Posterior ischemic optic neuropathy (PION) is an uncommon condition that occurs after acute hypoperfusion of the intraorbital optic nerve and is manifested as substantial vision loss.¹ The optic nerve head typically appears normal at the initial examination, despite a profound loss of vision. Pallor of the optic nerve head develops in 6 to 8 weeks. PION has been divided into 3 subtypes, according to the etiology:

• Perioperative PION occurs as a consequence of profound hypotension and anemia during surgical procedures²
• Arteritic PION is associated with systemic vasculitis, most often with giant-cell arteritis^2,3
• Nonarteritic PION has been associated with a variety of conditions, including internal carotid dissection, intranasal corticosteroids, methanol intoxication, migraine, sickle-cell disease, lung carcinoma, Aspergillus infection, and hemodialysis.⁴

Case Presentation

A 55-year-old woman with a history of hypertension, depression, and several suicide attempts was transported to the emergency department by emergency medical services after her husband found her unconscious next to an empty bottle of nifedipine. The precise amount ingested could not be determined accurately. Physical examination showed a lethargic and confused patient, with a heart rate of 20 to 30 beats/min and a systolic blood pressure of 60 to 74 mm Hg (diastolic blood pressures were not recorded by the emergency department). Initial management included normal saline, calcium chloride, dopamine, glucagon, and norepinephrine to treat her bradycardia and hypotension. A transcutaneous pacemaker was also used to treat her bradycardia. Because the transcutaneous pacemaker did not capture her ventricular sinus rhythm, she was transferred to the intensive care unit (ICU), where a transvenous pacemaker was placed, capturing her ventricular sinus rhythm at 80 beats/min. She was in the emergency department for a total of 55 minutes before being transferred to the ICU.

The patient regained full consciousness 6 days later. She was noted to use tactile sensation to locate objects at her bedside as opposed to vision. She reported that she could not see anything. The ophthalmology inpatient consultation service was called.

The initial ophthalmic examination revealed visual acuity of light perception (without projection) in the right eye and no light perception in the left eye. Her pupils were 7 mm (reacting to light sluggishly to 6.5 mm) in the right eye, and 7 mm (nonreactive to light) in the left eye. She had a relative afferent pupillary defect in the left eye. The optic discs appeared normal and did not show evidence of pallor or disc swelling (Figure 1). Visual field analysis and color vision examination could not be conducted because of the profound vision loss. A computed tomography (CT) scan of the head was unremarkable.

Figure 1 The right (A) and left (B) optic discs appear normal during the initial ocular examination of a patient with PION.

A presumptive diagnosis of PION was made based on the history and the ocular examination. The patient was scheduled for a follow-up visit in the neuro-ophthalmology clinic 8 weeks later. When she returned, her vision was unchanged in both eyes from the initial examination, but repeated funduscopic examination revealed diffusely pale optic discs, with sharp margins, and no swelling or atrophy (Figure 2). The retina, vessels, and choroid remained unchanged—a finding that lends support to the clinical diagnosis of PION secondary to an acute episode of hypotension and bradycardia after a calcium channel blocker overdose.

Figure 2 The right (A) and left (B) optic discs develop diffuse pallor 8 weeks after the initial diagnosis of PION.

Discussion

PION is caused by a compromised vascular supply to the intraorbital optic nerve through the posterior ciliary arteries. To our knowledge, this is the first report of PION as a consequence of calcium channel blocker overdose. Based on the patient's history, CT scan, and physical/ocular examination, PION was the most likely cause of her vision loss; however, other potential etiologies were entertained, including cortical blindness and toxic optic neuropathy. If the visual loss was secondary to cortical ischemia, pupillary responses would have been present, and the CT scan would have shown characteristic changes. According to available information about nifedipine, this medication has never been implicated as a cause of toxic optic neuropathy, although we cannot completely rule out toxicity as a potential contributor to this patient's visual loss.

One study suggests that normal doses of antihypertensive medications can lead to nocturnal arterial hypotension, which can reduce optic nerve head blood flow.⁵ The authors suggest that this mechanism may play a role in the pathogenesis of anterior ischemic optic neuropathy and glaucomatous optic neuropathy, but no mention of PION is included in the study.⁵

In contrast, another case report suggests use of calcium channel blockers at normal dosages for the treatment of ocular ischemic syndrome caused by vasospasm.⁶ Therefore, it appears that calcium channel blockers can be used to improve blood flow to the optic nerve in some conditions, but as our case suggests, a quantity large enough to cause bradycardia and hypotension can be detrimental to the optic nerve blood flow and lead to permanent visual loss.

Conclusion

PION, leading to visual loss, is a potential complication of bradycardia and hypotension secondary to a calcium channel blocker overdose. Because these medications are often prescribed for hypertension, all physicians should be aware of the possibility of PION occurring in patients who present with vision loss after ingesting quantities larger than the recommended dose.

Acknowledgment
This manuscript was supported by a grant from Research to Prevent Blindness, New York, NY.

References

1. Hayreh SS. Posterior ischemic optic neuropathy. Ophthalmologica. 1981;182:29-41.
2. Sadda SR, Nee M, Miller NR, et al. Clinical spectrum of posterior ischemic optic neuropathy. Am J Ophthalmol. 2001;132:743-750.
3. Hayreh SS, Podhajsky PA, Zimmerman B. Ocular manifestations of giant cell arteritis. Am J Ophthalmol. 1998;125:509-520.
4. Buono LM, Foroozan R, Savino PJ, et al. Posterior ischemic optic neuropathy after hemodialysis. Ophthalmology. 2003;110:1216-1218.
5. Hayreh SS, Podhajsky P, Zimmerman MB. Role of nocturnal arterial hypotension in optic nerve head ischemic disorders. Ophthalmologica. 1999;213:76-96.
6. Winterkorn JM, Beckman RL. Recovery from ocular ischemic syndrome after treatment with verapamil. Neuroophthalmol. 1995;15:209-211.