Approach to acute vision loss: Clinical sciences

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Introduction0:00–0:44

Acute vision loss is a relatively sudden worsening of visual perception. The underlying pathology could be anywhere along the visual pathway, including the eyes, optic nerves, optic chiasm, optic tracts, optic radiations, and the visual cortex.
Now, vision loss associated with eye pain is common for conditions like infectious keratitis, glaucoma, and optic neuritis.
However, painless vision loss is found with stroke, mass compression of the optic chiasm, retinal detachment, as well as central retinal artery or venous occlusion, or ischemic optic neuropathy.
If your patient presents with acute vision loss, first obtain a focused history and physical exam, as well as a fundoscopic exam.

H&P0:44–2:21

Patients typically report a sudden vision loss, while the physical exam demonstrates decreased visual acuity and possibly impaired visual fields.
Don’t forget to perform the swinging flashlight test. This test is used to assess the pupillary reflex pathway, which involves the optic nerve as the sensory afferent limb, and the oculomotor nerve as the motor efferent limb.
During the swinging flashlight test, you shine a light, such as with a penlight, back and forth between the two eyes. Normally, regardless of which eye the light is shining into, the sensory afferent limb of the optic nerve will send a signal to the Edinger-Westphal nucleus in the midbrain.
From here, the signal will be sent back via the oculomotor nerves and the ciliary ganglia to the pupillary sphincter muscles in both eyes, causing both pupils to constrict.
However, if there’s a lesion of the afferent pathway, when you swing the light from the normal eye to the affected eye, the stimulus will not reach the Edinger-Westphal nucleus.
In other words, efferent signals will not reach pupillary sphincter muscles, so the patient’s pupils will not constrict, instead, they will dilate.
This is known as a relative afferent pupillary defect or Marcus Gunn pupil. Finally, in some individuals with acute vision loss, the fundoscopic exam might reveal optic disc edema.
With these findings, you can diagnose acute vision loss, so your next step is to assess for eye pain. If there is pain associated with vision loss, examine the patient for conjunctival injection, meaning redness of the conjunctiva.

Painful vision loss2:21–2:40

The presence of conjunctival injection suggests ophthalmologic causes of vision loss, such as infectious keratitis and acute angle closure glaucoma.

Infectious keratitis2:40–4:19

Let’s start with infectious keratitis. These patients typically report tearing of the eye.
They might also have a history of unhygienic contact lens use, such as swimming with their contact lenses in. When it comes to the physical exam, it reveals corneal opacification, sometimes with corneal ulcers or mucopurulent drainage.
At this point, you should consider infectious keratitis, so obtain scrapings of the cornea and send samples for gram stain, culture, and PCR.
If gram stain or cultures detect bacteria or fungus, or PCR results come back positive for HSV or adenovirus, diagnose infectious keratitis.
Here’s a couple of clinical pearls to keep in mind! HSV keratitis commonly presents with dendritic ulcers, which have a branching appearance that look like dendrites.
These dendrites can be detected with a fluorescein stain exam. If you see them, start a topical or oral antiviral agent.
Now, while keratitis is inflammation of the cornea, other parts of the eye can also become inflamed and cause painful vision loss.
For example, inflammation of the eyelash follicles or Meibomian glands of the eyelid is known as blepharitis and causes similar symptoms in addition to eyelid swelling.
Next, your patient might present with inflammation of the conjunctiva, also known as conjunctivitis, which can occur due to bacteria, viruses, or allergies.
Some other common examples include periorbital and orbital cellulitis, uveitis, and dacryocystitis. Okay, let’s move on to acute angle closure glaucoma, which is the closure of the anterior chamber angle where aqueous humor is drained.

Acute angle closure glaucoma4:19–5:11

In addition to painful vision loss, these patients might report headache, nausea, or vomiting. They may also tell you that their symptoms were precipitated by entering a dark room.
This happens due to pupillary dilatation in the dark, which further narrows the anterior chamber angle, making it even more difficult for aqueous humor to drain.
On physical exam, you will find a fixed and dilated pupil. With these findings, consider acute angle closure glaucoma, Next, perform tonometry and gonioscopy.
If tonometry reveals elevated intraocular pressure, and gonioscopy confirms a closed anterior chamber angle, you are dealing with acute angle closure glaucoma.

Optic neuritis5:11–6:21

Now let’s go back and take a look at patients with no conjunctival injection. In this case, consider optic neuritis.
Optic neuritis can be caused by various conditions, including infectious, autoimmune, and granulomatous conditions. The most common ones are demyelinating disorders.
Your next step is to obtain an MRI of the brain and orbits. If it reveals optic nerve enhancement and edema, possibly with enhancing white matter lesions, diagnose optic neuritis.
Time for a clinical pearl! If your patient is a young, biological female with a first-time presentation of optic neuritis, suspect multiple sclerosis.
Another condition to consider is neuromyelitis optica spectrum disorder, which tends to be more severe with poorer recovery.
Patients with optic neuritis often report painful eye movements, as well as colors not appearing as bright as usual. This can be tested on exam by asking patients to look at a red object with each eye individually.
To the affected eye, the red color may appear lighter or washed out, known as red desaturation. Alright, let’s switch gears and discuss patients with painless vision loss.

Painless vision loss/Stroke6:21–7:17

In this case, your first step is to assess for hemianopsia, which can be homonymous or bitemporal. Homonymous hemianopsia, which is a loss of the same half of the visual field of both eyes, is suggestive of stroke.
Next, obtain a CT or MRI of the brain. If imaging reveals a stroke contralateral to the side of the visual field impairment, diagnose stroke as the cause of vision loss.
Here’s a clinical pearl! Strokes in the middle cerebral artery or posterior cerebral artery territory can cause contralateral homonymous hemianopsia.
A big difference is that a posterior cerebral artery stroke can result in homonymous hemianopsia with macular sparing, meaning your patient will have a small central area without vision loss.
On the other hand, bitemporal hemianopsia is a loss of the lateral half of the visual field of each eye. In this case, consider a sellar or suprasellar mass as a cause of vision loss, so, again, order a brain MRI.

Sellar/suprasellar mass7:17–8:06

If imagining reveals a mass lesion compressing the optic chiasm, diagnose sellar or suprasellar mass. Most commonly, you will find a pituitary adenoma, a craniopharyngioma, or a meningioma.
Here’s a high-yield fact! If there is also an acute onset headache with hypotension, think of pituitary apoplexy, which is a hemorrhage in the pituitary gland.
This is an emergency, as deficiency of pituitary hormones, especially ACTH can lead to hemodynamic instability. Okay, time to switch gears and discuss patients with painless vision loss but no hemianopsia.

Assess underlying cause8:06–8:21

In this case, further assess the underlying cause by taking a closer look at the history and fundoscopic exam. First up is retinal detachment.

Retinal detachment8:21–8:39

These patients report flashes of light or floaters prior to the onset of vision loss, and possibly a history of nearsightedness or recent eye trauma.
If the fundoscopic exam reveals a detached retina, diagnose retinal detachment. Next, let’s talk about central retinal artery occlusion.

Central retinal artery occlusion8:39–9:19

History typically reveals transient episodes of vision loss, known as amaurosis fugax, before experiencing a sustained loss of vision.
The patient might also report a history of carotid atherosclerotic disease ipsilateral to the affected eye or a history of atrial fibrillation.
The fundoscopic exam typically shows retinal whitening due to ischemia; pallor of the retinal arteries; and a cherry red spot over the fovea, which remains vascularized as it receives its blood supply from the choroid.
With these findings, diagnose central retinal artery occlusion. Now, let’s consider central retinal vein occlusion.

Central retinal vein occlusion9:19–9:49

Patients with this type of vision loss usually describe vision loss progressing over several hours to days. History might also reveal some risk factors, like hypertension, diabetes, and hypercoagulable disorders.
If, on fundoscopic exam, you see numerous retinal hemorrhages and dilated, tortuous veins, resulting in what is commonly called a “blood and thunder” appearance, that’s central retinal vein occlusion.

Non-arteritic anterior ischemic optic neuropathy9:49–10:11

Next up is non-arteritic anterior ischemic optic neuropathy. These patients may have a history of hypertension or diabetes.
If the fundoscopic exam shows severe optic disc swelling and disc hyperemia, diagnose non-arteritic anterior ischemic optic neuropathy.

Giant cell arteritis10:11–11:31

Finally, let’s discuss giant cell arteritis, which typically occurs in individuals age 50 or older. In addition to vision loss, history reveals a headache, pain over the scalp or temple, and pain with chewing, which is known as jaw claudication.
Additionally, there might be a history of polymyalgia rheumatica. The fundoscopic exam will show severe optic disc swelling and disc pallor.
At this point, consider giant cell arteritis, also known as temporal arteritis, which is a common cause of arteritic anterior ischemic optic neuropathy.
To confirm your diagnosis obtain labs, including ESR and CRP; and a temporal artery biopsy. If the ESR and CRP are elevated, and biopsy reveals transmural inflammation, multinucleated giant cells, and mononuclear infiltrates, diagnose giant cell arteritis.
Here’s a clinical pearl! Biopsy results might take time, so if you suspect giant cell arteritis, immediately start high-dose corticosteroids.
The goal is to prevent disease progression because giant cell arteritis can affect the healthy eye as well. In severe cases, inflammation can result in permanent vision loss.

Review11:31–12:00

Alright, as a quick recap… Painful vision loss is typically seen in infectious keratitis, acute angle closure glaucoma, and optic neuritis.
However, If your patient has painless vision loss with hemianopsia, consider either a stroke or a sellar or suprasellar mass.
If there is no hemianopsia, think about retinal detachment, central retinal artery or venous occlusion, non-arteritic anterior ischemic optic neuropathy, and giant cell arteritis.