The Blurry Border: You’ve Found Papilloedema, Now What?

It’s 4:00 AM. You’ve just managed to find a working ophthalmoscope and after wrestling with it and staring through the gloom, you spot the optic disc. The disc appears as an egg dropped from the roof, no margins and engorged vessels. You notice tachycardia, it’s yours not the patient’s! 😉

You go back to your notes and carefully document, “?papilloedema” but then what next??

Before we dive in, let’s take a quick 1-minute refresher about Papilloedema.

What is Papilloedema?

Papilloedema is bilateral optic disc swelling secondary to raised intracranial pressure (ICP). It’s distinct from other causes of optic disc oedema (e.g., optic neuritis, anterior ischaemic optic neuropathy—these are not papilloedema!). Causes range from benign (idiopathic intracranial hypertension-IIH) to sinister (tumour, Central nervous system (CNS) infection, haemorrhage, cerebral venous sinus thrombosis).¹

Pathophysiology

An increase in intracranial pressure is transmitted to the fluid around the optic nerve. This results in blockage of normal flow within the nerve at the optic disc. This results in a swollen disc with blurry edges, small haemorrhages may also be visible.^1,2 As both optic nerves are exposed to this pressure, papilloedema is usually bilateral. Unilateral cases are rare and tend to have alternative pathology.³

When should you look for it:

• Headache with red flags: fever or meningism, altered mental state, seizures, focal neurology or reduced Glasgow Coma Scale (GCS).
• Headache with visual symptoms such as blurred vision, transient visual loss or diplopia.
• Patients with features of malignant hypertension.

Differential diagnoses include:^4,5

• Idiopathic Intracranial Hypertension (IIH)
• Subdural hemorrhage/hygroma/empyema
• Subarachnoid Hemorrhage
• Intracranial masses (primary CNS tumor and metastases)
• Meningeal disease
  • Meningioma
  • Leptomeningeal carcinomatosis
• Encephalitis
• Cavernous Venous Sinus Thrombosis (CVST)
• Chiari malformations

The Mimics¹:

• Pseudopapilloedema: Often caused by optic disc drusen. The disc looks “heaped up” but the vessels aren’t obscured and there’s no haemorrhage.
• Optic Neuritis: Usually unilateral, associated with painful eye movements and a relative afferent pupillary defect (RAPD).
• Central Retinal Vein Occlusion (CRVO): The “blood and thunder” fundus.

Fig. 2 Image via LITFL

Now back to the main course – You’ve thought of it and now you’ve seen it, what next?

Step 1 Confirm and plan ahead

Once you’ve thought of papilloedema, do not spend the next half hour debating true vs pseudopapilodema. Focus on stabilisation and risk stratification and inform a senior/ colleague to brainstorm the way ahead.

Key actions at the bedside include:

• Check and record vision, this should include visual acuity and swinging light test for RAPD.^1,6
• Blood pressure (should have been done already, I hope) – High BP with papilloedema is end organ damage and should be treated as hypertensive emergency. Also, look out for evidence of other end organ damage (heart, lungs, kidneys).
• Brief but focussed neuro exam- look for cranial nerve palsies, motor/sensory deficits, cerebellar signs and level of consciousness. Any focal neurology or reduced GCS should be very concerning.
• Always remember with papilloedema the risk of over‑investigating is far lower than missing raised intracranial pressure.

Step 2 Classify the risk⁷

Is your patient sick now vs might be very sick soon!

Red flag features include:

• Focal neurology, reduced GCS, seizures of meningism
• Severe or malignant hypertension
• Progressive visual symptoms
• Systemic red flags including malignancy, pregnancy/postpartum, prothombotic state, infection

Patients without these features but with a classic IIH phenotype⁸ (younger woman, chronic daily headache, transient visual disturbances, pulsatile tinnitus, normal neuro exam) still need same‑day imaging and organised follow‑up.

Fig. 3 – RCEMLearning image generated with Google Gemini

Step 3 First line imaging

MRI Brain with MR Venography (laughs in ED) would be ideal to exclude mass lesions and cerebral venous sinus thrombosis and to assess features of raised ICP such as distended optic nerve sheath and flattened posterior globe.^1,2

In many EDs, the pragmatic step would be an urgent CT head ± CT venogram. Add venogram when you have prothrombotic states, infection or atypical headaches.

If you are a POCUS nerd, an Ocular US to measure the optic nerve sheath diameter is increasingly becoming a quick bedside tool. A diameter >5.5mm should make you concerned for raised ICP.⁹ (If you are rolling your eyes, hey, don’t shoot the messenger).

Step 4 Lumbar puncture – when, where, and why^1,10

If imaging has excluded a mass lesion or obstructive hydrocephalus and you still suspect raised ICP, lumbar puncture maybe the next logical step. I know, given the departmental pressures we face, this often comes under the domain of Acute Medics but humour me.

Some practical considerations:

Indications

• Suspected IIH– LP helpful to measure opening pressure and confirm normal CSF composition.​
• Suspected CNS infection or where papilloedema may represent raised ICP from meningitis or encephalitis.

Send CSF for standard infection and malignancy panels as per local Trust guidelines (cell count, protein, glucose, culture, cytology, oligoclonal bands where appropriate).

Step 5 Phone a friend

The provisional diagnoses will dictate referral decisions and patient disposition, keeping in mind local and Trust guidelines.

Acute medicine/ general medicine – If you are dealing with malignant hypertension and multiorgan involvement.

Neurology – If you are thinking about CVT, IIH and other diffuse raised ICP states, then a conversation with a neurologist would be advisable.

Neurosurgery – If imaging shows mass lesions, obstructive hydrocephalus, or evidence of impending herniation.​

Ophthalmology – If there is rapid acuity loss, confirmation of disc swelling and mimickers like drusen.

Phew, so that’s a rundown of an approach to the dreaded papilloedema. You don’t need to be an optic disc expert, however a robust process that identifies papilloedema, risk stratifies, appropriate imaging and referrals will keep the patient safe and your heart rate down.

References

1. Asuncion RMD, Margolin E. Papilledema. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025. [Cited 29 Jan 2026 ]. 
2. Ferreira BFA. Papilledema: A comprehensive assessment. J Neurosci Rural Pract. 2017;8(4):683–684. doi:10.4103/jnrp.jnrp_257_17.
3. Quesada D, et al. An unusual case of unilateral papilledema. Clin Pract Cases Emerg Med. 2019;3(4):444‑445. 
4. Bridwell R, Long B, Koyfman A. EM@3AM: Papilledema. emDocs. 24 April 2021. [Cited 1 February 2026].
5. Mollan SP, Davies B, Silver NC, Shaw S, et al. A practical approach to diagnosis, assessment and management of idiopathic intracranial hypertension. Pract Neurol. 2014;14(6):380‑390.
6. Xie JS, et al. Papilledema: A review of etiology, pathophysiology, diagnosis, and management. Surv Ophthalmol. 2022;67(4):1135-1159.
7. Passi N, Degnan AJ, Levy LM. MR imaging of papilledema and visual pathways: Effects of increased intracranial pressure and pathophysiologic mechanisms. Am J Neuroradiol. 2013;34(5):919-924. 
8. Wall M, Kupersmith MJ, et al. The idiopathic intracranial hypertension treatment trial clinical profile at baseline. JAMA Neurol. 2014;71(6):693-701. 
9. Ohle R, et al. Sonography of the optic nerve sheath diameter for detection of raised intracranial pressure compared to computed tomography: A systematic review and meta-analysis. J Ultrasound Med. 2015;34(7):1285-1294. 
10. Society for Academic Emergency Medicine. Lumbar puncture. SAEM Online Education, 2023. [Cited 1 Feb 2026].