Co-proxamol was an effective and cheap painkiller, specifically designed for chronic pain. Taken off the market because of a kneejerk reaction to it being used in a number of accidental deaths - even the academics that did the study said it should have had it's classification reviewed, not withdrawn.
People who accidentally and fatally overdosed were a) taking 10 or more at once and b) were obtaining them without a prescription.
Bring back this medicine and a lot of people currently on opioids could potentially transition back to a drug that suited them well, with few side effects and a low addiction potential.
I succeed in getting the army to stop buying co-proxamol.
The people in the army who died had all taken two tablets, with alcohol. The 'with alcohol' was the important aspect.
Those who had taken an overdose were very difficult to treat, the fatal respiratory depression could only partly be reversed with naloxone.
It was not a 'knee-jerk' reaction, it was a measured response to a dirty medication.
Toxicity[edit]
Overdose is commonly broken into two categories -
liver toxicity (from
paracetamol poisoning) and dextropropoxyphene overdose.
An overdose of dextropropoxyphene may lead to various systemic effects. Excessive opioid receptor stimulation is responsible for the
CNS depression,
respiratory depression,
aspiration pneumonia,
miosis, and gastrointestinal effects seen in propoxyphene poisoning. It may also account for
mood- or
thought-altering effects. In the presence of amphetamine, propoxyphene overdose increases CNS stimulation and may cause fatal convulsive seizures.
[13]
In addition, both propoxyphene and its metabolite
norpropoxyphene have local
anesthetic effects at concentrations about 10 times those necessary for opioid effects. Norpropoxyphene is a more potent local anesthetic than propoxyphene, and they are both more potent than
lidocaine.
[14] Local anesthetic activity appears to be responsible for the
arrhythmias and cardiovascular depression seen in propoxyphene poisoning.
[15]
Both propoxyphene and norpropoxyphene are potent blockers of cardiac membrane
sodium channels, and are more potent than lidocaine,
quinidine, and
procainamide in this respect.
[16] As a result, propoxyphene and norpropoxyphene appear to have the characteristics of a
Vaughn-Williams Class Ic antiarrhythmic.
These direct cardiac effects include decreased
heart rate (i.e. cardiovascular depression), decreased
contractility, and decreased
electrical conductivity (i.e., increased PR, AH, HV, and QRS intervals). These effects appear to be due to their local anesthetic activity and are not reversed by
naloxone.
[14][15][17] Widening of the QRS complex appears to be a result of a quinidine-like effect of propoxyphene, and
sodium bicarbonate therapy appears to have a positive direct effect on the QRS dysrhythmia.
[18]
Seizures may result from either opioid or local anesthetic effects.
[14] Pulmonary edema may result from direct
pulmonary toxicity,
neurogenic/
anoxic effects, or cardiovascular depression.
[15]
Balance disorder is possible, with risk of falls from standing height.