Citation Nr: 18141431 Decision Date: 10/10/18 Archive Date: 10/10/18 DOCKET NO. 16-05 142 DATE: October 10, 2018 ORDER Compensation benefits pursuant to 38 U.S.C. § 1151 for nonarteritic ischemic optic neuropathy (NAION) of both eyes (bilateral visual disorder) is denied. FINDINGS OF FACT 1. The Veteran’s bilateral NAION, resulting in visual field defect in both eyes, is not actually caused by VA medical treatment, to include treatment with Amiodarone therapy. 2. The Veteran’s bilateral NAION is not due to negligence, lack of proper skill, error in judgment, or similar instance of fault on the part of VA in furnishing medical care. 3. Visual defect is a known side effect of Amiodarone therapy. 4. The Veteran’s bilateral NAION is not due to an unforeseen event. CONCLUSION OF LAW The criteria for compensation benefits under 38 U.S.C. § 1151 for causation or aggravation of a claimed additional disability of a bilateral visual disorder (NAION) have not been met. 38 U.S.C. §§ 1151, 5103, 5103A; 38 C.F.R. §§ 3.102, 3.154, 3.159, 3.361, 3.800. REASONS AND BASES FOR FINDING AND CONCLUSION The Veteran, who is the Appellant, served on active duty from April 1973 to April 1977. This matter comes before the Board of Veterans’ Appeals (Board) on appeal from a January 2012 rating decision from the Regional Office (RO), which, in pertinent part, denied compensation pursuant to 38 U.S.C. § 1151 for a bilateral visual disorder. In this case, the Veterans Claims Assistance Act of 2000 (VCAA) notice requirements were satisfied by way of the September 2010 notice letter. The VCAA duty to assist has been met in this case. The complete service treatment records and all identified post-service treatment records are associated with the record, and a VA medical opinion was provided in July 2015, with adequate rationale. In the March 2012 Notice of Disagreement (NOD), the Veteran argued that “the compensation examination is errored and false in statement” as he now has very limited peripheral vision; however, a review of the record reflects that no VA compensation and pension examination (VA examination) had been rendered prior to the March 2012 NOD, or since receipt of the March NOD. In this case, a VA examination is not necessary, as the evidence of record establishes a current visual disability. Moreover, a VA medical opinion was obtained in July 2015, which addresses causation and the question of negligence or similar fault of VA in administering medical treatment. The VA medical opinion is supported by adequate rationale and notes a current peripheral vision defect, to include an altitudinal visual defect. As such, there appears to be no specific bases for the Veteran’s contention that a VA examination is in error, false, or otherwise inadequate, so no further development is necessary. 1. Entitlement to Compensation under 38 U.S.C. § 1151 Compensation under the provisions of 38 U.S.C. § 1151 shall be awarded for a qualifying additional disability or a qualifying death of a veteran in the same manner as if such additional disability or death were service-connected. A disability is a qualifying additional disability if (1) the disability was not the result of the veteran’s willful misconduct; (2) was caused by hospital care, medical or surgical treatment, or examination furnished to the veteran under any law administered by VA either by a VA employee or in a VA facility; and (3) the proximate cause of the disability was carelessness, negligence, lack of proper skill, error in judgment, or similar instance of fault on the part of VA in furnishing the hospital care, medical or surgical treatment, or examination; or an event not reasonably foreseeable. In determining whether a veteran sustained additional disability, VA compares his or her condition immediately before the beginning of the hospital care or medical or surgical treatment upon which the claim is based to his or her condition after such care or treatment has stopped. 38 C.F.R. § 3.361(b). To establish causation, the evidence must show that the hospital care or medical or surgical treatment resulted in the veteran’s additional disability or death. Merely showing that a veteran received care or treatment and that the veteran has an additional disability, or died, does not establish cause. 38 C.F.R. § 3.361(c)(1). Hospital care or medical or surgical treatment cannot cause the continuance or natural progress of a disease or injury for which the care or treatment was furnished unless VA’s failure to timely diagnose and properly treat the disease or injury proximately caused the continuance or natural progress. 38 C.F.R. § 3.361(c)(2). Additional disability or death caused by a veteran’s failure to follow properly given medical instructions is not caused by hospital care, medical or surgical treatment, or examination. In addition, the proximate cause of death is the action or event that directly caused the death, as distinguished from a remote contributing cause. 38 C.F.R. § 3.361(c)(3). To establish that carelessness, negligence, lack of proper skill, error in judgment, or similar instance of fault on VA’s part in furnishing hospital care, medical or surgical treatment, or examination proximately caused a veteran’s additional disability or death, it must be shown that the hospital care or medical or surgical treatment caused the veteran’s disability or death; and (1) VA failed to exercise the degree of care that would be expected of a reasonable health care provider; or (2) VA furnished the hospital care or medical or surgical treatment without the veteran’s informed consent. 38 C.F.R. § 3.361(d)(1). Determinations as to whether there was informed consent involve consideration of whether the health care providers substantially complied with the requirements of 38 C.F.R. § 17.32. Minor deviations from the requirements of 38 C.F.R. § 17.32 that are immaterial under the circumstances of a case will not defeat a finding of informed consent. 38 C.F.R. § 3.361(d)(1). Whether the proximate cause of an additional disability was an event not reasonably foreseeable is in each claim to be determined based on what a reasonable health care provider would have foreseen. The event need not be completely unforeseeable or unimaginable, but must be one that a reasonable health care provider would not have considered to be an ordinary risk of the treatment provided. In determining whether an event was reasonably foreseeable, VA will consider whether the risk of that event was the type of risk that a reasonable health care provider would have disclosed in connection with the informed consent procedures of 38 C.F.R. § 17.32. See 38 C.F.R. § 3.361(d)(2). The Veteran contends that the bilateral visual defect is due to medical treatment prescribed by VA. Specifically, the Veteran contends that Amiodarone prescribed to treat his non-service-connected heart disorder caused a stroke in his right eye. The Veteran argues that, once the VA cardiologist and physicians from the eye clinic assessed the effect of Amiodarone therapy on his right eye, VA should not have resumed treating his heart disorder with the medication, as resuming Amiodarone therapy subsequently caused a stroke in the left eye. See March 2012 NOD, July 2012 Statement in Support of the Claim. After a review of all the evidence, both lay and medical, the Board finds that the weight of the evidence is against finding that the Veteran’s bilateral visual disorder (NAION) was actually caused by VA hospitalization, medical or surgical treatment, submission to an examination, or the pursuit of a course of vocational rehabilitation. The record reflects that the Veteran has a medical history that is significant for hypertension, atrial fibrillation, cardiac arrhythmia, impaired fasting glucose, sleep apnea, and morbid obesity, among other comorbid medical conditions. See February 2009, and May 2012 VA treatment records. The evidence shows that the Veteran was started on Amiodarone therapy for non-service-connected cardiac disorder in January 2009, as such a baseline eye examination was conducted in February 2009 due to initiation of Amiodarone therapy. The February 2009 eye examination showed 20/20 visual acuity with presbyopia, but no ocular side effects of Amiodarone therapy. The treatment note reflects that new glasses were ordered and the Veteran was educated and advised to return in six months for a follow up examination of color vision and dilation. See February 2009, June 2008 VA treatment records. During a June 2009 optometry follow up, the Veteran initially reported a one-month onset of superior altitudinal visual field loss in the right eye with no symptoms in the left eye, but a June 2009 addendum note reflects that the Veteran clarified that he had a rapid onset of visual field loss in the right eye. Visual acuity remained 20/20 in both eyes on examination. The assessment was acute NAION in the right eye and Amiodarone therapy with vortex keratopathy of both eyes, for which Alphagan eye drops were prescribed and a follow up of right-sided temporal artery biopsy was planned. The June 2009 addendum note reflects that a question of Amiodarone-induced optic neuropathy was raised, but suspicion for this condition was deemed low because a more insidious onset with color vision loss bilaterally would have been expected in such a case. The June 2009 treatment note reflects that primary care and cardiology would be contacted regarding the findings. See June 2009 VA treatment records. July 2009 treatment notes reflect that cardiology agreed that the likelihood of Amiodarone toxicity was low, but recommended follow up with Amiodarone panel and discontinuance of Amiodarone therapy if there was any change in the contralateral eye. See July 2009 VA treatment record. After the July 2009 temporal artery biopsy and Amiodarone panel, the Veteran reported improving visual field defect in the superior temporal field of the right eye, but worsening visual field defect in the nasal and inferior visual field of the right eye. No visual defects were reported in the left eye and the temporal artery biopsy was negative. The July 2009 follow up note indicated that multiple blood pressure medications and Amiodarone use were both risk factors for NAION. The optometry clinic note indicates that while Amiodarone-induced optic neuropathy was controversial, the eye clinic would advise cardiology and primary care that discontinuance of the medication would be beneficial from an ophthalmology standpoint. In November 2009, cardiology discontinued Amiodarone therapy. The record reflects that the Veteran was admitted January 19, 2010 through January 22, 2010 for uncontrolled atrial flutter, and suspected congestive heart failure with secondary diagnoses of hypertension, impaired glucose, and severe obstructive sleep apnea. Amiodarone therapy was resumed during the hospital admission. See January 2010 VA treatment records. In May 2010, the Veteran reported an acute onset of blurred vision, floaters, and flashes in the left eye over the past week. Upon examination, the Veteran was assessed to have acute ischemic optic neuropathy of the left eye, which was previously noted in the right eye; however, the VA optometrist again noted that Amiodarone tends to cause a more indolent optic neuropathy. See May 2010 VA treatment records. Additional work up regarding bilateral NAION revealed a normal MRI of the brain, and stable visual acuity in both eyes with normal color vision; however, the eye clinic advised that it would be beneficial to discontinue of Amiodarone therapy from and optometry standpoint to avoid compound optic nerve damage given NAION in both eyes and advised cardiology to evaluate whether this was possible. Thereafter, cardiology discontinued Amiodarone therapy in July 2010. See May 2010, June 2010, July VA treatment records. A December 2011 treatment note reflects that the Veteran reported stable vision in both eyes and denied any problems with floaters or flashes of light in both eyes. A May 2012 follow up optometry note reflects that the Veteran had NAION in both eyes with stable visual field defects and a history of Amiodarone therapy with vortex keratopathy. See December 2011, May 2012 VA treatment records. To the extent that the Veteran has asserted that the current bilateral visual disorder is caused by Amiodarone use, the evidence does not demonstrate that the Veteran possesses the knowledge, training, or experience to provide a competent medical opinion regarding the etiology of ocular system disorders such as NAION. The etiology of the Veteran’s bilateral visual loss symptoms is a complex medical etiological question dealing with the origin and progression of the ocular system, and such a disability is diagnosed primarily on clinical findings and physiological testing; thus, while the Veteran is competent to relate bilateral eye symptoms experienced at any time, under the facts of this case, the Veteran is not competent to opine as to whether or not Amiodarone use was due to any fault on the part of VA. See Moray v. Brown, 5 Vet. App. 211 (1993) (regarding causation of retinitis pigmentosa, veteran’s testimony of aggravation of pre-existing disability in service was not competent evidence of aggravation, which was medical in nature). Moreover, the evidence of record reflects that although VA optometrist and cardiologist considered the potential effects of Amiodarone therapy in evaluating and treating the Veteran’s acute onset of a bilateral visual disorder, VA physicians noted that suspicion of Amiodarone-induced optic neuropathy was low, as the evidence did not show an insidious onset of symptoms with defective color vision bilaterally as would be expected. See June 2009, May 2010 VA treatment records. Moreover, VA physicians noted that use of multiple blood pressure medications was also a risk factor for NAION, and the record reflects a medical history that is significant for hypertension, which has been treated with Diltiazem, Hydrochlorothiazide, and Valsartan for management of blood pressure in addition to Amiodarone and Digoxin for cardiac disorders. See February 2009, June 2009, July 2009 VA treatment records. The July 2015 VA examiner’s opinion also supports a finding that there is no proximate causal link between Amiodarone use and the current bilateral visual loss disorder. The VA examiner assessed that Veteran has what appears to be classic NAION on the right eye in 2010 and the left eye in 2010. The VA examiner explained that risk factors for NAION include hypertension, diabetes, smoking, hyperlipidemia, possibly sleep apnea, and crowded optic disc, many of which Veteran has; his medical history is significant for hypertension, diabetes, atrial fibrillation, coronary artery disease, and sleep apnea. Moreover, medical literature reflects that over a five-year period patients who have had NAION in one eye have a 12 to 19 percent chance of developing NAION in the other eye. The VA examiner further noted that, while Amiodarone-associated optic neuropathy is a known entity, the most common presentation is an insidious onset unlike the acute onset the Veteran had. Furthermore, the Veteran retained normal color vision, which is less common with toxic optic neuropathies; and examination and test findings were similar to patients with NAION that never used Amiodarone. See July 2015 VA examination report. Considering the above, the Board finds that the evidence does not support a finding that the bilateral NAION was actually caused by Amiodarone use. Even if the current bilateral NAION/visual loss disorder was caused by Amiodarone, use the visual defect is a known possible side effect of Amiodarone therapy. The fact that visual defect is a known complication of Amiodarone therapy is supported by treatment notes that reflect that the Veteran underwent a baseline eye examination in February 2009 specifically due to the initiation of Amiodarone therapy in January 2009. The February 2009 treatment note reflected that the Veteran had no Amiodarone-associated ocular side effects at that time and that the Veteran was educated and advised to follow up within six months or sooner to evaluate color vision and dilation going forward, which is further evidence that visual defect was a known side effect of Amiodarone therapy. See February 2009 VA treatment record. Additionally, when the Veteran initially reported symptoms of visual field defects in the right eye in June 2009 and in the left eye in May 2010, VA optometrists immediately identified Amiodarone therapy as a potential risk factor for the visual defect, and Amiodarone use was also listed as a risk factor of NAION, among other risk factors, on a July 2009 VA treatment note while the VA eye clinic was actively monitoring and treating the new onset of visual defect. See June 2009, July 2009, May 2010, June 2010, July 2010 VA treatment records. Moreover, the July 2015 VA examiner opined that Amiodarone-associated optic neuropathy is a known side effect of Amiodarone use, although no actual causal link between Amiodarone use and the current bilateral NAION was assessed. See July 2015 VA examination report. The Board finds that the Veteran’s bilateral NAION and the resulting visual field loss was not due to negligence, lack of proper skill, error in judgment, or similar instance of fault on the part of VA in furnishing medical care. In other words, the complication was not caused by VA’s failure to exercise the degree of care that would be expected of a reasonable health care provider. As discussed above, VA physicians arranged for the Veteran to undergo baseline eye examination within one month of initiating Amiodarone therapy. When the Veteran reported an acute development of visual field defect in the right eye in June 2009, VA optometrist identified Amiodarone use as a potential risk factor in the development of the visual loss disorder and conducted a work up of the visual loss symptoms, to include a temporal artery biopsy, which was negative. VA optometrist also notified VA cardiology of the new findings on examination and both agreed to discontinue the medication despite low suspicion that Amiodarone use caused the NAION given testing and examination findings. See February 2009 through November 2009 VA treatment records. The Veteran contends that VA should not have resumed Amiodarone use in January 2010 to treat his cardiac disorder because the medication was known to have caused a visual defect in the right eye a year earlier; however, as previously discussed, the Veteran is a lay person and, under the facts of this particular case, does not have the requisite medical training or credentials to be able to render a competent medical opinion regarding whether the NAION/ loss of vision was caused by any fault on the part of VA physicians. The etiology of the Veteran’s bilateral eye symptoms is a complex medical etiological question dealing with the origin and progression of the ocular system, and such a disability is diagnosed primarily on clinical findings and physiological testing. Thus, while the Veteran is competent to relate bilateral eye symptoms experienced at any time, under the facts of this case, the Veteran is not competent to opine as to whether or not the medication residuals were due to any deficiency on the part of the VA physician in administering treatment. See Moray, 5 Vet. App. 211 (regarding causation of retinitis pigmentosa, veteran’s testimony of aggravation of pre-existing disability in service was not competent evidence of aggravation, which was medical in nature). The record reflects Amiodarone therapy was resumed in January 2010 due the Veteran’s acute onset of chest discomfort, atrial flutter, and possible congestive heart failure; however, when the Veteran reported an acute onset of left eye visual field loss months after resuming Amiodarone therapy, the VA eye clinic again did a work up of the symptoms, to include an MRI of the brain that was normal, and coordinated care with cardiology to assess whether it was safe to discontinue the medication from a cardiology standpoint to prevent potential exacerbation of optic neuropathy in both eyes. After coordinating care between the eye clinic and cardiology, VA physicians discontinued Amiodarone use and continued to monitor symptoms of visual field loss in both eyes in the following years. See January 2010, May 2010-August 2010 VA treatment records. The July 2015 VA examiner opined that the eye exams, treatment, and recommendation were all well within the standard of care because the conditions were promptly recognized and addressed, which included recognizing that the Veteran was prescribed Amiodarone during both events and that the use of this medication needed to be addressed by its prescribers, the VA cardiologist. The VA examiner explained that the prescribers of Amiodarone would have the necessary expertise to determine the cardiac/life threatening risk of discontinuing Amiodarone, and that reasonable care was exercised by the VA physicians under the facts of this case. See July 2015 VA examination report. Based on the foregoing, the Board finds that the weight of the evidence of record is against finding that the bilateral visual loss disorder was caused by medication provided by VA, or any other VA hospitalization, medical or surgical treatment, submission to an examination, or pursuit of a course of vocational rehabilitation. The evidence of record reflects that bilateral NAION, with subsequent loss of vision, although not caused by Amiodarone use, even though it is a well-known risk of Amiodarone therapy. Further, the VA treatment reports concerning the acute onset of bilateral NAION reflect that Amiodarone was immediately identified as medication the Veteran was prescribed, and the appropriate treatment, recommendations, and coordination of care with the prescribers was administered before the medication was discontinued. For these reasons, the Board finds that a preponderance of the evidence is against the claim for VA benefits under 38 U.S.C. § 1151 for claimed disability of bilateral NAION (visual loss disorder), and the claim must be denied. 38 U.S.C. §5107(b); 38 C.F.R. § 3.102. J. PARKER Veterans Law Judge Board of Veterans’ Appeals ATTORNEY FOR THE BOARD S. Moore, Associate Counsel