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Gastrointestinal Adverse Effects in GDD. And a few words on noncontrast MRI diagnosis.

A very common complex of symptoms in GDD relates to the entire digestive system - top to bottom. Frequently complaints are vomiting, abdominal pain, diarrhea, and constipation. The core issue is that Gd can insert itself in place of Ca in the actin/myosin physicochemical process, which is involved not only in striated muscles (like biceps) causing fasciculations, but in smooth muscle throughout the entire digestive tract. This causes a true sabotage, and interrupts/ delays any or all segments of the digestive system so rather than the normal antegrade propulsion of bowel contents, known as peristalsis, there is varying levels of delayed passage, from slowing, known as hypotonia, to paralysis, known as ileus. Stomach is a common organ to experience paralysis and this is termed gastroparesis. Gastroparesis can be truly awful: in most sufferers with gastroparesis they will say, I will take severe pain any day over gastroparesis, it can be unbearable.

Although it has not been described, it is conceivable that the delayed passage through small bowel may not simply be slow peristalsis but may also involve comparable features as seen in striated muscle, which is fasciculations,

One of the most deadly consequence of ileus is in the small bowel: small bowel bacterial overgrowth, which can result in sepsis and death. If small bowel does not maintain the forward peristalsis, it allows for bacteria from the colon to creep back into the small bowel reeking havoc. Fortunately this complication is rare in GDD.

Constipation of the colon of varying severity can also occur.

Constipation can be due to various stages of GDD: the primary disease, and also the consequence of redistribution (with a poor chelator) but also re-equilibration, even with an effective chelator. The constipation secondary to re-equilibration with an effective chelator almost always resolves. It seems for many re-equilibration issues (GI, vision, cardiac arrhythmias) chelation # 8 seems to be the turning point to recovering for these. Steroid use may also add to this, that is also one of the major reasons that I progressively reduce the amount of steroids with successive chelations, and never have patients on continuous steroids.

For many adverse findings during the course of chelation, it can be difficult to sort out the contribution of the primary disease, re-equilibration, or steroids. Overall I treat the vagaries of these possibilities by continuing chelation to certain pause points (that the number of GBCA injections help determine) which may be 10 or 15 chelations, while simultaneously decrease the amount of steroids with subsequent chelations.

Effective treatment does involve some level of nuance, which can at times be enormous.

MRI and the digestive tract.

As perhaps the most experienced radiologist on the general topic of bowel MRI, a few words on that does seem appropriate.

Noncontrast MRI is very effective at elucidating many aspects of bowel.

Motility. It is possible to observe bowel motility, using even the simple strategy, of multiple single shot acquisition of single shot T2 or trueFISP images to generate an image series that is comparable to most cartoon movies: single images run together as a movie picture. Cute, but I rarely think is necessary.

Various esophageal abnormalities, one example achalasia, are well shown on MRI. Gastroparesis shows a fluid- and debris-dilated thin-walled stomach and distal decompressed small and large bowel. Dilated small bowel and transitions in dilation are well shown on single shot T2 images, such as high fluid distended small bowel with transitions to small caliber small bowel in obstruction. Small bowel ileus, as in paralysis,( as can occur in GDD), the small bowel all dilated; and in contrast if obstruction present, as in scarring fibrous strands or tumors, proximal dilation with distal small bowel narrowing.

Dilated colon: fluid (bright on T2) in the setting of diarrhea, dark on T2 with both air and stool, with air showing susceptibility artifact..

Stool has an interesting appearance on MRI. The somewhat revulsion of stool, that I have even as an abdominal imaging authority, inhibits me from being excited about it. But formed firm stool is actually quite dark on single shot T2 weighted images, and restricting attention to these images for diagnosis will result in the missing of even a massively dilated colon filled chock-a-block with firm stool. So firm solid constipating stool can simulate the appearance of air on single shot T2 weighted images. It is on T1 weighted images that one can visualize that it is stool and not air: air will be dark- and one can see, essentially always, susceptibility artifact (ballooning-type) artifact from air, whereas stool is usually intermediate muscle tissue signal or somewhat high signal (bright) on T1 weighted images. I have to mention this about stool, because although generally decent God-fearing folk do not like to speak of it (this includes myself) this generally means even abdominal imagers are not good at identifying it and the appearances of other related findings as well.

One observation I have made, that probably does have considerable clinical importance. The clinical history on the patient may read: Irritable bowel syndrome with diarrhea - IBS with d, on the MR study the colon is actually completely full of dense stool, so it is IBS with constipation (c). What has been happening clinically then is the colon is so completely full of firm solid stool that the only thing that can get out is small volumes of fluid stool. So severe constipation mimicking diarrhea, and ofcourse the treatments of the two being polar opposite. False diarrhea in a severely constipated colon if managed with anti-diarrheal agents will only make the clinical condition worse, and probably much, much worse. A simple easy observation to be made on MRI: if you know what to look for, and surprisingly easy to overlook, if you don't. I do not advocate the use of MRI for sorting out diarrhea vs constipation: there is already far too much imaging overuse.

Richard Semelka, MD


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