It cannot be emphasized enough that prior to undergoing a contrast enhanced imaging study, this applies to iodine contrast enhanced CT as much as to GBCA-enhanced MRI, the individual must be adequately hydrated prior to receiving the contrast agent. One can add to that, that the patient should not be in an acidotic state.
Over the years, and especially in regards to iodine contrast enhanced CT, with the intention of warding off contrast-induced nephropathy (CIN), a number of scientific articles have described a variety of strategies to minimize the risk of getting CIN, which have described techniques such as using N-acetyl-cysteine or sodium bicarbonate or other chemicals. I always prefer simple strategies, and somehow using chemicals to avoid other chemical adverse events seems like a less than ideal approach. In the end, my opinion is that adequate hydration is the best strategy. This certainly is effective against CIN and iodine contrast, but I also believe it has beneficial effects to mitigate against Gadolinium toxicity. I have been talking about Gadolinium Deposition Disease (GDD), so minimizing risk of severe GDD, but this approach probably does not avoid GDD completely. The question one may have is, how do I know if I am dehydrated? I recall reading an article in the New England Journal of Medicine a few years back in which essentially the conclusion was the best estimate of dehydration is that the patient is thirsty> initially I found the conclusion humorous, almost silly, because it was so simplistic, but in reality it is correct. Rather than relying on serum sodium concentration or other biochemical indicators - if the patient is thirsty they are dehydrated.
Rule #1: don't undergo contrast administration with either iodine-contrast enhanced CT or GBCA-enhanced MRI if you are thirsty. If you are thirsty, ask the technologist for something to drink, water fine (and ideal), and drink till you are no longer thirsty.
Somewhat related, it is better to not be in an acidotic state when receiving contrast, as metabolic acidosis tends to lead to worse outcomes with CIN and GDD. How to avoid this? For most individuals not engaging in strenuous activity before or immediately after a contrast enhanced CT or MR study is a simple way to avoid acidosis. This is ofcourse not so simple for individuals who by the nature of their disease: severe infection, uncontrolled diabetes, they are acidotic. This is where the concept of sodium bicarbonate is not unreasonable. A simple strategy to avoid acidosis is to drink alkalinated water - and most grocery stores offer this for sale. It may also be reasonable that patients with GDD already should as a matter of life style drink alkalinated water. Almost certainly does no harm, and most likely does some good.
Rule #2: don't engage in strenuous activity immediately prior to or after a contrast-enhanced imaging study. Consider drinking alkalinated water
Post 5: Revised Main Clinical Criteria for Gadolinium Deposition Disease
I have received some well-informed recommendations from patient experts on the disease. The revision to main criteria I am revising sooner than I had anticipated. I had wanted to change it earlier, and the reader would have noted I used 3 on atleast one occasion where I should have written 4. Observations from 2 physician sufferers have contributed to my revising these criteria as well. Here goes:
There are 5 primary clinical diagnostic findings for the Disease. In my extensive interactions with sufferers and publication of peer-reviewed studies and surveys there are 5 symptoms that stand out to me as critical. It is imperative that individuals have atleast 1 of these, and of course I prefer to see 4/ 5 to make the diagnosis absolutely certain:
1. Intense burning of the skin and skin substrate. Arising in early stage (early on after GBCA): This can be an all over feeling in the body, but often may be localized to the trunk region or distal extremities.
2. Intense boring pain in bones or joints. Arising in early stage (early on after GBCA): This can be any bones or any joints. Often the joints may be peripheral, but can also be large joints like the knee or hip. Any bones can have severe point pain, but rib pain is quite distinctive for the disease.
3. Brain fog. Arising in early stage (early on after GBCA): Many terms have been used for this: mental confusion sounds more scientific, but brain fog gets the point across well and succinctly. Brain fog is also a prominent feature of lead toxicity, which is another heavy metal toxicity. The fact that sufferers from both GDD and lead toxicity both have brain fog, tells me that this may be a feature of heavy metal poisonings in general. Practitioners should not let the name suggest that it is trivial or innocuous; brain fog can be devastating, and a number of sufferers have described that they have lost their job and livelihood because of it.
4. Muscle vibrations (muscle fasciculations) and skin pins and needles/tingling (early on after GBCA). These symptoms may represent part of the same process that is causing brain fog. Muscle vibrations/twitching and pins and needles skin sensations generally reflect nerve disease (neuropathy). My initial opinion of the pins and needles was that it was an early or lesser version of the intense skin/skin substrate burning pain (reflecting skin deposition), but on further reflection may represent a separate process of neuropathy. The subject of brain fog and my opinion of underlying cause will appear in a later blog, but relies on the concept of neural synapse dysfunction due to Gd substituting in for calcium in glutamate-based neurotransmitters. In a number of individuals this neuropathy may represent the only abnormality they experience, which suggests it may be a distinct sub-type of GDD. As I now realize that since this may be the only abnormality patients present with, it has moved from a secondary to a primary feature.
5. Distal arm and leg skin/skin substrate thickening, discoloration, and pain. Arising in the subacute stage (2 weeks +):
This is very much like the principal features of NSF, but generally less severe. Instead of woodiness, doughiness; instead of redness, pinkness; instead of extreme joint contractures, stiffness of joints and decreased range of motion. This symptom complex should be expected in these sufferers. If the major issue in NSF is prolonged retention of GBCA in patients because of advanced renal failure, why shouldn't some disturbing retention occur in subjects without advanced renal failure, and ofcourse why shouldn't lesser but similar symptoms occur if there is not significant retention, if the other critical aspect of the NSF disease is the presence of GBCAs? Although the critical aspect with NSF is that it almost only occurs with the least stable of the linear GBCAs, GDD appears to arise following all GBCAs. My opinion, because it is also related to acute hypersensitivity reactions; and represents a merger with NSF-type disease.
I want to remind readers, especially patient-experts that recognition of the disease is new, and actually even not accepted by many (perhaps the great majority) physicians. As it is new, criteria may be added or deleted, and I depend on patient-experts and other experts to help with all aspects of the disease. So do not hesitate to reach out to me if you have informed recommendations. I may not agree with your recommendations, and may disagree for a number of reasons, not all based purely on science. My goal however is to find the truth, and not what I believe (or any one person) what the truth is. One need only to reflect back on NSF and how criteria and described risks had been revised over several years. I want to arrive at solid critical criteria over a period of months, if I can, with GDD.