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Retina & Vitreous

Saturday Night Retinopathy

Saturday Night Retinopathy (SNR) is an acute ischemic retinopathy caused by prolonged external compression of the eyeball during loss of consciousness due to substance abuse or excessive alcohol consumption.

First reported and named by Jayam et al. in 1973, the typical scenario is a person who becomes heavily intoxicated on a Saturday night, falls down, and remains in that position until morning. It is classified as a type of ocular artery occlusion (OAO). The incidence is extremely rare, with only a few reported cases.

Q What is the origin of the name "Saturday Night Retinopathy"?
A

The name is based on the typical situation where a person loses consciousness due to substance abuse or excessive drinking over the weekend, remains in a position with the eyeball compressed overnight, and develops symptoms the next morning. It was named in the 1973 report by Jayam et al.

  • Acute unilateral vision loss: Often noticed after regaining consciousness. It is severe and sudden visual impairment.
  • Visual field defect: Accompanied by extensive visual field loss in one eye.

Findings reflecting sustained external compression and ischemia of the eyeball are characteristic.

Acute Phase Findings

Fixed and dilated pupil: Accompanied by loss of light reflex. Due to ischemia of the iris sphincter.

Ophthalmoplegia: Restriction of eye movement due to ischemic damage to the extraocular muscles.

Pale retina: Extensive retinal pallor due to ophthalmic artery ischemia. No emboli are observed.

Unclear cherry red spot: In OAO, unlike CRAO, the cherry red spot becomes unclear 1).

Findings after the course

Proptosis: May be observed in the acute phase but resolves spontaneously.

Optic atrophy: Progresses in the chronic phase. Reflects degeneration of the optic nerve due to ischemia.

Retinal thinning: Irreversible change observed after a long-term course.

Complete loss of electroretinogram: An objective indicator of ischemia involving the full thickness of the retina.

In OAO, complete ischemia of the ophthalmic artery damages both the retina and choroid. Therefore, the cherry red spot, which is typically seen in CRAO, becomes unclear, which is a key point in differentiation 1).

Q How to differentiate from central retinal artery occlusion (CRAO)?
A

In CRAO, choroidal circulation is preserved, so a cherry red spot appears in the macula. In contrast, in SNR (OAO), occlusion occurs at the ophthalmic artery level, causing ischemia of both the retina and choroid, making the cherry red spot unclear 1). Additionally, the presence of emboli and history of compression are important differentiating information.

The essence of SNR is collapse and ischemia of the ophthalmic artery due to prolonged continuous external compression of the eye. The following situations are known as causes.

  • Substance abuse / excessive alcohol consumption: After loss of consciousness, the eye compression posture persists for a long time. The most typical cause.
  • Prone position surgery under general anesthesia: May occur during spinal or spinal cord surgery performed in the prone position due to improper head fixation or compression of the face by instruments.
  • Other states of unconsciousness: A similar mechanism can occur after coma or epileptic seizures.

SNR is primarily a diagnosis of exclusion. After confirming a history of loss of consciousness and the possibility of ocular compression, other causes of ophthalmic artery occlusion or retinal artery occlusion should be ruled out.

The main examinations and their purposes are listed below.

ExaminationMain Purpose
CT/MRIExclude intracranial lesions or embolic sources
Fluorescein angiography (FA)Confirm the site of vascular occlusion
ElectroretinographyObjective assessment of full-thickness retinal damage
  • CT/MRI: To rule out intracranial diseases. Essential for differentiating cerebral infarction, vascular malformations, dissection, etc.
  • Fluorescein angiography (FA): To confirm the location and extent of ophthalmic artery occlusion and evaluate the presence of emboli.
  • Electroretinography (ERG): In OAO, the ERG completely disappears, reflecting full-thickness retinal ischemia. It serves as an objective indicator of severity.
  • Blood tests (ESR/CRP): Giant cell arteritis (GCA) must be ruled out. GCA is an emergency condition that can cause similar vascular occlusion, and screening with ESR/CRP is recommended 1).

Acute retinal artery occlusion and ophthalmic artery occlusion require management as ophthalmic emergencies 1).

Q Why is it necessary to rule out giant cell arteritis (GCA)?
A

GCA is a systemic vasculitis that occludes the ophthalmic artery and posterior ciliary arteries, causing acute vision loss, and requires emergency treatment with steroids. Since it presents with ophthalmic artery occlusion similar to SNR, active exclusion with ESR/CRP is recommended in elderly patients 1).

There is no established treatment for SNR. Current management is as follows:

  • Anterior chamber paracentesis for reperfusion attempt: In the acute phase, intraocular pressure may be lowered to improve ocular perfusion pressure. However, efficacy is limited and general evidence is lacking.
  • Observation of proptosis: Proptosis may occur in the acute phase but usually resolves spontaneously. Surgical intervention is often unnecessary.
  • Prognosis disclosure: Visual impairment is often permanent. Adequate explanation to the patient and family is necessary.

Acute retinal artery occlusion and OAO should be treated as ophthalmic emergencies, with intervention as early as possible 1).

Acute Management

Anterior chamber paracentesis: Attempts reperfusion by lowering intraocular pressure. Efficacy is low if time has passed since onset.

Emergency evaluation: Promptly rule out GCA and intracranial diseases.

Ophthalmic emergency: Acute RAO/OAO should be treated as emergencies 1).

Observation

Proptosis: Spontaneously resolves after decompression. Observation is the mainstay.

Visual prognosis: In most cases, severe visual impairment is permanent. Recovery is unlikely.

Complication management: Monitor for optic atrophy and secondary glaucoma.

6. Pathophysiology and detailed mechanisms

Section titled “6. Pathophysiology and detailed mechanisms”

The pathogenesis of SNR involves a cascade of ophthalmic artery collapse due to sustained external ocular compression, followed by ischemia and reperfusion injury.

  • Sustained external compression: Direct compression of the globe increases intraocular pressure, exceeding the perfusion pressure of the ophthalmic artery and central retinal artery.
  • Ophthalmic artery collapse: When intraocular pressure exceeds ophthalmic artery systolic blood pressure, the ophthalmic artery collapses, interrupting blood flow to the entire globe.
  • Total ischemia: Occlusion at the ophthalmic artery level causes simultaneous ischemia of the retina, choroid, and optic nerve. This is the pathological basis for the absence of a cherry red spot, unlike in CRAO 1).
  • Reperfusion injury: Even after blood flow is restored upon decompression, oxidative stress from reactive oxygen species accumulated during ischemia further exacerbates tissue damage.
  • Irreversible damage: Retinal ganglion cells and optic nerve axons are vulnerable to ischemia, and irreversible degeneration occurs after several hours of ischemia.

In the pathology of OAO, ophthalmic artery occlusion blocks both retinal and choroidal circulation, resulting in a worse prognosis than central retinal artery occlusion1).

The main differences between SNR and CRAO are shown below.

ItemSNR (OAO)CRAO
Occlusion siteOphthalmic arteryCentral retinal artery
Choroidal circulationImpairedPreserved
Cherry red spotUnclearTypically present
Main causesExternal compression of the eyeEmbolism/thrombosis

  1. American Academy of Ophthalmology. Retinal and Ophthalmic Artery Occlusions Preferred Practice Pattern. Ophthalmology. 2020;127:P259-P287.
  2. Gonzales AF, Lee MJ. Saturday Night Retinopathy. Ophthalmol Retina. 2023;7(3):260. PMID: 36609036.
  3. Malihi M, Turbin RE, Frohman LP. Saturday Night Retinopathy with Ophthalmoplegia: A Case Series. Neuroophthalmology. 2015;39(2):77-82. PMID: 27928336.

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