual loss is of varying intensity greater if the occlusion is massive with effects on blood flow (ischemic form called immediately). The fundus shows dilated and tortuous veins with petechiae scattered throughout the territory.

The occlusion may sit at the central retinal vein, a higher or lower venous hémitronc or only one branch (often at an arteriovenous crossing).

Angiography Retinal fluorescein is indicated to distinguish between forms edematous and ischemic forms, the latter requiring treatment to pan retinal photocoagulation laser, essential to prevent neovascular complications (vitreous hemorrhage, neovascular glaucoma … ).

However, be aware that an edematous form can turn into ischemic form and thus ophthalmologic monitoring remains necessary. Edematous form is responsible for a decrease in vision, usually less than the ischemic form.

Neuropathy acute anterior ischemic optic:

The diagnosis of acute anterior ischemic optic neuropathy (NOIAA) is to be considered in the elderly. The damage may be total, but can also be altitudinal (cit challenge horizontal stops on the horizontal line).

Visual acuity is variable. There is a relative afferent pupillary defect or Gunn pupil.

The field shows very often an altitudinal deficit called “vascular”. The eye background is a pale papillary edema with few petechiae. The causes are mostly non arteritic (arteriosclerosis, rarely hypoperfusion during a state of shock for example) but the fear is still and always the GCA which is the most common visual manifestation, and must absolutely be diagnosed (seen: functional symptoms, physical signs, ESR and CRP) and treated in an emergency, without waiting for temporal artery biopsy can wait several days. The prognosis is related to the possible breach of the second eye, sometimes very fast, thus leading to a disastrous bilateral total blindness.

Also be aware that non-arteritic forms (that is to say, not giant cell, non Horton) and are the most common, are readily associated with a particular morphology of the papilla, small and full. This criterion can only be studied on the papilla of the affected eye is often the seat of a white edema that blurs the edges, but will be appreciated on examination of the fundus contralateral (papillae are usually symmetrical) . A bilateralization is feared in the years to come and we can offer the power antiplatelet agent and in any case we must avoid all situations of drug blood pressure (antihypertensive medications, Viagra …) or surgical (give written information to the patient’s other doctors). We must find and treat any ocular hypertension and sleep apnea.

Retrobulbar optic neuritis:

If this drop deep unilateral abrupt visual acuity occurs in a young person, especially a woman, often settling on a few hours in a context of pain exacerbated by eye movements, the most likely diagnosis is a neuritis optical retrobulbar (NORB), possible first manifestation of multiple sclerosis.

The visual loss is very variable depth. The examination of the pupils shows a relative afferent pupillary defect of the eye concerned that signs the diagnosis of optic neuropathy, much easier to highlight that achievement is profound.The fundus is normal, “the patient sees nothing and neither ophthalmologist.” The field has a variable morphology deficit. EPI would show damage to the optic nerve. The MRI is king because it allows, besides the examination of nerve and a potential viewing a plaque on its way to highlight signal abnormalities suggestive of white matter in September

Note that for several years, US multicenter studies have shown it is against inappropriate to treat NORB by a single oral corticosteroid therapy because it appears to increase the risk of transition to multiple sclerosis.

DEFICIT OF VISUAL FIELD PART OF AN EYE – EYE IS NOT RED:

Retinal detachment, sometimes preceded by a posterior vitreous detachment:

Initially, the disease is localized at the periphery of the visual field and is not accompanied by loss of visual acuity. But cit challenge progresses more or less quickly from the periphery to the center. When he joined the visual center, there is collapse of visual acuity. Day or previous weeks, the phosphenes have been perceived (white flashes better seen in the dark) and floaters sudden appearance (described as flying flies by patients, appointed by the ophthalmologist floater), the together constitute the symptoms of a posterior vitreous detachment (PVD) (Box 2). Phosphenes however, are not constant. Sometimes the patient reports having seen smoke rising, which often means the presence of a bleeding down by gravity into the vitreous inside the eye. This is probably a retinal detachment and to behave is urgent, especially if there is no visual loss. Indeed, retinal detachment treated early with macula has not peeled off much better chance by surgery alone, to be cured with Functional Safety of vision, while at the stage where acuity collapsed by macular uprising visual recovery may be poor despite anatomical retinal reattachment. Support ophthalmic is therefore urgent by a specialist ophthalmologist in the rétinovitréenne surgery and which, moreover, optionally ask the indication of a laser prevention on the other eye.

Box 2. Recommendations to bring the patient during a DPV
It is good to give the following recommendations to the patient: after onset of floaters, floaters, and if at the ophthalmological consultation, examination of the fundus dilated pupil has confirmed that this is a posterior detachment of the vitreous uncomplicated, self-monitoring is useful. As long as there phosphenes, the glass did not fi nish to its rear detachment and there remains a risk of retinal tear and thus retinal detachment. This active period in which the patient sees phosphenes can last weeks or months. It is therefore essential that it assumes itself monitoring, since there is obviously no question of subjecting it to a daily dilated fundus. It must determine, by eye eye, a central point to be aware at the same time to see the entire visual field. If in the visual field of the eye in question appears a missing zone absent, gray, etc., it is essential to consult a specialist very quickly. Indeed, this device permanent injury is suggestive of retinal detachment still localized. Treated early, the prognosis will be better.
A DPV which was accompanied by a vitreous hemorrhage sign that there has indeed been torn, otherwise the retina, at least the vessel wall, and monitoring should be much closer, retinal detachment because of the risk rises to about 50%. Similarly, when the CAE is accompanied by significant bleeding at the point of masking the fundus, it is essential to practice ocular ultrasound to diagnose the earliest retinal detachment and treated surgically before it is getting worse.
Finally the floater usually subside with time, but may persist, which the patient must
be warned.

Occlusive arterial branch:

In a patient who has a disease (particularly cardiac) potentially embolic, the appearance of a deficit of a field of vision in one eye may be due to occlusion of retinal arterial branch. This deficit that the patient can draw and objectify the visual field is not systematized. The fundus shows a localized area of ischemia and sometimes bolus, willingly blocked an arterial bifurcation. Later, in the fundus signs of ischemia disappear, but the defi cit persists the most.

DOWN WITH VISUAL ACUITY OF PERCEPTION scotoma CENTRAL OR NOT METAMORPHOPSIA:

A positive central scotoma scotoma is seen by the patient, that is to say, he sees a black spot that conceals him the place fixed. He can draw on an Amsler grid or other grid paper with materialization of a central point to be set. This central scotoma may be associated with metamorphopsia or micropsies.

It is then very likely with maculopathy.

Macular degeneration:

If the subject is old, the probability is high of a macular degeneration (AMD) in its wet form (atrophic form gives no metamorphopsia but only a central scotoma or negative para-central). The wet form with recent worsening and appearance of metamorphopsia is an emergency to contact a competent center for the supplementary examinations and highly specialized treatments indicated (angiography, laser, possibly PDT, intravitreal injections of anti-VEGF). In these circumstances also, early treatment has a better chance of success.

The risk of bilateralization unfortunately significant and means of prevention at this stage are relatively low.Nevertheless, one can cite the protection against ultraviolet, stopping a possible smoking and it seems a diet rich in antioxidants or vitamin and food supplements (lutein, zeaxanthin, omega-3).

Fuchs spot of high myopia:

If the patient is young with a very strong myopia, again, it may be a macular involvement that requires the same behavior in the emergency (the myopic maculopathy is the main cause of permanent loss of visual acuity in young subjects).

Central serous chorioretinopathy:

If there is a young person who does not have high myopia, more likely male, especially stressed and complaining at a metamorphopsia eye with micropsies (the images are seen smaller) and often hypermétropisation, (that is to say, the ophthalmologist manages to improve it by adding one or two positive diopters its correction), the most likely diagnosis is a central serous chorioretinopathy (CRSC). The fundus shows the presence of a serous detachment bubble macular neuroepithelium, angiography detects the confi rms and the vanishing point. OCT (Optical Coherence Tomography),simple noninvasive examination allows monitoring.

The improvement is often spontaneous.

Avoid any corticosteroid (even under local form, apparently in low doses) because it has a role aggravating or triggering.

Or various other:

Whatever the age, but especially in a young person, bear in mind the possibility of inflammatory maculopathies reached by toxoplasma, rarely sarcoidosis.

One can also cite the exudative retinal detachment without retinal tear causal, often bilateral disease Vogt-Koyanagi-Harada or, rarest of toxemia of pregnancy.

DROP VISUAL ACUITY WITH RED EYE: CAUSES THE THREE CLASSIC

When the drop of unilateral visual acuity is accompanied by redness of varying intensity with pain, the causes are schematically three in number: glaucoma attack acute angle closure, uveitis and keratitis.

All are potentially severe.

Recognizing the redness is important because it can be relatively unobtrusive. It predominates around the limbus (that is to say, it prevails around the cornea, hence its name périkératique circle), in contrast to the redness of conjunctivitis that predominates in the conjunctival cul de-sacs. Also unlike conjunctivitis, no wake sticky secretions eyelashes, and there is a decrease in visual acuity.

Glaucoma attack acute angle-closure:

The glaucoma attack acute angle closure typically occurs in older women having not yet operated cataract and often sighted. In fact it can occur in people much younger and not necessarily farsighted. The pathogenesis is the occurrence of pupillary block on a predisposed eye because of its narrow anterior chamber, making the anterior chamber angle able to close. Intraocular pressure increases rapidly and can reach 70 mmHg (normal is around 10 to 20).

Eye pain is in the foreground and may be accompanied by nausea and vomiting, may divert attention to the digestive tract. Similarly, it may be accompanied by headache and make wandering explorations to neurological causes. Eye examination will easily rectify the diagnosis by showing a unilateral ocular redness marked by a circle périkératique, a cornea less transparent (because edematous) with a dull reflection, a dilated pupil semi mydriasis and bi-digital palpation frankly hard look (conventionally described glass ball), easier to appreciate by comparing to the fellow eye.

Vision is lowered variably. There may be a triggering factor or not (taking medication with anticholinergic effect, atropinization during general anesthesia …).

The support must be urgent, first by slow intravenous injection in Diamox® or, failing its oral administration for hypotoniser the globe. Once hypotonisation achieved, sometimes at the cost of administration of mannitol intravenously, the ophthalmologist will tighten the pupil by suitable eye drops and practice iridotomy has YAG laser immediately if feasible, if not necessarily the waning of crisis. The other eye (also at risk for reasons of anatomical symmetry) must be protected from such attack by preventive practice a laser iridotomy.

Uveitis:

The decline in acuity of varying importance. There is often a significant photophobia. The top may be more or less rapid. The eye may be more or less tearful. The examination shows relative miosis compared to the other eye. There may already be familiar ground spondyloarthritis with HLA B27 positive (in which case, the anterior uveitis are synechia, which requires the urgently address to avoid irido- crystalline lens adhesions, including eye drops corticosteroid and mydriatic administered more times a day or corticosteroid injections periocular).

The examination at the slit lamp shows a Tyndall effect in the anterior chamber and rushed backward descemétiques (that is to say deposited on the posterior surface of the cornea). Tone may be increased or lowered. The fundus must imperatively, and may reveal a chorioretinal home. The management by an ophthalmologist is urgent and it can refer serious cases to an internist for research and management of the associated potential systemic manifestations.

A special case is the visual loss + redness and pain in the early postoperative period of eye surgery; then it is of endophthalmitis to address extremely urgent in an eye clinic.

Keratitis:

There photophobia and foreign body sensation. The visual loss is variable depending on the location of corneal involvement.

The state often tearful eye also contributes. It can be a superficial punctate keratitis, traumatic ulcers or herpes … A drop of Fluorescein often, even to the naked eye, to highlight the ulcer.

It can also be a corneal abscess, particularly in contact lens wearers, especially hydrophilic soft. The review shows a white infiltrate of variable size. This is a serious emergency to take care of immediate way by an aggressive and appropriate treatment. On a preventive level, recommend to the holders of contact lenses a very rigorous hygiene in particular vis-à-vis the tap water (amoebic contamination varies with region but difficult to treat and potentially extremely serious ).

DROP VISUAL ACUITY OF LAND KNOWN AT RISK:

Diabetic retinopathy:

This is especially diabetic with over 10 years of diabetes, poorly controlled, poorly monitored on an eye level. The visual loss may be due to macular edema or even proliferative diabetic retinopathy that requires support specialized with angiography, and laser or surgery. Proliferative retinopathy can be opened by an episode of bleeding in the vitreous or complicate a tractional retinal detachment, even, result in neovascular glaucoma. The best prevention is glycemic control and blood pressure, as well as regular ophthalmologic monitoring.

Toxic or hereditary optic neuropathy:

Toxic or hereditary neuropathies most often result decreased bilateral progressive visual acuity, for example an alcohol and tobacco neuropathy, neuropathy ethambutol. In the case of alcohol and tobacco neuropathy, stopping the poisoning, the correction of vitamin challenge cit and malnutrition are essential on pain of further visual deterioration.Visual impairment is fairly symmetrical rule with the field level centrocaecal a scotoma.

An alcohol and tobacco neuropathy does not improve the actual cessation of intoxication or occurring in the absence of intoxication can be related to Leber’s disease (Leber’s disease is an isolated optic neuropathy, due to hereditary a mutation of the DNA mitochrondrial (so maternally) of the patient. women are only transmissive, but does not transmit to all their descendants. the visual loss is often sharp and abrupt, bilateral or immediately occurring with a less than 2-month lag. the average age of onset is around thirty, but there may be cases before 10 years or after 50 years. the diagnosis of certainty is achieved by the search for mutations mitochondrial DNA. another diagnosis, often poorly known, is the dominant optic atrophy.

Toxic or drug maculopathies:

A visual loss can also be caused by a toxic maculopathy. This is true of bilateral visual impairment in maculopathy to antimalarials, rare condition occurring most often beyond

from 100 to 250 grams of Plaquenil® in cumulative doses. The decline is gradual and final, but fortunately exceptional when ophthalmologic monitoring is performed. This is mainly based on color vision, visual field 10 ° (achievement is indeed peri-foveal), EOG (Electro-eye-gram) and, if available in the ERG (electroretinography) multifocal.

Hereditary macular:

Stargardt’s disease or fundus flavi maculatus is one of the most common hereditary eye conditions.

REVELATION OF SUDDEN DROP VISUAL ACUITY PROGRESSIVE:

It is not uncommon for a patient is surprised by the seemingly sudden revelation of an unknown low vision in one eye, which he realizes that the day he hides the good side. “Would you have had this long fall without realizing it? “Is the question.

Presbyopia:

The visual loss of presbyopia that occurs around the age of 45 years can thus appear as relatively sharp. The patient sees relatively well from a distance with his usual correction, but can not read closely.

The age of onset of discomfort is earlier for the farsighted especially uncorrected and later in myopia. Simply send it to an eye doctor for a prescription of glasses, which will use this consultation to screen for glaucoma, retinal damage, incipient cataract …

Cataract:

The visual loss from cataracts can in fact, too, seem brutal, especially if it was already on a sealing eye. This is an old subject that has a visual loss of near and far and often dazzling light, but the sharpness is not collapsed (with rare exceptions). It can sometimes guess a white reflection behind the pupil. Ophthalmic consultations will lead to surgery if a change of glasses enough t do more to give adequate visual acuity. It should be noted that anti-cataract eye drops are ineffective and potentially deleterious to the surface of the eye due to the conservative and should be banned.

Chronic open angle glaucoma:

Chronic open angle glaucoma is not an immediate cause of visual loss.

It translates to the top by only negative paracentral scotomas in the visual field, which are very long inapparent to the patient and are highlighted by the instrumental examination of the automated visual field. Decreased vision occurs at the terminal stage of definitive near-blindness and therefore can not serve as a sign of useful call. The screening systematic reviews with taking eye pressure and examination of the fundus is a public health goal because glaucoma is with AMD diabetes and a major cause of blindness in developed countries.

Therefore routine screening for all at the first presbyopia consultation, screening much earlier for those at risk (family history, black race, diabetes, high myopia …). Routine screening for risk of subacute attacks and few symptoms of angle closure on older non-operated eyes from cataracts.

DROP VISUAL ACUITY BY ACHIEVING NEUROLOGIC:

revealing visual loss of neurologic impairment, such as a tumor of the optic nerve, pituitary or chiasm, which will highlight the MRI, possibly after the discovery of an edematous optic disc in FO (Reminder: a normal eye bottom does not eliminate intracranial hypertension).

Finally cortical blindness is a very rare because of declining bilateral sharp visual acuity by ischemic injury of the occipital lobes. There is no abnormality of the anterior segment of the eye or at the fundus or at the pupillary reflexes.By cons, there is no blink reflex threat nor of accommodation-convergence reflex and the patient also does not clearly feels this visual loss due to hallucinations. The look is empty, there is no movement of fixation and pursuit. The context is very evocative.

CONCLUSION:

It is important to recognize the serious nature of visual loss (as opposed to a simple little difficulty is that far or near, and that requires glasses), analyze its characteristics, associated symptoms (redness, context) to direct the patient urgently to the ophthalmologist or cardiologist. GCA must be an ongoing concern in the elderly (ESR, CRP very broad indication).

macular degeneration, glaucoma and diabetes are the leading causes of decreased vision or even blindness in our developed countries.

Consultation with the ophthalmologist at the age when presbyopia leads there the patient is the right opportunity to allow the screening of potentially blinding conditions and often preventable or treatable.