AMIODARONE EYE PROBLEMS
Posted , 15 users are following.
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?
1 like, 20 replies
professor
Posted
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.
KARAOKE
Posted
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
stewart79639 KARAOKE
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derek76
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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.
derek76
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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.
The_Conductor
Posted
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..
roger8547 KARAOKE
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roberta_51995 roger8547
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Sassyfrass KARAOKE
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derek76 Sassyfrass
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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
Sassyfrass KARAOKE
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derek76 Sassyfrass
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Sassyfrass KARAOKE
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derek76 Sassyfrass
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Sassyfrass KARAOKE
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