|Year : 2022 | Volume
| Issue : 1 | Page : 188-189
Inadvertent antihypertensive double dosing with concurrent Tadalafil use - A double whammy on the optic nerve!
Samuel A Minaker, Arun N E Sundaram
Department of Ophthalmology and Vision Sciences, Sunnybrook Health Sciences Center, University of Toronto, Toronto, ON, Canada
|Date of Submission||25-Apr-2021|
|Date of Acceptance||24-Aug-2021|
|Date of Web Publication||07-Jan-2022|
Dr. Arun N E Sundaram
Sunnybrook Health Sciences Center, M1202c, 2075 Bayview Avenue, Toronto, Ontario
Source of Support: None, Conflict of Interest: None
Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common acute unilateral optic neuropathy in adults over the age of 50. Nocturnal hypotension has been hypothesized as the potential cause of NAION. Phosphodiesterase type 5 inhibitor (PDE5I) has been a known cause of NAION. We report an interesting case of NAION that was triggered by inadvertent double dosing of antihypertensive medication and concurrent use of a PDE5I.
Keywords: NAION, nonarteritic anterior ischemic optic neuropathy, phosphodiesterase 5 inhibitor, Tadalafil
|How to cite this article:|
Minaker SA, Sundaram AN. Inadvertent antihypertensive double dosing with concurrent Tadalafil use - A double whammy on the optic nerve!. Indian J Ophthalmol Case Rep 2022;2:188-9
|How to cite this URL:|
Minaker SA, Sundaram AN. Inadvertent antihypertensive double dosing with concurrent Tadalafil use - A double whammy on the optic nerve!. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 Jan 28];2:188-9. Available from: https://www.ijoreports.in/text.asp?2022/2/1/188/334977
Nonarteritic anterior ischemic optic neuropathy (NAION) causes acute unilateral visual loss with associated optic disc edema. Estimated annual incidence of NAION is approximately 2.3–10 cases per 100,000., Nocturnal hypotension resulting in hypoperfusion of the optic nerve head is the hypothesized etiology. Congenital structural predisposition of a “crowded” optic nerve head, termed “disk-at-risk,” that is susceptible to inadequate perfusion and infarction is felt to play a major role in the pathogenesis. Other risk factors include advancing age, diabetes mellitus, hypertension, hypercholesterolemia, obstructive sleep apnea, perioperative hypotension, anemia, post-cataract surgery, and optic disc drusen.,,, There is a two-fold increase in the relative risk for developing NAION within two days after the use of PDE5I.
| Case Report|| |
A 60-year-old man with history of hypertension, remote cryptogenic lacunar stroke, and erectile dysfunction was referred to Neuro-Ophthalmology clinic for assessment of left optic neuropathy of two months duration. His medications included clopidogrel 75 mg daily, olmesartan 10 mg daily and tadalafil PRN. Two months prior to our assessment, the patient went on a transatlantic flight and inadvertently took two doses of olmesartan within a few hours due to the confusion with the time-zone change. After arrival at the destination, he also took tadalafil before going to sleep. The second dose of the olmesartan was taken approximately 4 hours before he went to bed. When he awoke, he noticed painless visual loss in the inferior visual field of the left eye. He also felt light-headed and measured his blood pressure to be 100/55 mm Hg, which was lower than his baseline. His inferior visual field defect worsened over the next day and it had remained stable since. Two days later, he was seen by an ophthalmologist who detected optic disc edema OS. He was referred to us after he returned home. A review of symptoms was negative and he denied any symptoms of giant cell arteritis (GCA).
His best-corrected visual acuity was 20/20 OD and 20/40 OS. He had a relative afferent pupillary defect OS. Anterior segment examination was unremarkable. Funduscopic exam revealed bilateral crowded optic discs (disk-at-risk OD) and optic disc pallor OS [Figure 1] and [Figure 2]. Visual field analysis was normal OD and showed inferior nasal defect and partial superior arcuate defect OS. His neurologic exam was normal. Temporal arteries were nontender. Serological investigations, including ESR, CRP, CBC, and autoimmune screen, were unremarkable. He was diagnosed with NAION OS. The patient was counseled regarding the risk of sequential NAION in the fellow eye. He was instructed to discontinue the tadalafil immediately and to be careful not to overdose on the olmesartan, and to avoid taking it at bedtime. We advised his family physician of our recommendations and suggested optimization of his cardiovascular risk factors.
|Figure 1: Color fundus photo of normal, crowded optic disc OD (disk-at-risk)|
Click here to view
|Figure 2: Colour fundus photo of the left eye showing small optic disc with pallor|
Click here to view
| Discussion|| |
Our patient with crowded optic discs woke up with painless visual loss OS after unintentional double-dosing of olmesartan, with additional exposure to tadalafil. He had documented optic disc edema in the acute phase, which resolved spontaneously at the time of our assessment in two months. His NAION was triggered by the hypotensive spell and the concurrent use of tadalafil.
Visual loss in NAION is typically painless. This is in contrast to inflammatory and/or demyelinating optic neuropathies where up to 92% of patients report retrobulbar pain. Up to 73% of NAION patients first notice visual loss after waking, which supports the theory of impaired autoregulation of blood pressure and nocturnal hypotension. The mechanism of NAION with the use of PDE5I is not clearly understood. It has been hypothesized that PDE5I may accentuate physiological nocturnal hypotension resulting in poor perfusion pressure of the posterior ciliary arteries that supply the optic nerve head. Another possible mechanism is the PDE5I induced activation of the nitric oxide–cyclic GMP pathway, which may decrease the perfusion of the optic nerve head or disrupt autoregulation resulting in NAION. Visual acuity is relatively preserved compared to other optic neuropathies, with one study demonstrating half of the patients examined within two weeks having visual acuity better than 20/30. Infarction of the optic nerve head in NAION happens in the watershed regions located either in the superior or the inferior poles of the optic disc, typically resulting in an altitudinal visual field defect in up to 58% of patients. Although most commonly the visual field defects are inferior, any pattern of visual field loss may be present depending on the extent of infarction of the optic nerve head. NAION will demonstrate edema of the optic nerve in the acute phase. Classically, the optic disc edema is segmental; however, diffuse edema may be present in more extensive involvement. Hemorrhages around the optic disc are common and present in up to 75% of NAION patients, whereas only 5%–15% of inflammatory optic neuropathies have hemorrhages., The optic disc edema, which is typically hyperemic, resolves over a few weeks resulting in optic disc pallor.
All patients with NAION must be screened for GCA. The management of NAION is challenging because there is no proven treatment to reverse the visual loss. The goal is to prevent sequential involvement of the fellow eye. The Ischemic Optic Neuropathy Decompression Trial demonstrated a 5-year risk of NAION recurrence in the same eye of less than 5% and in the fellow eye of 14.7%. Patients should be screened for vascular risk factors including obstructive sleep apnea. Additionally, NAION patients must be educated that hypotension, anemia, hypovolemia, and the use of PDE5I may cause sequential NAION and devastating visual loss in the good eye.
| Conclusion|| |
Our case highlighted the appalling combination of hypotension that was induced by unintended double-dosing of antihypertensive medication and the concurrent use of PDE5I in a patient with crowded optic discs. This underscores the importance of cautioning NAION patients not to overdose on antihypertensive medications and to avoid them at bedtime. It is recommended that physicians discuss the potential risk of NAION with all patients taking PDE5I and stop this medication immediately when a patient had NAION in an eye.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Levin, LA. Lessons learned from the ischemic optic neuropathy decompression trial: A decade later. Arch Ophthalmol 2007;125:1570-1.
Johnson LN, Arnold AC. Incidence of nonarteritic and arteritic anterior ischemic optic neuropathy: Population-based study in the state of Missouri and Los Angeles County, California. J Neuro-Ophthalmol 1994;14:38-44.
Riva CE, Hero M, Titze P, Petrig B. Autoregulation of human optic nerve head blood flow in response to acute changes in ocular perfusion pressure. Graefe's Arch Clin Exp Ophthalmol 1997;235:618-26.
Ischemic Optic Neuropathy Decompression Trial Study Group. Characteristics of patients with nonarteritic anterior ischemic optic neuropathy eligible for the ischemic optic neuropathy decompression trial. Arch Ophthalmol 1996;114:1366-74.
Bilgin G, Koban Y, Arnold AC. Nonarteritic anterior ischemic optic neuropathy and obstructive sleep apnea. J Neuroophthalmol 2013;33:232-4.
Gittinger Jr JW, Lessell S, Bondar RL. Ischemic optic neuropathy associated with optic disc drusen. J Clin Neuroophthalmol 1984;4:79-84.
McCulley TJ, Lam BL, Feuer WJ. Nonarteritic anterior ischemic optic neuropathy and surgery of the anterior segment: Temporal relationship analysis. Am J Ophthalmol 2003;136:1171-2.
Campbell UB, Walker AM, Gaffney M, Petronis KR, Creanga D, Quinn S, et al
. Acute nonarteritic ischemic optic neuropathy and exposure to phosphodiesterase type 5 inhibitors. J Sex Med 2015;12:139-51.
Optic Neuritis Study Group. The clinical profile of optic neuritis: Experience of the optic neuritis treatment trial. Arch Ophthalmol 1991;109:1673-8.
Hayreh SS. Erectile dysfunction drugs and non-arteritic anterior ischemic optic neuropathy: Is there a cause and effect relationship? J Neuroophthalmol 2005;25:295-8.
Hayreh SS, Zimmerman MB. Nonarteritic anterior ischemic optic neuropathy: Natural history of visual outcome. Ophthalmology 2008;115:298-305.
[Figure 1], [Figure 2]