Saturday night retinopathy (SNR) is a rare condition caused by compression of the orbit and globe during a prolonged period of unconsciousness in a face-down position following the use of sedating drugs or heavy alcohol. The resulting unilateral acute ischemic retinopathy and choroidopathy can cause severe irreversible vision loss.
Jeyem et al. first documented the condition in 1974 and named it after the initial case involving heavy alcohol and methadone abuse at a Saturday night party.1 Similar clinical findings may also arise from complications of surgical positioning, particularly in patients under general anesthesia placed face-down on a cushioned headrest.2
Due to the association of Saturday night retinopathy and drug use, there will likely be an increase in cases as the incidence of opioid abuse continues to rise. Therefore, it is important that eyecare providers are familiar with this condition even though it is rare. The condition may also be underreported due to the affected population not seeking or having access to health care.
Pathophysiology of Saturday night retinopathy
The hypothesized mechanism of SNR includes the collapse of orbital vessels due to prolonged external pressure on the orbit.2 The use of sedatives dampens the typical pain response that would cause someone to actively alleviate the pressure sensation.
When orbital pressure is eventually relieved, the ischemic vessels will dilate and reperfuse. This leads to fluid moving into the surrounding tissues, causing orbital edema, ocular motility defects, proptosis, and retinal edema.
Vision loss is thought to be due to lack of blood flow through either the central retinal or ophthalmic artery, resulting in ischemia.3 Although ophthalmoplegia, proptosis, and retinal edema improve within the following days or weeks, the resulting retinal atrophy can limit vision to hand motion or light perception.
Risk factors for Saturday night retinopathy
History of substance abuse often emerges as a key risk factor in SNR. The state of unconsciousness leading to this condition typically stems from excessive drinking and narcotic or opioid use. In some cases, a combination of sleep medications and alcohol consumption has also led to the development of retinopathy.4
Presentation of SNR
Patients will typically present with acute, monocular vision loss with periorbital edema upon awakening from a long period of unconsciousness. The shortest published duration of unconsciousness in SNR involves a patient who lost consciousness for 3 hours.4 Exam findings include a fixed and nonreactive pupil with an obvious relative afferent pupillary defect.
In some cases, injury to the anterior segment may impair reperfusion and cause a spike in intraocular pressure (IOP), resulting in corneal edema and conjunctival chemosis.5 Some case series have found proptosis and ophthalmoplegia to be signs of a more severe orbital reperfusion injury. Patients who are able to partially relieve orbital compression or have shorter periods of compression will typically present with milder signs and symptoms.6
Posterior segment findings include evidence of an ophthalmic or central retinal artery occlusion. This manifests as a pale optic nerve with mild hyperemia and a cherry red spot macula.6 No emboli are noted at the nerve in SNR.
The examiner should also note other findings that may point towards recent inebriation or altered mental state, such as facial bruising or swelling, peripheral track marks, or peripheral nerve palsies. Multiple SNR case reports mention nerve palsies in the foot, leg, or arm due to the period of unconsciousness.6
Diagnosis and testing of SNR
- In SNR, optical coherence tomography (OCT) shows significant edema and hyperreflectivity within the central retina. Over approximately 1 month, the retina becomes atrophic as the swelling resolves.7
- Other case reports have also noted subretinal and sub-retinal pigment epithelium (RPE) fluid on OCT.
- Fluorescein angiography (FA) exhibits decreased and delayed choroidal and retinal filling.
- After 1 month, RPE pigment changes can be noted.
- Computed tomography (CT) of the head and orbits typically reveals preseptal soft tissue engorgement. Magnetic resonance imaging (MRI) with contrast uncovers swelling of the extraocular muscles and orbital tissue with proptosis.6
Differential diagnoses of Saturday night retinopathy
SNR should be treated as a diagnosis of exclusion. Profound vision loss, ophthalmoplegia, and proptosis in any patient is an ocular emergency. It is important to rule out other causes of proptosis and extraocular muscle (EOM) restriction, such as orbital cellulitis, orbital pseudotumor, orbital myositis, and orbital sarcoidosis.8
Carotid cavernous fistula should also be considered as a differential and the patient should be examined for pulsatile exophthalmos and orbital bruit. Due to the involvement of the ophthalmic or central retinal artery, it is important to rule out other causes of occlusion, such as carotid, cardiac, and hypercoagulable etiologies.
The patient's social history is a key component to determine if SNR should be on the differential list.
Management and follow-up of SNR
There is no consensus on the management of SNR. If an IOP spike is noted, treat with topical IOP-lowering medications. Monitor for anterior/posterior segment neovascularization (e.g., sequelae of severe retinal ischemia) to prevent a blind painful eye. Counsel the patient on poor visual prognosis, with final visual acuity ranging from no light perception to hand motion.8
Patients should be evaluated for other sequelae of narcotics abuse—such as dry eye disease, mild keratopathy, endophthalmitis, and occipital lesions—and referred appropriately. These patients will likely require a multidisciplinary approach to address their healthcare needs.
Key takeaways
With the increasing incidence of opioid abuse, awareness among eyecare providers about this disease is paramount to ensure prompt recognition and intervention.
Here are the key takeaways you need to know to recognize and manage SNR:
- SNR represents a rare but significant ocular emergency, characterized by acute, monocular vision loss resulting from prolonged unconsciousness in a face-down position due to sedative drug use or heavy alcohol consumption.
- Understanding the pathophysiology, risk factors, and clinical presentation of SNR is crucial for timely diagnosis and management.
- It is essential to differentiate SNR from other causes of vision loss and proptosis through thorough clinical evaluation and patient history.
- The hypothesized mechanism involves compression of orbital vessels leading to ischemia, subsequent reperfusion injury, and irreversible vision loss.
- Management of SNR involves addressing elevated IOP, monitoring for neovascularization, and counseling patients on the poor visual prognosis.
