IIDB

born_again

https://forums.moneysavingexpert.com/discussion/comment/82140762#Comment_82140762

Any history of claims for this drug on the internet. If it's such a widely used one?

Newcad

There a couple of recent FOI's about this subject on Whatdotheyknow, one to the DWP and one to the MOD. Both were refused on cost grounds.

I can't find any mention of IIDB being awarded for side effects of taking Disulfiram/Antabuse.

However in the DWP's guidance reactions to medications are not prescribed industrial diseases.

That being the case then getting an award if IIDB based on such an adverse reaction could prove problematic to say the least.

You would have to prove that the medication was prescribed or dispensed in error thus making it an accident.
If it was not prescribed or dispensed error then it was not an accident and you were simply unlucky to suffer side effects.

peteuk

https://forums.moneysavingexpert.com/discussion/comment/82140762#Comment_82140762

I’m guessing it was something along the lines of your alcoholic, attend this course or get fired. As a Civvy you were under no obligation to”orders” to compel any undertaking. You will find it hard to proof any wrong doing from a medical point of view, unless there was something in your medical history that was ignored/over looked at the time of prescription.
How long were you on the drug? Who continued to prescribe it? Did you drink whilst taking the drug?

I will be honest, I’m struggling to accept your complicated story, given my experience of military hospitals. Are you still in the area? Hospital records are kept by the hospital, eg if I was seen in Southampton General, but move to Doncaster, my record of a broken leg and surgery will stay at Southampton. My Gp will have access to the notes sent to my Gp at the time. Have you asked Portsmouth/Plymouth who ever for access to those notes?

I know his because my current Gp has all my notes, even the “Lloyd George” notes from infancy, and the 20 odd years I was Serving Her Majesty Queen Elizabeth II.

Although what your claiming may be a side effect of the drug, could it also be due to something else, lets say headaches are common side effects when taking a drug, but ultra rare side effects are hand twitching. If you have hand twitching can you say it’s solely caused by a drug you took 30 yrs ago.

MouldyOldDough

https://forums.moneysavingexpert.com/discussion/comment/82141126#Comment_82141126

The issue is that at the time - NHS did NOT have any records of me attending the alcohol course - and when I was found collapsed outside of my front door I had hit my head on the kerb - the NHS assumed that I was suffering the effects if alcohol and failed to consider any other reason.. I was in respiratory failure - my blood pressure was almost 200 - my gases were :

• PCO₂ 8.63 → extreme carbon dioxide retention
• PO₂ 6.72 → severe lack of oxygen
• Oxygen saturation 88.4% → dangerously low
• Base excess +21.4 → profound metabolic disturbance

I was dying and nobody knew the reason - It was not alcohol - these readings do not match alcohol at any level…..

My IIDB claim is not based on alcohol misuse. It is based on the proposition that the collapse which occurred in May 1990 resulted from the neurological and metabolic consequences of disulfiram treatment and withdrawal, potentially compounded by medication interactions and inadequate continuity of care.

The objective medical evidence from the time of the collapse demonstrates a severe acute physiological event rather than simple intoxication. Hospital records document acute renal impairment, profound electrolyte disturbance (including severe hyponatraemia and hypokalaemia), metabolic acidosis, markedly elevated AST, and the need for treatment with chlormethiazole (Heminevrin), carbamazepine and parenteral medication. These findings are consistent with a major neurological and metabolic crisis requiring emergency intervention.

Following this event, I sustained bilateral pallidal necrosis involving the basal ganglia. The resulting neurological deficits became permanent and affected speech, gait, coordination, handwriting and cognitive function. The severity and permanence of the injury were subsequently reflected in medical discharge, occupational health restrictions, inability to return to my original engineering duties, and long-term workplace adjustments.

The basis of my IIDB claim is therefore that a work-related sequence of events, including mandatory occupational intervention, prescription of disulfiram, subsequent neurological collapse and resulting hypoxic/toxic-metabolic brain injury, caused permanent disablement. The injury is not being presented as a consequence of alcohol consumption itself, but as a consequence of the medical and neurological events that followed treatment with Antabuse and culminated in bilateral basal ganglia injury.

In short, I am claiming IIDB because I contend that the disabling condition for which I remain impaired today originated from an employment-related incident chain in 1990, culminating in documented neurological injury and permanent functional impairment.

peteuk

I totally understand that your IIDB claim isnt for alcohol misuse. But I still believe your pinning you hopes on something that is beyond your grasp.

Long term alcohol misuse can lead to a metabolic imbalance, head injury and collapse can cause respiratory failure…

Think of it this way, when did you start the Antabuse? When was the collapse? When did you stop drinking? When did you stop taking the Antabuse? Did you drink whilst taking it?

I think you’ll have a hard time pinning the collapse onto the Antabuse? I have no doubt that the respiratory failure would have caused the issues you now face, but proving the cause of the collapse is the issue? Equally for me this is not an IIDB issue. What happens if the collapse was caused by something else (metabolic imbalance caused by long term alcohol abuse - Im not saying this is the cause, but when it comes to probability - do you have any other bloods taken at the time to disprove alcohol wasn’t a factor?

But why claim now? What have you been doing for the last 30 odd years?

Gandalf644

https://forums.moneysavingexpert.com/discussion/comment/82141948#Comment_82141948

Were you a member of a trade union as an MOD civilian, such as the PCS or Unite (or their predecessor unions) either at the time of the incident or even now as a active/retired/unemployed member?

They might be the ones to assist you, if as you say, it is work related or stems from work related.

Robbie64

All you can do is apply for IIDB and take it from there. As long as you can prove that the injury or disablement occurred in consequence of your employment then you may have a valid claim.

Did you ever pursue a medical negligence claim against the MOD?

teaselMay

Doesn't disulfram cause metabolic acidosis rather than alkalosis? (Base excess +21.4)

I think you'll struggle to argue that this was an industrial injury rather than the consequence of alcoholism even if disulfram played a part, especially if as I think was the case disulfram was pretty standard management at the time.

MouldyOldDough

https://forums.moneysavingexpert.com/discussion/comment/82142183#Comment_82142183

That's what I put :

The objective medical evidence from the time of the collapse demonstrates a severe acute physiological event rather than simple intoxication. Hospital records document acute renal impairment, profound electrolyte disturbance (including severe hyponatraemia and hypokalaemia), metabolic acidosis, markedly elevated AST, and the need for treatment with chlormethiazole (Heminevrin), carbamazepine and parenteral medication. These findings are consistent with a major neurological and metabolic crisis requiring emergency intervention.

Disulfiram is more commonly associated with metabolic acidosis, not metabolic alkalosis.

The confusion often arises because disulfiram can cause several different metabolic disturbances depending on the clinical context:

• Disulfiram toxicity/overdose has been reported to cause high anion gap metabolic acidosis, particularly in severe poisoning.
• The metabolite carbon disulfide and other toxic effects can impair cellular metabolism, potentially leading to lactic acidosis.
• If a patient develops severe vomiting after a disulfiram-alcohol reaction, they could theoretically develop metabolic alkalosis from loss of gastric acid, but that would be secondary to vomiting rather than a direct effect of disulfiram itself.

So if someone stated that disulfiram itself causes metabolic alkalosis, that would generally be inaccurate. The primary acid-base disturbance directly linked to significant disulfiram toxicity is metabolic acidosis.

MouldyOldDough

Standard Bicarbonate 2️0.4,

O₂ sat 99.1%”
• PCO₂ 6️.2️5️ kPa → respiratory compromise
• H⁺ 5️2️.2️ nmol/L → acidotic
• PO₂ 2️2️.83️ kPa → extremely high due to oxygen therapy
• HCO₃⁻ 2️0.4 mmol/L → low
• Base Excess -4.9 → metabolic acidosis
“Urea 14.1, Creatinine 2️6️6️ , Potassium 5️.2️, Sodium 13️5️”
The creatinine of 2️6️6️ μmol/L showed acute kidney stress. The urea of 14.1 mmol/L showed dehydration.

Plus - I had fractured the base of my skull.

I was released from hospital the next day - which is probably the most incredible thing of the lot.