Severe difficulties with eating in ME/CFS

As well as issues with oral feeding requiring enteral feeding to avoid malnutrition being important to consider in very severe ME, the limited cases we know of suggest that enteral feeding also can breakdown and may not be sufficient to prevent malnutrition.

If there are problems of gut motility and/or muscle weakness, enteral feeding though it gets food further on along the alimentary canal may not ultimately overcome the inability to progress a bolus through the remainder of the digestive system, nor would enteral feeding overcome an inability to absorb nutrition from the gut.

If there are problems of being unable to tolerate food, enteral feeding might not overcome any resulting vomiting and/or other associated symptoms.

Problems with moving food through the gut or absorption issues may need to be overcome by a central line into a major blood vessel, eg a Broviac Line or Hickman line, where a catheter is used to create a veinous port where nutrition can be introduced directly into a major vein (see Hickman Line in Wikipedia https://en.wikipedia.org/wiki/Hickman_line ). However if there problems tolerating nutrition even when introduced directly into the blood system, there still may be problems using a central line to avoid malnutrition.

Given we are looking at very small numbers of people with ME requiring enteral feeding or a central line, would rather specialists in these feeding techniques be best taking the lead here rather than ME specialist especially as @Jonathan Edwards points out we don’t know why or how these problems arise in people with very severe ME.
 
So glad you're bringing this up. I find it a bit alarming that there has been little attention to it when the people with ME who do die all seem to have severe GI problems at the end. I was delighted to see that Fluge, Mella and co have taken an interest:

https://www.tandfonline.com/doi/fig...3.2173533?scroll=top&needAccess=true&role=tab

I'm also interested on a personal level since a few months before this study, I developed similar symptoms (extreme fullness, unable to eat beyond tiny amounts), ended up in hospital and lost a lot of weight. Certainly I am being treated as if this is nothing to do with my ME. Domerid and a dietitian have helped enormously, but I had to get the dietitian myself - you'd think a BMI of 15-16 and rapid loss of more than 10% body weight would have made that a priority, but it wasn't.

Separately, I'm concerned that people with ME seem to be fed by NG tube for long periods of time eg in the Baxter et al case series. In the hospital where I worked, the guideline was 2 weeks for NG feeding - after that it should be PEG or a similar alternative (although in reality, NG feeding did often continue a bit beyond 2 weeks). I believe this is because of the damage NG tubes do to the nose, pharynx and oesophagus, but this should be checked with a dietitian.

Also Baxter et al argue for NG tube changes at home - this is very very unsafe. I was working on a ward when a patient died after being fed via an NG tube that was in her lung. The doctor had received a verbal report from X-ray that it was OK and went ahead before receiving the official report that the NG tube was in the patient's lung. It is not possible to eliminate this risk without a chest X-ray. If ME patients aren't able to do this, then they must make this decision in the knowledge that there is a risk of death.
 
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I've always assumed the ME/CFS label is just superseded by another diagnosis that is more specific/less controversial in situations when these patients do actually receive appropriate care.

The tertiary clinics i've attended, which includes a Gastro clinic where most of the people in the waiting room had nasogastric tubes, intentionally avoided listing ME/CFS in my clinic letters.

I'm more surprised that death certs are even issued with ME/CFS as a cause - given the general attitudes I'd think that's quite brave and that most would want to pin it on something else.
 
Regarding safe reinsertion of NG tubes, see these references (copied from https://imj.ie/wp-content/uploads/2...afety-Standards-in-a-Radiology-Department.pdf)

1. The National Patient Safety Agency alert NPSA/2011/PSA002 ‘Reducing the harm caused by misplaced nasogastric feeding tubes in adults, children and infants’, available at: http://www.nrls.npsa.nhs.uk/resources/type/alerts/?entryid45=129640 (accessed 12 October 2020).

2. National Patient Safety Agency - Reducing the harm caused by misplaced nasogastric feeding tubes 2005, available at: http://www.nrls.npsa.nhs.uk/resources/type/alerts/?entryid45=59794&p=4 (accessed 12 October 2020).

3. National Patient Safety Agency Rapid Response Report: Harm from flushing of nasogastric tubes before confirmation of placement 2012, available at: http://www.nrls.npsa.nhs.uk/resources/type/alerts/?entryid45=133441 (accessed 12 October 2020).

4. NHS England Patient Safety Alert: Stage 1 - Placement devices for nasogastric tube placement DO NOT replace initial placement checks 2013 available at: http://www.england.nhs.uk/wpcontent/uploads/2013/12/psa-ng-tube.pdf (accessed 12 October 2020).

5. NHS Improvement ‘Resource Set: Initial placement checks for nasogastric and orogastric tubes’ July 2016, available at: https://improvement.nhs.uk/resource...cementchecks-nasogastric-and-orogastric-tubes (accessed 12 October 2020).
6. NHS England Never Events Policy and Framework 2015, available at: http://www.england.nhs.uk/patientsafety/never-events (accessed 12 October 2020).

5. NHS Improvement ‘Resource Set: Initial placement checks for nasogastric and orogastric tubes’ July 2016, available at: https://improvement.nhs.uk/resource...cementchecks-nasogastric-and-orogastric-tubes (accessed 12 October 2020).
 
There have been a couple of papers on delayed gastric emptying (gastroparesis) in CFS:

Burnet, R.B., Chatterton, B.E. Gastric emptying is slow in chronic fatigue syndrome. BMC Gastroenterol 4, 32 (2004). https://doi.org/10.1186/1471-230X-4-32

(Abstract only) Gastric emptying in patients with chronic fatigue syndrome
Sand, A.; Hulstaert, J.; Wanet, P.; Uyttersprot, A.; Meirleir, K. de, 2002 https://inis.iaea.org/search/searchsinglerecord.aspx?recordsFor=SingleRecord&RN=34035565

I cannot speak for other severe ME patients but for me, my inability to eat correlates perfectly with overexertion. The days that I am crashing, my gastroparesis symptoms are awful, but conversely they ease when I rest aggressively and I can eat more then.

I don’t think that gastroparesis represents the entirety of the issue, however. After all, mine is moderate and my gastric emptying is much better on a liquid diet. Not to forget that some severe ME patients who can’t eat don’t have gastroparesis. The issue is that whenever I eat more calories than my body can seemingly handle on a given day, whether in solid or liquid form, I crash (and I have to eat less to recover the following days). I don’t know why.

Since liquids do not require the stomach to contract (they empty by gravity), they should require little to no exertion to digest. So is it that absorbing nutrients from the GI tract alone takes too much energy?

In any case, whenever I eat, my symptoms peak about 2h to 2h30 after finishing a meal. It feels as though blood is coming out of my stomach and getting redistributed throughout my body, and forcefully so. I get “wired” from it and am very sensitive to any sensory stimulus. Also, when I “overeat”, I get breathless and I have palpitations.
 
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Evergreen said:
Separately, I'm concerned that people with ME seem to be fed by NG tube for long periods of time eg in the Baxter et al case series. In the hospital where I worked, the guideline was 2 weeks for NG feeding - after that it should be PEG or a similar alternative (although in reality, NG feeding did often continue a bit beyond 2 weeks). I believe this is because of the damage NG tubes do to the nose, pharynx and oesophagus, but this should be checked with a dietitian.
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Guidelines for when a PEG should be used instead of an NG tube varies between 2-6 weeks. With ME given that there are no guidelines making any approximation for how long the tube might be needed will be difficult.

cassava7 said:
Since liquids do not require the stomach to contract (they empty by gravity), they should require little to no exertion to digest. So is it that absorbing nutrients from the GI tract alone takes too much energy?
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Even though the stomach doesn't have to knead liquids as much as whole foods, the enzymes needed to break down the nutrients must still be synthesized, blood still has to be shunted to the stomach area and muscles have to work to push the food further down the GI tract.

Edit: Typically, we attribute ~10% of energy towards "thermic effect of food" in people having a "normal" level of activity (so typically assumed total energy expenditure of 1800-2500 kcals depending on gender).

If I remember correctly those numbers are from direct calorimetry measurements, ie. placing people inside chambers and measuring heat expenditure while they're in there. Likely they then have been eating "normal" food, so the energy expenditure from easier to digest foods would be uncertain. Though I guess it's still good to have an estimate.
 
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In the Norwegian ME Association report on severe pwME, they write this on nutrition care of the very severe:
Norwegian ME Association report said:
38 % manage to eat something without help every day, while 45% are never able to. Only eight of the 47 very sewere say they can eat "normal" once in a while. Participants report that when they say "normal" they mean being able to move the food to the mouth themselves, not that they can eat enough or follow a "normal" diet. Half of the patients have stomach pains, while four out of ten experience nausea and problems swallowing. Many need help to eat (for example spoon feeding), while 32% (8 patients) are fed by tube, PEG/PEJ (6 patients) or through parenteral feeding (1 patient).
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As my illness slowly worsens over the years, i have gotten more and more food intolerances. At this point, i cannot eat most foods. I also often get a very uncomfortable sensation in my stomach (typically when i wake up) that i can only quell by eating. I eat a lot, but I've always been underweight. Most doctors would say malabsorption but i get the feeling it's something a bit different. It's as if, somehow, with ME my body cannot "handle" the food. Like if you tried to do weight training and your muscles didn't grow but with food instead.

Steroids do nothing to help this so i don't think it's anything like other GI illness, even if at times it does feel like "inflammation". But I've tried many immune GI (and systemic) drugs and they don't work.

Brain and stomach seem to be most affected in ME. The brain is hard to access, the stomach is not. We should be doing biopsy studies on stomach tissues. I wouldn't be surprised if the same pathology happening in the brainstem is also happening in the stomach. It is a mistake imo that we are overlooking this.
 
Trish said:
That makes sense to me except for one specific factor relation to ME diagnoses. Not commenting on this specific case, which I know nothing about, I think the problem some pwME have confronted is lack of belief by clinicians in the physical inability to eat. The ME diagnosis being misinterpreted as psychosomatic.
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This is definitely what happened in Maeve O'Neill's case, according to the documentation.
 
The puzzle is that nowhere is there a policy that people should be denied nutritional support because of a lack of belief in a physical inability to eat. People with anorexia nervosa get nutritional support by whatever means needed, as I understand it. The psychosomatic/physical attribution does not alter treatment policy - it certainly didn't in situations I have experienced. I think it is a pity that this was raised in the case report series. Failing to take PWME's problems seriously is a big issue but the more people focus on this distinction the more likely it is to go on contributing to that dismissal in my view. Advisors should be saying forget what is causing what, just make sure the patient gets enough nutrition. If one lot of doctors tell patients to believe one thing and another lot tell them not to, trust fails and disaster follows.

And in the longer term research should go into finding out what really is causing the problem.
 
Jonathan Edwards said:
The puzzle is that nowhere is there a policy that people should be denied nutritional support because of a lack of belief in a physical inability to eat. People with anorexia nervosa get nutritional support by whatever means needed, as I understand it. The psychosomatic/physical attribution does not alter treatment policy - it certainly didn't in situations I have experienced. I think it is a pity that this was raised in the case report series. Failing to take PWME's problems seriously is a big issue but the more people focus on this distinction the more likely it is to go on contributing to that dismissal in my view. Advisors should be saying forget what is causing what, just make sure the patient gets enough nutrition. If one lot of doctors tell patients to believe one thing and another lot tell them not to, trust fails and disaster follows.

And in the longer term research should go into finding out what really is causing the problem.
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I'm not familiar with the UK system, but "psychosomatic/physical" attribution definitely plays into it if a patient get nutrition support with the reasoning that one does not want to "reward" the mistaken belief the patient can't eat. So instead look for reasons why a patient does not eat, or just adopt a "wait and see" and "they'll eat when they are hungry enough" attitude. It doesn't help that nutrition screening in often not performed, and knowledge about malnutrition (and how to treat it) can vary a lot. Not that long ago a Norwegian anorexia nevrosa patient died of refeeding syndrome at a ward that specialised in treating eating disorders (!).
 
Jonathan Edwards said:
We simply do not have any medical knowledge about how to manage inability to eat in ME that is any different from inability to eat without ME. Knowing about ME does not change the options. There are no special drugs or protocols with published evidence of benefit or even well described uncontrolled studies.
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For nutrition support, this is true for more than ME. We have few studies, and a lot of practice is instead based on "best evidence".

For a dietitian, knowing a patient has an ME diagnosis could lead thoughts along the need for a careful start/maintenance of enteral and/or parenteral nutrition, easier digestable food/supplements in the case of enteral feeding and ways to reduce nausea.
 
As someone that suffers primarily with gastro issues (about 75% of my overall symptom burden) and having traveled to many major universities for testing...

I think we are actually on the cusp of being able to diagnose the cause of just about all GI disorders. Many of these causes can look like ME/CFS, but it turns out being something else. Where I learned the most about my issue was going to Wake Forest to Dr Kenneth Koch and going to the University of Miami to see 2 gastro specialists there as well.

We found that my UES is dysfunctional and I have been diagnosed with RCPD, or in other words... I literally can't belch any air. It lead the specialists to finding an overly tight UES on manometry. Then, the lower esophagus was found distended on barium imaging due to air buildup, along with the rest of the GI tract.

All other testing has come back normal from smart pill, imaging, endoflip, scopes, camera pill, breath testing for intolerances/SIBO, E.G.G, and 48hr reflux monitoring. My hope is the botox injection into the UES will help and it might possibly fix all of the GI symptoms. I can't get it done until April 12, fingers crossed.

Perhaps, it could maybe eliminate the poor sleep, fatigue, and muscle tension/tension headache in my upper body. If that is the case, then I'm cured. Maybe I don't have CFS after all...

The other neat thing is now some clinics can do a full thickness biopsy of the GI tract via endoscopy to inspect for many various immune infiltration, damage, etc. I have not had this done but considering motility seems to be ok, it's not currently warranted.

Autoimmunity is a very very common cause of motility disorders when other known causes have been easily ruled out. 80-85% of motility patients are female, which also fits the 80%-85% of autoimmune patient population as well. Paraneoplastic panels are commonly run now, at the places I have been to. I showed a slight positive once for N-VGCC, but follow up testing was negative.

I strongly believe patients diagnosed with CFS that have severe gastro issues might not have CFS at all, but something mimicking it.

I hope to update everyone soon. Reducing sugar and fodmap intake has helped my 'disease state' but will not obviously solve the problem.
 
To answer J's question, I'm not aware of any formal literature. I just know it's urgent work. It's clear from recent cases that the NHS doesn't know what to do with these patients, but surely we can't allow a situation where nobody is willing to take charge of the care of gravely ill young people because there's no protocol.

At minimum, a team of clinicians needs to document the process of managing real cases. Even if the illness is so intractable that they still sometimes run out of options and lose patients, experience will be gained and evidence gathered. At the moment nobody seems to be learning anything, either from these patients' lives or from their deaths.
 
In the recently posted thread it was stated the patient has Ehlers-Danlos Syndrome AND ME/CFS. EDS has known correlation with intestinal problems and might offer useful comparisons, although what seems like a frequent confounding of EDS with ME/CFS may make EDS as a comparator less helpful.

Two papers from Google Scholar search:

Gastrointestinal disorders in joint hypermobility syndrome/Ehlers-Danlos syndrome hypermobility type: A review for the gastroenterologist

Abstract

Joint hypermobility syndrome (JHS)/Ehlers-Danlos syndrome hypermobility type (EDS-HT) is the most common hereditary non-inflammatory disorder of connective tissue, characterized by a wide range of symptoms, mainly joint hyperextensibility and musculoskeletal symptoms. A majority of patients also experiences gastrointestinal (GI) symptoms. Furthermore, JHS/EDS-HT has specifically been shown to be highly prevalent in patients with functional GI disorders, such as functional dyspepsia and irritable bowel syndrome.
Purpose

The aim of this review was to examine the nature of GI symptoms and their underlying pathophysiology in JHS/EDS-HT. In addition, we consider the clinical implications of the diagnosis and treatment of JHS/EDS-HT for practicing clinicians in gastroenterology. Observations summarized in this review may furthermore represent the first step toward the identification of a new pathophysiological basis for a substantial subgroup of patients with functional GI disorders.

Sci Hub link to full article: https://sci-hub.se/10.1111/nmo.13013

Gastrointestinal and eating problems in women with Ehlers–Danlos syndromes

Abstract

Ehlers–Danlos syndromes (EDS) are a group of heritable conditions in which abnormal collagen synthesis leads to features such as joint hypermobility, skin abnormalities, and tissue fragility. Gastrointestinal (GI) symptoms are common among those affected. These may negatively impact eating behaviors, leading to weight/nutritional problems. We aimed to compare GI symptoms, disordered eating, and body mass index (BMI) between EDS patients and healthy controls, and to explore the link between these variables in EDS patients.

Sci Hub link to full article: https://sci-hub.se/10.1007/s40519-021-01146-z
 
dave30th said:
Jonathan, can you explain the protocol for needing to be at least at a 30% incline for tube-feeding?
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I guess it is to avoid aspiration of gastric contents. The presence of a tube is likely to make the oesophageal sphincter inefficient. If acid comes back up and goes into the lungs that is potentially lethal. There is also always the possibility that the tube will pull back if maybe the person turns and it catches and then feeding matter could get in the lungs. Rules like that usually have a sound basis in a history of disasters.
 
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