AMIODARONE EYE PROBLEMS

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I WAS PRESCRIBED AMIODARONE FOR AN AF CONDITION. THIS DRUG TAKES APPROX. 8 WEEKS TO BE ABSORBED BY ALL THE TISSUES IN THE BODY BEFORE IT BECOMES EFFECTIVE. AFTER 9 WEEKS, I STARTED WITH BLURRED VISION (A KNOWN SIDE-EFFECT). I CONSULTED MY GP, SHOWED HIM THE DRUG WARNING LEAFLET, WHICH STATES 'EYE PROBLEMS'. BUT HE DENIED IT WAS NOT THE DRUG. AND KEPT ME ON AMIODARONE. IT STATES IN THE BNF THAT BLINDNESS CAN OCCUR WITH THIS DRUG. I HAVE FOUND LITERATURE, FROM USA, BY DR MICHAEL ROSENBERG, WHERE HE BELIEVES THAT THE MICRO DEPOSITS OF THE DRUG CLING TO THE WALLS OF THE TINY BLOOD VESSELS, RESTRICTING THE FLOW OF BLOOD TO THE OPTIC NERVE. I AM NOW REGISTERED BLIND AND I BELIEVE THAT THE DRUG WAS RESPONSIBLE. HAS ANYBODY ELSE SUFFERED EYE PROBLEMS OR BLINDNESS AND NOT RELATED THEM TO THE DRUG?

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  • Posted

    I have just been confirmed partially blind. I have been taking amiodarone for about six months.

    My Eye doctor found it immediatly upon exam.I have ld it is not reversible been told it is perminant. I have not been given any other information other than that I will be going to a blind support clinic next month.

    i am having a real problem getting around.

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  • Posted

    Hi Professor. I was never told of the dangerous side effects of this highly toxic drug (eyes, lungs, liver and thyroid). Consequently, I did not relate my eye problems (blurred vision) to Amiodarone. My Doctor was reluctant to associate the cause of my blindness to Amiodarone for, I believe, fear of Litigation. Consequently, I was left on this drug for a further seven weeks, by which time, severe irrepairable damage was caused to my optic nerves. Even having stopped the drug, at that moment in time, the drug still remains active in your body because of the long half-life, thus still causing damage. After gathering information from the BNF, which states 'if blurred vision occurs you must stop taking the drug immediately as this can lead to blindness' and information from the internet (Dangers of Amiodarone) I decided to stop taking the drug myself. Since then, I can now relate to other vascular blood supply side effects which also occured at the same time my blurred vision started, and which, I believe, on the grounds of probability (51%), could be attributed to Amiodarone being the cause.

    YOU MUST get your Eye Doctor or yourself to report this via the Yellow Card Scheme. It is important!!

    I live in the Manchester area and if there is any way I can support you, I would love to discuss this further with you. I am a member of the North West RNIB. C.Bishop

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    • Posted

      My GP calls it a dirty drug, but it does the job. only the sight in one eye from birth. (you don't miss what have never had), but just  looking forward to getting off it. My sight has an immenual value, (Pardon the pun) Looking forward to see what the electronic boffins can do.
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  • Posted

    My wife once suggested to her doctor that he should yellow card a medication that gave her a severe allergic reaction. He said that it was not necessary as the reaction is well known. It does now show as a warning when her new doctor brings up her records.

    Soon after starting Amiodarone I developed floaters in each eye. My GP referred me to an eye specialist but in the meantime I had stopped taking it and the floaters had gone but the deposits remained.

    I went into AF again and had to go back on Amiodarone and the floaters returned. A different eye consultant said, coincidence.

    However the main problems for me with the drug are an unsteady gait and disturbed sleep. Each a similar reaction to when I was previously taking it.

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  • Posted

    This is a brief extract from a site called, dailymed on Amiodarone.

    Indications and Usage

    Because of its life-threatening side effects and the substantial management difficulties associated with its use (see “WARNINGS”below), amiodarone HCl is indicated only for the treatment of the following documented, life-threatening recurrent ventricular arrhythmias when these have not responded to documented adequate doses of other available antiarrhythmics or when alternative agents could not be tolerated.

    1. Recurrent ventricular fibrillation.

    2. Recurrent hemodynamically unstable ventricular tachycardia.

    As is the case for other antiarrhythmic agents, there is no evidence from controlled trials that the use of amiodarone favorably affects survival.

    Amiodarone should be used only by physicians familiar with and with access to (directly or through referral) the use of all available modalities for treating recurrent life-threatening ventricular arrhythmias, and who have access to appropriate monitoring facilities, including in-hospital and ambulatory continuous electrocardiographic monitoring and electrophysiologic techniques. Because of the life-threatening nature of the arrhythmias treated, potential interactions with prior therapy, and potential exacerbation of the arrhythmia, initiation of therapy with amiodarone should be carried out in the hospital.

    Contraindications

    Amiodarone HCl is contraindicated in severe sinus-node dysfunction, causing marked sinus bradycardia; second- or third-degree atrioventricular block; and when episodes of bradycardia have caused syncope (except when used in conjunction with a pacemaker).

    Amiodarone HCl is contraindicated in patients with a known hypersensitivity to the drug or to any of its components, including iodine.

    Warnings

    Amiodarone HCl is intended for use only in patients with the indicated lifethreatening arrhythmias because its use is accompanied by substantial toxicity.

    Amiodarone has several potentially fatal toxicities, the most important of which is pulmonary toxicity (hypersensitivity pneumonitis or interstitial/alveolar pneumonitis) that has resulted in clinically manifest disease at rates as high as 10 to 17% in some series of patients with ventricular arrhythmias given doses around 400 mg/day, and as abnormal diffusion capacity without symptoms in a much higher percentage of patients. Pulmonary toxicity has been fatal about 10% of the time. Liver injury is common with amiodarone, but is usually mild and evidenced only by abnormal liver enzymes. Overt liver disease can occur, however, and has been fatal in a few cases. Like other antiarrhythmics, amiodarone can exacerbate the arrhythmia, e.g., by making the arrhythmia less well tolerated or more difficult to reverse. This has occurred in 2 to 5% of patients in various series, and significant heart block or sinus bradycardia has been seen in 2 to 5%. All of these events should be manageable in the proper clinical setting in most cases. Although the frequency of such proarrhythmic events does not appear greater with amiodarone than with many other agents used in this population, the effects are prolonged when they occur.

    Even in patients at high risk of arrhythmic death, in whom the toxicity of amiodarone is an acceptable risk, amiodarone poses major management problems that could be life-threatening in a population at risk of sudden death, so that every effort should be made to utilize alternative agents first.

    The difficulty of using amiodarone effectively and safely itself poses a significant risk to patients. Patients with the indicated arrhythmias must be hospitalized while the loading dose of amiodarone is given, and a response generally requires at least one week, usually two or more. Because absorption and elimination are variable, maintenance-dose selection is difficult, and it is not unusual to require dosage decrease or discontinuation of treatment. In a retrospective survey of 192 patients with ventricular tachyarrhythmias, 84 required dose reduction and 18 required at least temporary discontinuation because of adverse effects, and several series have reported 15 to 20% overall frequencies of discontinuation due to adverse reactions. The time at which a previously controlled life-threatening arrhythmia will recur after discontinuation or dose adjustment is unpredictable, ranging from weeks to months. The patient is obviously at great risk during this time and may need prolonged hospitalization. Attempts to substitute other antiarrhythmic agents when amiodarone must be stopped will be made difficult by the gradually, but unpredictably, changing amiodarone body burden. A similar problem exists when amiodarone is not effective; it still poses the risk of an interaction with whatever subsequent treatment is tried.

    Mortality

    In the National Heart, Lung and Blood Institute’s Cardiac Arrhythmia Suppression Trial (CAST), a long-term, multi-centered, randomized, double-blind study in patients with asymptomatic non-life-threatening ventricular arrhythmias who had had myocardial infarctions more than six days but less than two years previously, an excessive mortality or non-fatal cardiac arrest rate was seen in patients treated with encainide or flecainide (56/730) compared with that seen in patients assigned to matched placebo-treated groups (22/725). The average duration of treatment with encainide or flecainide in this study was ten months.

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  • Posted

    Hi all..

    I have the same problem. I've been on this medication since November. My eyesight has become so bad I need to ware glasses just to read. Went to my eye clinic for a checkup a couple weeks back, they told me I might lose the sight in my right eye if I don't get things under control. I didn't think of the connection back then.This drug is responsible for so many of the know side effects in me & it seems in others. The problem is, it's hard to get off these meds, even with all the side effects. Doctors don't listen and think we're all going mad, in the meanwhile our lives are turning to mud.

    I'm also on Sotalol, which seems to be responsible for giving me Prinzmetal Angina..

    ARrggghhhh!! If anyone finds a way off this stuff, write in..

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  • Posted

    I was prescribed Amiodarone April of 2015 for my A Fib conditon. I have worn glasses for the past 20 years with the prescription changing only slightly from year to year. But since Amiodarone, I've been getting slightly blurred vision in gthe left eye and am having trouble getting my new eye glass prescription fitted correctly. And all of a sudden I've gone from normal eye pressure to pressure reading in the 20's. Have just seen an opthamologist and was told I am probably in the early stages of Glaucoma. There has been no history of it in my family and the Dr. told me to check all my meds.for such warnings. Sure enough! Amiodarone warns it may cause blindness. I'm stopping the Amiodarone. I will deal with the A Fib rather than go blind.
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  • Posted

    Amioderone made my mum legally blind.    She went to Wills Eye Hospital in Philadelphia, USA and they told her to get off it immediately.   Pale optic nerves - amioderone toxicity......   Very sad....
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    • Posted

      I woke up one morning early this year suddenly rather short sighted and slightly out of focus. It gradually wore off after two or three days. I had an appointment at the eye hospital during that time and they noted the change in my sight from after checks when I had cataract surgery the year before.

      The suggestion was it had been a type of neuropathy caused by a sudden drop in BP or a glucose surge during the night. They also noted that the optic nerves were pale. They asked what medications I was taking but I did not go back to discontinued ones like Amiodarone

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  • Posted

    My mother in America is now legally blind due to amioderone....     It states in her medical records amioderone toxicity.....   Sue........     We were too late.   You must sue within two years of taking the drug.   Her optic nerve specialist said he would have given a deposition......
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  • Posted

    Statute of limitations.   That's what the lawyers said......
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    • Posted

      In the UK for 'injury' it is two years. In America it varies sate by state from one to six years. In PA it is two years but it seems no time at all and we seem to hear of people joining Class Actions over long periods.
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