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Tube feed or not tube feed in gut-brain disorders? – three underlying questions to aid management

Updated on: 24 Jan 2022   First published on 17 Jan 2022

Author name: Dr Peter Paine

Author institution: Salford Royal Foundation Trust

Key words

  1. Nutrition
  2. Gut-brain disorders
  3. Gastroparesis
  4. Functional dyspepsia
  5. PEG


CIPO – chronic intestinal pseudo-obstruction
GES – gastric emptying study
CT – computed tomography
BMI – body mass index
NICE – National Institute for Clinical Excellence
FD – functional dyspepsia
GP – gastroparesis
CANH – clinically assisted nutrition and hydration
U&Es – urea and electrolytes
NJ – nasojeunal feeding

Learning points

  1. Objective markers of nutrition and hydration status (body-mass-index, anthropometrics and U&E’s), evidence of indication and the goal of CANH in patients with gut-brain disorders should be reviewed in a multi-disciplinary setting. Evidence of benefit reduces and risks of harm increases for subjective symptom-oriented CANH interventions.
  2. It is essential to attempt to identify specific gut-brain disorder diagnoses where possible, and any potentially reversible underlying mechanisms to guide CANH and symptom management decisions.
  3. The concept of optimised “effortful oral feeding as least-worst option” with ongoing MDT monitoring can be useful to avoid iatrogenic invasive escalation and to enable cautious CANH weaning.

Case study

A patient presents with a 3 year history of nausea, occasional but rare vomiting, and reports post-prandial pain even for liquid oral supplements. Co-morbid diagnoses include fibromyalgia, chronic constipation, anxiety, depression, fatigue, Postural Orthostatic Tachycardia syndrome, and hypermobile Ehlers Danlos Syndrome.

Medication: fentanyl patch, regular oramorph, and anti-emetics.

Investigations: normal bloods; normal gastroscopy; gastric emptying study (on opioids) shows slight delay with loss of proximal accommodation; normal small bowel on CT scan.

The patient has on-going nausea, pain, and bloating, but not weight loss.

Body Mass Index is 26 and bloods are normal.

Should the patient have clinically assisted nutrition and hydration (CANH) with enteral tube feeding?

What are the real questions?

Does the patient need CANH support objectively?

Enteral tube feeding is an evidence-based intervention for patients with objective features of malnutrition or hydration/electrolyte disturbance who are not meeting their nutrition and hydration requirements with oral intake and supplementation alone.

NICE guidelines suggest a BMI less than 18.5 kg/m², unintentional weight loss greater than 10% within the last 3-6 months or BMI <20 kg/m2 and unintentional weight loss greater than 5% within the last 3-6 months should prompt consideration of nutrition support1. Serial anthropometric measurements can be a useful adjunct to BMI in objective nutritional assessment. It is easy to lose sight of this primary underlying question however, and to make an incipient shift into trying to help foregut symptoms by tube feeding in patients not meeting objective nutritional criteria.

The evidence that tube feeding helps symptoms in foregut gut-brain disorders is poor and with increasing invasiveness comes increasing risks of iatrogenesis from CANH-related morbidity and mortality. The primary question therefore is one of a risk/benefit balance analysis of more clearly defined objectively evidenced nutritional indicators and goals versus subjective drivers that may be associated with less clear benefit and more potential risk. This risk/benefit analysis will require an on-going multi-disciplinary assessment, subject to frequent review.

Careful monitoring of objective markers by a multi-disciplinary team, including an experienced dietitian, a clinical psychologist, and a gastroenterologist with an interest in nutrition and an understanding of gut-brain disorders is therefore essential.

The patient in our case currently lacks absolute objective markers for escalation to enteral tube feeding and optimised medical management focussed on the likely diagnosis should be considered (Table 1), with objective nutrition and hydration markers monitored closely.

Foregut gut-brain disorder diagnosis Key features Diagnostic basis and tests Management options Optimal nutrition approach
Rumination Syndrome High pressure gastric contractions precede regurgitation/vomiting. Typical history. Concurrent impedance/manometry with meal provocation. Diaphragmatic breathing, baclofen, Nissens fundoplication (selected patients). Optimised effortful oral feeding, short term bridging NJ to therapies only if malnourished.
Cyclical Vomiting Syndrome & Cannabis Hyperemesis Bouts of hyperemesis with intervals of normality. History of migraines and relief from hot baths. Clinical history is typical and exclusion of other structural or central neural causes. May respond to tricyclics and migraine prophylaxis. Abstinence from cannabis. Short bouts may need parenteral fluids/electrolytes. NJ likely to be unstable and unnecessary.
Chronic nausea and vomiting Low grade background constant nausea and vomiting. Clinical history and exclusion of other structural or central neural causes. Pro-kinetics, anti-emetics, gut-brain neuromodulators. Optimised effortful oral feeding, avoid NJ unless malnourished.
Functional dyspepsia and Gastroparesis Overlapping spectrum of varying degrees of sensorimotor impairment of gastroduodenal function. Clinical history and solid meal gastric emptying test off of confounding medication (but not based on gastric emptying study alone). Pain management (avoid opioids), psychosocial support, buspirone, gut-brain neuromodulators inlcuding mirtazapine, pro-kinetics. If malnourished with predominantly gastric muscle failure (gastroparesis), then trial of NJ with view to longer term post-pyloric feeding tube.
CIPO and enteric (small bowel) dysmotility (ED) Non-mechanically obstructed dilated small bowel (CIPO) or significantly abnormal small bowel manometry or transit (ED). CIPO – dilated small bowel radiologically. ED – small bowel manometry or abnormal transit. Full thickness biopsy if undergoing venting surgery. Pro-kinetics, small intestinal bacterial overgrowth therapy, non-opioid analgesia with gut-brain neuromodulators. CIPO more likely to need parenteral nutrition than ED which should be manageable with optimised effortful oral or enteral feed.
Centrally mediated abdominal pain and narcotic bowel syndrome (NBS) Chronic continuous abdominal pain with neuropathic features. Escalating opioid doses in NBS. Clinical history and exclusion of other causes. Non-opioid analgesics (e.g. duloxetine). Opioid stabilisation and reduction. Mu-opioid antagonists. Avoid enteral tube and parenteral feeding.
Somatoform disorder/central sensitivity syndrome Overlapping multiple functional symptom syndromes. Psychiatric evaluation. Clinical psychology/liaison psychiatry. Central neuromodulators. Avoid iatrogenesis due to escalating invasive approaches.
Avoidant Restrictive Food Intake Disorder (ARFID) Restrictive and avoidant behaviours not body image driven, but anxiety, fear, food related symptom and fixed (e.g. health) beliefs. Psychiatric evaluation. Clinical psychology and liaison psychiatry input. If severely malnourished may need short term bridging enteral tube feeding to therapies, but needn’t be post-pyloric.

Table 1: Summary of the main foregut gut-brain disorders, key features, diagnostic basis and tests, management options and optimal nutrition approach.

What are the main foregut gut-brain disorder differential diagnoses, mechanisms, and management options?

The main differential diagnoses together with key features, diagnostic basis and tests, management options and optimal nutrition approaches are summarised in Table 1. Familiarisation with these in more detail is encouraged2.

We will focus on the functional dyspepsia (FD)-gastroparesis (GP) spectrum disorders however, as the commonest foregut gut-brain disorder presentations for which enteral tube feeding is considered and are most likely in our patient.

The FD and GP constructs display considerable overlap and are difficult to fully differentiate3,4.  They likely represent a pathophysiological spectrum from a chiefly sensory disorder (epigastric pain sub-variant of FD) to a mixed sensory/motor disorder (post-prandial distress syndrome sub-variant of FD) to a chiefly motor disorder (GP).

An over-reliance solely on gastric emptying studies (GES) for gastroparesis diagnostic labelling may skew the approach away from addressing sensory and psychosocial components, and drive iatrogenic invasive tube feeding escalation. Failure of proximal stomach accommodation and delayed or rapid gastric emptying can all be frequently seen on GES in the much commoner condition of FD. Many drugs, including opioids as in our patient, can affect the GES result and should be stopped in sufficient time before testing5,6.  This can be challenging in practice, and a multi-disciplinary pain management team may be helpful in enabling opioid weaning, which might be substantially and negatively contributing to patients’ symptoms.

The patient in our case presents with functional dyspepsia features, including those of both the epigastric pain syndrome and post-prandial distress sub-variants, and these are likely being exacerbated by opioids.

If a patient has gross motor failure evident on a well conducted GES, with vomiting as the predominant symptom, objective evidence of malnutrition and absence of small bowel failure, then these patients are most likely to benefit from post-pyloric tube feeding. A trial of nasojejunal feeding to confirm tolerance and nutritional gains before converting to a longer term more invasive enteral tube is usually sensible. For all other patients, in the absence of objective evidence of malnutrition, escalation of invasive intervention should be avoided whilst pain management (including stopping opioids), gut-brain neuromodulators, anti-emetics, pro-kinetics, and psychological input are optimised, as summarised in Table 1.

Might optimised “effortful oral feeding” be the least worst option?

In the absence of overt malnutrition, the concept of optimised “effortful oral feeding as least worst option”, in the face of on-going symptoms, can be the safest and most appropriate approach compared with the risks associated with tube feeding. Optimised effortful oral feeding may include changes in food with a lower fat content, more liquid consistency and smaller particle size, and the use of liquid oral nutritional supplements, which can help symptoms in a nutritionally balanced way in many patients7,8. Lower volume but higher calorie concentration feeds might be better tolerated.

In patients who have already escalated to tube feeding, tube feeding–related symptoms and tube-related problems will require a re-evaluation of the risk/benefit balance. For some patients, again with careful monitoring, a stable BMI below the healthy range maintained with optimised effortful oral feeding may also be a ‘least worst’ option compared with tube feeding.

De-escalation by weaning to return to optimised oral effortful feeding can be challenging but should be frequently revisited with regular community dietetic support in primary care. Slow weaning can be safely achieved by close dietetic supervision of the patient, especially with the inclusion of anthropometric measurements by the same dietitian to minimise inter-observer error.

It is appreciated that with chronic intractable symptoms, patients and their carers can become distressed, which can strain the therapeutic relationship.  Psychological assessment and supervision therefore are essential as part of the multi-disciplinary team to aid engagement and support self-efficacy of the patient in the review process and treatment plan, and can help artificial feed weaning over time. Once weaned, ‘safety netting’ with comprehensive ongoing MDT support in partnership with primary care can avoid the need to re-escalate to tube feeding in the absence of objective parameters of significant malnutrition, even in the face of on-going symptoms.


“Tube feed or not tube feed?” is an unduly simplistic and misleadingly binary forced choice question, which is unhelpful for safe and effective management and communication for patients with gut-brain disorders. A pragmatic and helpful way forward can be to ask three further underlying questions: Firstly, what are the objective versus subjective indicators and goals for CANH in an on-going risk/balance analysis? Secondly, what are the main foregut gut-brain disorder differential diagnoses, mechanisms, and management options? and thirdly, whether optimised “effortful oral feeding” might be the least worst and safest option? These three underlying questions can aid formulation of safer and more effective nutritional and symptomatic longer-term management in patients with gut-brain disorders.


  1. Nutrition support for adults: oral nutrition support, enteral tube feeding and parenteral nutrition. Available: https://www.nice.org.uk/guidance/cg32/chapter/1-guidance [Accessed 17 Jul 2019].
  2. Paine P, McMahon M, Farrer K et al. Jejunal feeding: when is it the right thing to do? Frontline Gastroenterology. 2019 5 397-403
  3. Fosso CL, Quigley EMM. A critical review of the current clinical landscape of gastroparesis. Gastroenterol Hepatol 2018;14:140–5.
  4. Stanghellini V, Tack J. Gastroparesis: separate entity or just a part of dyspepsia? Gut 2014;63:1972–8.
  5. Vijayvargiya P, Jameie-Oskooei, S, Camilleri M, et al. Association between delayed gastric emptying and upper gastrointestinal symptoms: a systematic review and meta-analysis.
  6. Gut 2019;68:804–13. Vijayvargiya P, Camilleri M, Chedid V, et al. Effects of promotility agents on gastric emptying and symptoms: a systematic review and meta-analysis. Gastroenterology 2019;156:1650–60.
  7. Camilleri M, Diet N. Novel diet, drugs, and gastric interventions for gastroparesis. Clin Gastroenterol Hepatol 2016;14:1072–80.
  8. Olausson EA, Störsrud S, Grundin H, et al. A small particle size diet reduces upper gastrointestinal symptoms in patients with diabetic gastroparesis: a randomized controlled trial. Am J Gastroenterol 2014;109:375–85.

Author Biography

Dr Peter Paine is a consultant gastroenterologist at Salford Royal Foundation Trust. His doctoral research explored psychophysiological mechanisms in visceral and somatic pain.

He runs a tertiary regional neurogastroenterology & motility clinic with a particular interest in chronic abdominal pain, severe dysmotility and their interface with nutrition.

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