Approach to the patient with flashes and/or floaters

Authors: Dr. Lauren Hughes (biography, no disclosures) and Dr. Heather L. O’Donnell (biography and disclosures)

What care gaps or frequently asked questions I have noticed

The acute onset of monocular flashes and/or floaters is a common presentation to primary care providers. Most often, this represents a posterior vitreous detachment (PVD), an age-related condition with a prevalence that increases from 24% in adults aged 50 to 59 to 87% among those aged 80 to 89 years.¹ However, the differential diagnosis also includes concerning retinal pathology, such as a retinal tear or detachment. These are less common, with a 0.1% lifetime risk of developing a retinal detachment, but a threat to vision and must be ruled out.² Other conditions, such as acephalgic migraine, can also present with flashing lights. The objective of this article is to outline clinical features that differentiate these diagnoses and aid the primary care physician in determining the urgency of ophthalmologic assessment. What this article will do: help you decode flashing lights. What this article will not do: a comprehensive migraine review… perhaps another TCMP article.

Data that answers these questions or gaps

Patient Evaluation

The most common mimicker of PVD is visual aura with or without a migraine. On history, patients describe a pattern of lights, jagged lines, or colours “marching” through the visual field, sometimes surrounding a central area of visual field loss. This phenomenon is bilateral and involves the sensation of coloured lights, as opposed to monocular flashing lights seen in retinal pathology and white lights seen in PVD. Further, the flashing lights seen with PVD are rapid, peripheral, and short-lived. Patients often describe “a camera flash at the side of my vision.” Migraine with typical aura is defined as gradual development of positive and negative visual and/or sensory and/or speech/language symptoms, but no motor weakness. Each symptom lasts no longer than one hour and is completely reversible.³ The aura may not be accompanied nor followed by a headache of any sort within 60 minutes, representing an acephalgic migraine. Most of these patients have a known migraine history. The ocular exam will be normal with a visual acuity that is 20/20 or unchanged from previous.

Additional differential diagnoses to be mindful of are occipital disorders such as ischemia or infarction, hemorrhage, AV malformation, seizure disorder, and neoplasm. It is important to consider a neurologic etiology with questioning around constitutional and focal neurologic symptoms, as well as a focused neurologic exam. Finally, orthostatic hypotension can produce brief flashes or dimming of vision in all or part of the binocular visual field. Features including transient visual symptoms accompanying light-headedness or ataxia precipitated by orthostatic posture change support the diagnosis. It would be prudent to perform orthostatic vital signs.

14% of PVD’s result in retinal tears, 33% to 46% of which could progress to a retinal detachment, a vision threatening condition, if left untreated.¹ When evaluating a patient presenting with flashes and/or floaters, one must identify patients with high-risk historical features for retinal tear or detachment. Patients with high myopia, other retinal pathology like lattice degeneration, family history of retinal detachment, previous retinal breaks, prior ocular surgery, or history of trauma are at higher risk.^1,4,5,6 In addition, a progressive monocular visual field defect (“curtain of darkness”) in the affected eye or subjective vision loss is a retinal detachment until proven otherwise increases the likelihood of an acute retinal detachment and needs emergent assessment.¹ A comparison of the common diagnoses presenting with acute onset flashes and/or floaters can be found in Table 1.

Table 1. Comparison of common conditions presenting with acute onset flashes and/or floaters. (Download Table1. PDF)

Physical exam should include best corrected visual acuity, preferably measured with a Snellen chart, as well as confrontational visual fields, with close attention to a monocular visual field defect in the affected eye. A pupil exam should also be performed. If available, slit lamp exam may reveal vitreous pigment (“tobacco dust” or “Shafer’s sign”) or hemorrhage in the case of a retinal tear. The examiner should focus the beam behind the lens into the anterior portion of the vitreous. Have the patient look up, immediately down, then immediately straight ahead to improve visualization of vitreous hemorrhage or pigment. Direct ophthalmoscopy should be performed to visualize the fundus, which may reveal a billowing retinal detachment. These latter physical exam maneuvers will be difficult for emergency physicians as they aren’t dilating the pupil and family physicians as they don’t have access to slit lamps in the office.

Ultimately, subjective vision reduction (Likelihood Ratio (LR) 5.0), the presence of vitreous hemorrhage (LR 10), and/or the presence of vitreous pigment (LR 44) are most suggestive of acute retinal tear in patients presenting with flashes and/or floaters.¹ Preservation of a patient’s usual visual acuity decreases the likelihood of a retinal tear (LR 0.60).¹

Triage, Management, Follow-up

Patients with progressive monocular visual field loss suggestive of acute retinal detachment or high-risk features for retinal tear such as subjective visual reduction, objective visual reduction, vitreous pigment, or vitreous hemorrhage on exam require same-day ophthalmology assessment. As above, visualization of vitreous pigment or vitreous hemorrhage will be difficult for emergency and family physicians. Ultimately, if your patient presents flashes, floaters, and decreased vision, they need to be seen urgently by ophthalmology. Physicians working in rural communities should speak to an ophthalmologist over the phone and arrange for transfer as soon as possible or as advised by the consulting ophthalmologist. In the case of an acute retinal tear, patients can expect to be managed with laser therapy or cryotherapy within a few days, however, treatment is individualized depending on the size and location of the tear as well as symptomatology and etiology. As previously mentioned, retinal tears pose a risk of progression to retinal detachment, particularly superior tears. As such, patients must be told to report any worsening of symptoms immediately. In the case of a retinal detachment, management may include laser therapy, injecting a gas bubble into the eye to reattach the retina, a pars plana vitrectomy, or scleral buckling. The urgency of therapy and visual prognosis depends on whether the macula is involved. Macula-on detachments require more urgent intervention to preserve central vision and carry a significantly better prognosis. Given high myopia is a risk factor for retinal detachment, these patients should be counselled on the importance of wearing protective eyewear during high contact sports to prevent a subsequent detachment.

Patients with new-onset floaters and/or flashes with suspected ocular cause but without high-risk features for retinal tear or detachment should be referred to ophthalmology on a less urgent basis (1-2 weeks) and advised to seek immediate medical attention should they develop monocular visual field defects or decreased vision. There is no acute management necessary for a PVD. Patients found to have a PVD should be informed that they will likely develop a PVD in their fellow eye. An uncomplicated PVD caries a small risk (3.4%) of subsequently developing a retinal tear within six weeks of diagnosis.¹ A sudden increase in floaters (change from <10 to ≥10) or new subjective vision loss is predictive of new retinal tear. Patients should be told to return immediately if these symptoms develop, at which time they should be assessed urgently by ophthalmology.

Beyond the acute management described above, patients with a retinal detachment, retinal tear, or PVD can expect to be followed and re-examined routinely by an ophthalmologist for the first six to 12 months.

If your clinical assessment has led you to a diagnosis of acephalgic migraine, there is limited evidence for specific treatment. Patients should be reassured and instructed to avoid driving during events. Identification of triggers can help reduce frequency of events. Patients should return to their care provider if there is a change to the frequency or duration of the symptoms for neurologic evaluation. Aura symptoms resolve spontaneously without intervention. Any scintillating scotoma that does not resolve warrants assessment by ophthalmology.

What I recommend (practice tip)

1. Consider a broad differential diagnosis when evaluating patients with flashes and/or floaters.
2. Perform a thorough evaluation of a patient with flashes and/or floaters with particular attention to associated monocular visual field defects suggesting a retinal detachment or high-risk features for a retinal tear such as subjective visual reduction, objective visual reduction, vitreous pigment, or vitreous hemorrhage. The presence of any of these features requires same-day ophthalmology assessment. Physicians working in rural communities should speak to an ophthalmologist over the phone and arrange for transfer as soon as possible or as advised by the consulting ophthalmologist.
3. There are many additional ophthalmic conditions that cause photopsia and if patients have ongoing flashing lights in their vision, review with ophthalmology is necessary.

References

1. Headache Classification Committee of the International Headache Society. The international classification of headache disorders. 3^rd ed. Cephalalgia. 2018;38(1):1–211. DOI: 10.1177/0333102417738202. (Request with CPSBC or view with UBC)
2. Hollands H, Johnson D, Brox AC, Almeida D, Simel DL, Sharma S. Acute-onset floaters and flashes: Is this patient at risk for retinal detachment? JAMA. 2009;302(20):2243–2249. DOI: 10.1001/jama.2009.1714. (Request with CPSBC or view with UBC)
3. Bagheri N, Wajda B. Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease. 7^th ed. 2016. (Request with CPSBC or view with UBC)
4. Crim N, Esposito E, Monti R, Correa L, Serra H, Urrets-Zavalia J. Myopia as a risk factor for subsequent retinal tears in the course of a symptomatic posterior vitreous detachment. BMC Ophthalmol. 2017;17(1):226-230. DOI: 10.1186/s12886-017-0629-6. (View)
5. Flitcroft D. The complex interactions of retinal, optical and environmental factors in myopia aetiology. Prog Retin Eye Res. 2012;31(6):622–660. DOI: 10.1016/j.preteyeres.2012.06.004. (View with CPSBC or with UBC)
6. Shah D, Dilwali S, Friedman D. Current aura without headache. Curr Pain Headache Rep. 2018;22(11):1–8. DOI: 10.1007/s11916-018-0725-1. (Request with CPSBC or view with UBC)

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Approach to the Patient with Flashes and/or Floaters

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