Patient with OP poisoning - letter to GP

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Since adding this anonymised letter to my website, I have further developed my treatment of OP poisoning. Please see these 2 links for further detail:

Although from the 1990's, and even though much has moved on in terms of treatment, it is still very useful to read a case study, as below, to gain further insight into the causes and presentation of OP poisoning.

Text of letter to GP

J came over to see me with his wife because I have a particular interest in organophosphate poisoning. I have now seen many farmers and other such people who have been occupationally exposed to organophosphates and I am beginning to understand some of the problems and complications.

The first point is that J has been substantially exposed to organophosphates and other pesticides throughout his farming career. As a child and a young man he regularly helped on the farm dipping sheep and handling them. During these early years dieldrin an organochlorine would have been used. Organochlorines have less toxicity in the short term, but are cumulative poisons and this is why they were withdrawn from the market. During the late 1970s they were replaced by organophosphate dips, which not only contained OPs but many other equally toxic compounds. These include the industrial solvents, glycol esters, epichlorhydrin, phenols, cresols and thiram (this inhibits liver enzymes turning all farmers into slow metabolisers). Furthermore, the OPs used in these dips were inherently unstable and broke down to form even more toxic impurities. Furthermore, work by Vyvyan Howard demonstrated that these cocktails of chemicals are very much more toxic than the parent compounds. As a result, the formulation of sheep dip was changed in the 1990s and then all these products were subsequently withdrawn from the market so that whilst there were originally 274, there are now only two.

Furthermore, J was investigated by Professor Nicola Cherry who demonstrated that he was a slow metaboliser and that this is genetically determined. J has both genes that result in low levels of paraoxonase, which means that his system is inefficient at clearing OPs from the blood. This means that any OP which gets into the system persists for much longer than normal.

Because J has been a large scale sheep farmer with anything up to 700 ewes and followers, he has been daily exposed to OPs as a result of normal farming sheep handling activities. This is because OPs persist in the wool (which gives them long lasting protection against ectoparasites) and they are readily inhaled and absorbed through the skin by humans.

It is this combination of facts which explains why sheep dippers are so much worse affected by OPs than other members of the farming profession or people in other occupations. His exposure would not have been helped by a fire in 1986 where the only available liquid to extinguish the flames was sheep dip remaining in the bath and obviously there would have been substantial exposure then.

However, his clinical problems began in October 1986 when he was admitted with chest pain and pins and needles in his left arm. At that time there was no evidence of ischaemia, with normal cardiac enzymes and no ischaemic change on his EEG. However, monitoring in the hospital did show episodes of ventricular tachycardia and I have no doubt that it was this which caused his chest pain (he was diagnosed at the time as being angina). Obviously a VT would drop the blood pressure and reduce coronary artery perfusion. Organophosphate chemicals are extremely toxic to the heart and cardiac arrhythmias are a well recognised complication of poisoning. Unfortunately this was not recognised at the time, but I have little doubt that this was the cause of his dysrhythmia. Although he was a very modest smoker, there were no other risk factors for arterial disease. Furthermore, since that episode he has not had any further chest pain. This accords with him reducing his farming activities and therefore reducing his exposure to organophosphate pesticides. Indeed he estimates his last exposure to OPs was in 1988, since when he has had no arrhythmias.

I know that he should have had an angiogram immediately after this admission, but this was overlooked. If as I believe the dysrhythmia was caused by poisoning and not arteriosclerosis, then there would have been no indication for angiography anyway, so perhaps this was a fortuitous oversight!

On discharge from the hospital J was prescribed atenolol, which gave him a profound bradycardia of 40 beats per minute. Again this reaction to atenolol may well have been exacerbated by OP poisoning. He certainly felt very much better for stopping atenolol. At the time of his admission no murmurs were noted.

J gradually recovered from this episode, but has increasingly developed many of the symptoms suggestive of a chronic fatigue syndrome, namely quite marked physical fatigue, muscle fatigueability and weakness, cognitive dysfunction (which means that he has poor short term memory and great difficulty acquiring new information, sometimes difficulty word finding and following a line of argument) and also painful and aching muscles. All activities have to be carefully paced and if he overdoes things then he pays for it.

However, during the past ten years another problem has arisen. In addition to the above he has developed increasing shortness of breath and orthopnoea and two years ago at a routine examination it was noticed to have a pan systolic murmur. Obviously in the last ten years he has developed a mitral incompetence and as a result has mild left sided heart failure. On examination he had a clear pan systolic murmur, loudest in the mitral area, but I could not hear a diastolic murmur and do not think he has mitral stenosis as well. He also had fine creps at both bases suggesting early left ventricular failure, but has never had ankle oedema suggesting the right side of the heart is functioning normally.

So this begs the question as what is causing his mitral incompetence? His father suffered from the same problem, but had rheumatic fever, but there is no other family history of heart problems. I think it is quite likely that J is magnesium deficient – this is a feature of patients with fatigue syndromes and OP poisoning and I have sent off blood to look at this. Selenium deficiency is also associated with cardiomyopathy and again I have sent off bloods to check this. The only risk factor which has not been checked for arterial disease is homocysteine and again I have looked for this. I will write again with the results.

The next point is that his chronic fatigue syndrome needs treating and I have a fairly structured work up to doing this. Nutritional tests frequently show deficiencies of B vitamins, zinc and magnesium, and I have recommended the appropriate supplements. Boron is necessary for normal calcium and magnesium metabolism and may well explain why so many of my patients with muscle aching do well on this and so I have added this into his regime.

I have become interested in work done by Dr Gordon Skinner, Consultant Physician, at Birmingham who has been treating CFS patients with low dose T4. He has found that many of these patients have T4 levels at the low end of the normal range, which correlates well with their clinical picture. Furthermore some patients fail to convert inactive T4 to active T3. By giving small amounts of T4, 50-100mcgms and/or T3, he brings their thyroid hormones into the higher normal range and patients feel much better as a result. I have taken blood and will let you have a copy of the result.

Fatigue can certainly be caused by diet and in my experience the four common influences are carbohydrates during the day, food intolerance, gut dysbiosis and chemicals. I have developed a diet which encompasses all these factors and I would like J to try this.

B12 is now widely used to treat chronic fatigue syndrome. It is thought to be helpful because it improves the liver's ability to deal with xenobiotic chemicals. B12 can be used in two ways - in physiological doses to treat pernicious anaemia. In this case, serum levels are low. However it can be used in much higher pharmacological doses (say 2-6mgs a week) to treat fatigue. Clearly in this case blood levels are going to be normal and it is pointless to measure them. B12 is extremely safe, there are no documented cases of overdose in the literature. Many of my patients inject themselves with B12 and adjust the dose themselves according to their response. Please, would you consider trying this?

Finally, we now know that patients with chronic OP exposure are at greater risk of osteoporosis and I do think J should be referred for a bone density scan and I would be grateful if you would do this. Dr Michael Davie, Consultant Radiologist at Oswestry has a particular interest in the osteoporosis for OP poisoning and I would be grateful if you could refer J there.

I will write again when the results of the bloods come through.

Yours sincerely,

Enc to patients: Test results, CFS diet sheet, Nutritional supplement handout

Enc to GP: Skinner letter to BMJ re: hypothyroidism

cc: J

  • J's thyroid test results are now back showing:

Free T3 - 4.8 (2.3 to 4.9) pmol/L

Free T4 - 17.1 (11.5 to 23.0) pmol/L

TSH - 0.6 (0.4 to 4.5) mU/L

These results are normal and no action is required in this respect.

  • The Plasma Homocysteine result is back at 9.8 (4.50 – 12.5) umol/L. This is also a normal result and no action is necessary.
  • The red cell results are back showing:

Red Cell Magnesium 2.00 mmol/l (2.08 to 3.00)

Red Cell Selenium 81 ug/l (66 to 132)

The selenium result is fine, but the magnesium is low. Initially I would suggest increasing the minerals EAP to four capsules daily. I hope this will improve levels and I would like to recheck in three months time. Magnesium deficiency may be a cause of mitral valve prolapse (see enclosed) and it would be very interesting if cardiac function could be improved by increasing the magnesium level.

Supporting External Links to the text of the letter

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