Welcome to the learning and teaching companion website for Transient Visual Loss by Randy H. Kardon, MD, PhD, University of Iowa, Iowa City, Iowa USA.
Below you’ll find a Primer of Transient Visual Loss and multiple Case Studies that are meant to completed before viewing the lectures by Dr. Kardon.
Bilateral – retina vs. occipital cortex; is center of visual field going out first (occipital drop in perfusion pressure) or is peripheral visual field going out first (retinal drop in perfusion pressure)? The retina macula arterioles have the highest perfusion pressure, so drops in blood pressure affect the peripheral retina first. The occipital pole in visual cortex often lies in a watershed zone of perfusion between the distal branches of the posterior cerebral artery and the middle cerebral artery, so that drops in blood pressure often affect the occipital pole first (corresponding the central visual field).
Unilateral - which part of the visual field went out – peripheral, first, then central (implies drop in ocular perfusion pressure), altitudinal (implies embolic), area of vision spared (central due to cilioretinal artery) or central field only – may be involvement of cilioretinal artery
Transient visual obscurations (seconds) – often occurs in the context of a swollen optic nerve due to severe papilledema with superimposed postural drops in blood pressure
Amaurosis (minutes) – usually due to emboli
Hours – Uveitis Glaucoma Hyphema Syndrome (UGH syndrome) from haptic of intraocular lens rubbing against back of iris after cataract surgery, occipital lobe epilepsy (post-ictal temporary blindness after the seizure)
Darkening of vision (negative phenomena)? – usually ischemic
White out of vision (positive phenomena)? – usually migraine
“Positive” complex visual phenomena – sparkles, colors, geometric shapes (migraine like aura)
Valsalva from coughing or laughing or straining – – may be paradoxical embolism through patent foramen ovale and Valsalva may accentuate right to left shunt of venous thrombi (e.g. from extremity). Sometimes an intense coughing episode may dislodge an intimal plaque or cause a dysrhythmia.
change in posture – orthostatic drop in blood pressure
sitting at rest – suspect either embolism or drop in blood pressure due to dysrhythmia
rubbing their eye – may cause transient spike of intraocular pressure with resulting decrease in ocular perfusion pressure and decrease in blood flow
transient visual loss precipitated by eye movement in extreme gaze – suspicious for compressive optic neuropathy in the orbit (e.g. optic nerve sheath meningioma)
transient visual loss with increase in body temperature (environmental, exercise, hot shower) – suspect demyelination with Uthoff’s phenomena from delayed nerve conduction caused by increases in core body temperature
looking at a bright light and then seeing an afterimage – may be due to photoreceptor dysfunction. Dark spot in the center of vision may also be noticed on awakening in patients with macular disease due to increase in metabolic demand of photoreceptors in darkness; the membrane dark current is maintained by Na+/K+ pump which is ATP energy dependent.
post-prandial, after eating – (“steal phenomena” in the setting of flow significant stenosis)
occurring with exposure to bright daylight – – increase in metabolic demand that cannot be met by increases in blood flow due to flow significant arterial stenosis
palpitations, irregular heartbeat – – transient drops in blood pressure with reduced ocular perfusion pressure, decrease in blood flow; if there is a superimposed arterial stenosis, then the transient visual loss may be unilateral
darkness – angle closure from mydriasis and pupil block with raised IOP
Peripheral field goes out first – consider retinal hypoperfusion episode due to transient hypotension (peripheral retinal arterioles have a lower perfusion pressure compared to macular arterioles)
Central field goes out first –– consider occipital pole of visual cortex (lying within a watershed zone) responding to transient hypoperfusion in the setting of a drop in blood pressure.
Regional visual field change such as altitudinal loss – common with embolic cause
Light headedness – think about transient hypotension
Unilateral weakness or numbness (TIA) – consider embolic cause
Global amnesia or cognitive dysfunction or motor activation - consider seizure activity
Anterior segment – signs of causes of acute rises in IOP (pigmentary dispersion, narrow angles) or signs of hyphema or microhyphema, iris transillumination defects, IOL haptic rubbing on posterior iris surface.
Posterior segment – signs of emboli (platelet, calcific, cholesterol), venous stasis retinopathy with cilioretinal artery. Digital pressure on globe during exam to determine if small increases in IOP can collapse the central retinal artery or cilioretinal artery due to low ocular perfusion pressure (e.g. carotid stenosis); sometimes this will reproduce the transient darkening of vision. Disc edema associated with raised intracranial pressure may give rise to transient visual obscurations with drops in blood pressure brought on by postural changes or Valsalva maneuver.
Neck bruits
Pulse - any irregularities due to dysrhythmia?
Vascular imaging – Duplex ultrasound of carotid and vertebral arteries (is there a significant stenosis or the presence of intimal plaques? But this only samples the cervical portion of the carotid – need MRA or CTA or angiogram to evaluate more distal vascular pathology.
Cardiac echography – is there an embolic source (valves) or patent foramen ovale (bubble study)?
Holter monitor - to discover transient dysrhythmia +/- 24 hour ambulatory blood pressure monitoring to uncover transient episodes of hypotension.
Fluorescein angiography –is there a delay in choroidal filling (giant cell arteritis)? Is there a prolonged arteriole-venular filling time indicative of low ocular perfusion pressure?
CT and/or MRI - to evaluate for any compressive lesion adjacent to the optic nerve. After trauma with orbital fractures, assess if there is intra-orbital air.
Blood testing for coagulopathies – (antiphospholipid antibodies, clotting disorders)
Diagnosis | Unilateral vs Bilateral | Duration | Activity | Pattern of VL | Other Symptoms | Medications |
---|---|---|---|---|---|---|
Acute Elevation in Intraocular Pressure | Unilateral | minutes to hours | being in a dark environment may precipitate angle closure; physical activity may cause pigmentary dispersion and sudden increase in IOP, ocuarl trauma with hyphema and spike in IOP, eye rubbing | may be diffuse blurring if corneal edema results from high IOP; decrease in ocular perfusion pressure will cause peripheral loss of vision first, then central | ocular pain | adrenergic agents or anticholinergic agents given either systemically or from eye exposure |
After-image after viewing bright light | Unilateral/Bilateral | seconds to minutes | viewing bright light, worse after mydriasis | usually central after-image | none | none |
Carotid Artery Stenosis with Episode of Hypotension | Unilateral | minutes (amaurosis fugax) | orthostatic or decrease in cardiac output from heart dysrhythmia | peripheral field loss first, then possibly followed by central field loss | may experience pre-syncopal symptoms or TIA | anti-hypertensive agents with over-treatment |
Corneal Surface Disease / Dry Eye | Unilateral | seconds to minutes | often tasks requiring concentration which reduces spontaneous blinking, wind or air movement | diffuse blurring or monocular diplopia, which may become less after each blink | irritation of eye | anticholinergic drugs reducing tear production |
Giant Cell Arteritis | Unilateral/Bilateral | seconds to minutes | orthostatic changes in posture | may be partial or complete loss | headaches, jaw claudication, transient diplopia, scalp tenderness,s constitutional symptoms (fatigue, weight loss) | none |
Hypotension | Unilateral/Bilateral | seconds to minutes | orthostatic changes in posture | peripheral field loss first, then possibly followed by central field loss, if retinal ischemia is present, but if occipital pole is affected by low blood pressure, then central field may go out first | may experience pre-syncopal symptoms or TIA | anti-hypertensive agents with over-treatment |
Migraine | Bilateral | minutes to almost an hour | no particular activity, sometimes activities that precipitate a migraine | usually homonymous; very rich, moving;often black and white, scintillaiton, shimmering, jagged edges | headache, unilateral finger numbness and perioral numbness, vertiginous symptoms | none |
Occipital Seizures | Bilateral | minutes to hours | positive, visual phenomena | none, some associated with seizures | ||
Optic Disc Drusen | Unilateral/Bilateral | seconds to minutes | none | may be entire visual field darkening or a portion of the visual field | none | none |
Optic Disc Edema | Unilateral/Bilateral | seconds | orthostatic changes in posture | graying out, some report flashes | headaches, nausea, vomiting, light sensitivty, oulsatile tinnitus, neck and back pain | none |
Optic Nerve Sheath Meningiomas / Orbital mass | Unilateral | seconds to a minute | extreme gaze | may be entire visual field darkening or a portion of the visual field | diplopia on extreme gaze | none |
Orbital Emphysema | Unilateral/Bilateral | minutes | coughing, sneezing, vomiting, Valsalva | may be entire visual field darkening or a portion of the visual field | orbital pain | none |
Retinal Emboli | Unilateral | 1-15 minutes | coughing, bending over | may be entire visual field darkening or a portion of the visual field (e.g. altitudinal visual field loss) | may experience TIA | none |
Retinal Vasospasm | Bilateral | 10-20min up to an hour | none | may be partial or complete loss | migrainous headache | none |
Transient Ischemic Attack | Bilateral/Unilateral | seconds to minutes | none | negative(hemianopia or blindess) | brow headache, vertigo, diziness, imbalance, diplopia, bilateral weakness | none |
Uhthoff's Phenomenon | Unilateral | several minutes | activities that raise core body temperature (exercise, hot tub, hot shower, outdoor activites on a hot day) | difuse darkening or blurring of vision | may experience paresthesias at the same time | none |
Uveitis-glaucoma-hyphema (UGH) Syndrome | Unilateral | hours to a day | no particular activity, sometimes eye rubbing or fast eye movements | diffuse white haze | pain, if IOP is also elevated, glare | none |
Venous Stasis Retinopathy | Unilateral | seconds to minutes | coughing, orthostatic positional changes | usually central in retinal area supplied by cilioretinal artery | none | none |
Referral Reason: | Link | Wrap-Up |
---|---|---|
80-year-old white female that has noticed repeated episodes of sudden darkening of vision. | Start | 31921374-Commentary |
Bilateral Transient Visual Loss | Start | 31921375-Commentary |
64-year-old women who has been experiencing episodes of haziness in vision | Start | 31921376-Commentary |
41-year-old woman has had two episodes transient vision loss. | Start | 31921377-Commentary |
26-year-old male was taken to the emergency room after being involved in a motor vehicle accident with subsequent transient visual loss. | Start | 31921378-Commentary |
72-year-old with 4 episodes of vision loss. | Start | 31921379-Commentary |