FUNCTIONAL GASTROINTESTINAL DISORDERS

Symptoms occur in the absence of any demonstrable abnormalities in the digestion and
absorption of nutrients, fluid and electrolytes and no structural abnormality in the GI tract.

There is inevitably overlap, with some symptoms being common to more than one disorder.

Table 6.26 lists the common functional gastrointestinal disorders as defined by Rome III
criteria. These conditions are extremely common world-wide, making up to 80% of patients
seen in the gastroenterology clinic.
Table 6-25. Chronic gastrointestinal symptoms suggestive of a functional
gastrointestinal disorder(FGID)
Nausea alone
Vomiting alone
Belching
Postprandial fullness
Abdominal bloating
Abdominal discomfort/pain (right or left iliac fossa)
Passage of mucus per rectum
Frequent bowel actions with urgency first thing in morning

Table 6-26. Modified Rome III functional gastrointestinal disorders

Functional oesophageal disorders
Heartburn
Chest pain of presumed oesophageal origin
Dysphagia
Globus
Functional gastroduodenal disorders
Non-ulcer dyspepsia
Belching disorders
Nausea and vomiting disorders
Rumination syndrome in adults
Functional bowel disorders
Irritable bowel syndrome
Functional bloating
Functional constipation
Functional diarrhea
Unspecified functional bowel disorder
Functional abdominal pain syndrome
Functional gallbladder and sphincter of Oddi (SO)
disorders
Pathophysiology and brain-gut interactions
1. A greater GI motility response to life events than normal subjects (poor association
between symptoms and motility changes.
2. Abnormalities in visceral sensation and have a lower pain threshold when tested
with balloon distension (visceral hyperalgesia). Which is possibly relates to:

 Altered receptor sensitivity at the viscus itself.

 Increased excitability of the spinal cord dorsal horn neurons.
 Altered central modulation of sensations.

The excessive release of serotonin is thought to contribute to symptom development.

The brain-gut axis describes a combination of intestinal motor, sensory and CNS
activities. Thus extrinsic (e.g. vision, smell) and intrinsic (e.g. emotion, thought) information
can affect GI sensation because of the neural connections from higher centres.
Conversely, viscerotropic events can affect central pain perception, mood and behavior.

Psychological stress can exacerbate gastrointestinal symptoms.

FGID should be regarded as a dysregulation of brain-gut function.

FUNCTIONAL OESOPHAGEAL DISORDERS

1. Globus
This presents as:

 Persistent or intermittent sensation of a lump or foreign body in the throat.

 Occurrence of the sensation between meals.
 The absence of dysphagia and odynophagia.

Treatment is with explanation and reassurance and a trial of antireflux therapy.

Antidepressants may be tried.

2. Functional chest pain, of presumed oesophageal origin

 Episodes of mainly midline chest pain, not burning in nature, that is potentially of
oesophageal origin.
 Absence of a cardiac cause, GERD and achalasia.
A history of psychiatric disorder is found in more than 60% of patients

More than half of patients will respond to high-dose acid-suppression therapy in the first
week; some will respond to nitrates and calcium-channel blockers.

Antidepressant therapy, e.g. amitriptyline or the SSRI citalopram, have been shown to be
effective.

FUNCTIONAL GASTRODUODENAL DISORDERS

1. Functional dyspepsia
This is the second most common FGID (after IBS). Patients can present with a spectrum of
symptoms including upper abdominal pain/discomfort, fullness, early satiety, bloating and
nausea.

Functional dyspepsia subgroups

Two subgroups based on the predominant (or most bothersome) single symptoms are
suggested:

 Epigastric pain syndrome with pain centred in the upper abdomen as the

predominant symptom. PPIs may be used.
 Postprandial distress syndrome with an unpleasant non-painful sensation
(discomfort) centred in the upper abdomen being the predominant symptom. This
sensation may be associated with upper abdominal fullness, early satiety, bloating
and nausea. Prokinetic agents may be used.

Investigations
Many young patients (< 50) require no investigation. Older patients or those with alarm
symptoms require endoscopy. Gastroscopy often shows gastritis but whether this is the cause
of the symptoms is doubtful.
Treatment
Reassurance, explanations and lifestyle changes. Reducing intake of fat, coffee, alcohol and
cigarette smoking may help. Placebo response rates are high (20-60%).

H. pylori eradication therapy can be effective in some patients with functional dyspepsia.

2. Aerophagia
A repetitive pattern of swallowing or ingesting air and belching. It is usually an unconscious
act unrelated to meals. Usually no investigation is required. Explanation that the symptoms
are due to swallowed air and reassurance are necessary, as is treatment of associated
psychiatric disease.

3. Functional vomiting
Rare. Chronic nausea is a frequent accompaniment in all FGIDs. Clinically it is
characterized by:

 Frequent episodes of vomiting, occurring on at least 1 day/ week.

 Absence of criteria for an eating disorder, rumination or major psychiatric
disease.
 Absence of self-induced and medication-induced vomiting.
 Absence of abnormalities in the gut or CNS and metabolic disease.

Investigation is often not required but always excludes non-GI disorders.

Treatment is with anti-nausea drugs and antidepressants; behavioural therapy and

psychotherapy are helpful. Dietary changes occasionally help.

4. Rumination syndrome

 Persistent or recurrent effortless regurgitation of recently ingested food into the

mouth with subsequent re-mastication and re-swallowing. Regurgitation is not
preceded by retching.
 Absence of nausea and vomiting, abdominal discomfort, heartburn.
 Cessation of the process when the regurgitated material becomes acidic. The
regurgitant contains recognizable food with a pleasant taste.

Central factors are culprit and the disorder is common in individuals with learning
difficulties.

FUNCTIONAL BOWEL DISORDERS

1. Irritable bowel syndrome (IBS)
IBS is the commonest FGID. Reported in up to 1/5 people. IBS - a multisystem disorder.

IBS patients suffer from a number of non-intestinal symptoms. The non-intestinal symptoms
of IBS can be more intrusive than the classical features of IBS. IBS coexists with chronic
fatigue syndrome, fibromyalgia, and temporomandibular joint dysfunction.
Table 6-27. Non-gastrointestinal features of irritable bowel syndrome.
Gynaecological symptoms
Painful periods (dysmenorrhoea), Pain following sexual intercourse (dyspareunia), Premenstrual tension.
Urinary symptoms
Frequency, Urgency, Passing urine at night (nocturia), Incomplete emptying of bladder.
Other symptoms
Back pain, Headaches, Bad breath, unpleasant taste in the mouth, Poor sleeping, Fatigue.

Table 6-28. Subtyping irritable bowel syndrome by predominant stool pattern

 IBS with constipation
(IBS-C)
IBS with diarrhoea (IBS-
D)
Mixed IBS (IBS-M)
Unsubtyped IBS
Hard lumpy stools ≥ 25% and loose (mushy)
or watery stools < 25% of bowel movements
Loose (mushy) or watery stools ≥ 25% and hard
or lumpy stools < 25% of bowel movements
Hard or lumpy stools ≥ 25% and loose (mushy)
or watery stools ≥ 25% of bowel movements
Insufficient abnormality of stool consistency
to meet criteria for IBS- C, D or M

These criteria state that in the preceding 3 months there should be at least 3 days per
month of recurrent abdominal pain or discomfort associated with two or more of the following:

 Improvement with defecation.

 Onset associated with a change in frequency of stool.
 Onset associated with a change in form (appearance) of stool.

Pointers to the need for thorough investigation are the presence of the above symptoms in
association with:
 Rectal bleeding.
 Nocturnal pain.
 Fever.
 Weight loss.
 A clinical suspicion of organic diarrhoea (stool wt > 250 g/day).

Treatment
The initial promise of the emerging receptor active drugs (HT3 receptor antagonists for
diarrhoea- predominant IBS, HT4 receptor agonists for constipation-predominant IBS).
Kappa opioid agonists for use in patients in whom visceral hyperalgesia.
Probiotics and prebiotics
Probiotics are live or attenuated bacteria or bacterial products that confer a significant
health benefit to the host. the symptomatic response was associated with normalization of the
ratio of an anti-inflammatory to a proinflammatory cytokine suggesting an immune modulating
role for this organism in IBS.

Prebiotics are non-digestible food supplements that are fermented by host bacteria thereby
altering the microbiota of the host often by stimulating the growth of healthy bacteria. A trans-
galacto oligosaccharide prebiotic has now been shown to be bifidobacteria enhancing in IBS
patients and to alleviate symptoms. This group of compounds may have considerable
potential as therapeutic agents in IBS.
Box 6.11 Some factors that can trigger onset of irritable bowel
symptoms

 Affective disorders, e.g. depression, anxiety

 Psychological stress and trauma
 Gastrointestinal infection
 Antibiotic therapy
 Sexual, physical, verbal abuse
 Pelvic surgery
 Eating disorders

Approaches to management of the irritable bowel syndrome (IBS)

End organ treatment Action
 Smooth muscle relaxants for pain Dicycloverine hydrochloride
Mebeverine hydrochloride, Peppermint
oil
Explore dietary triggers Refer to dietician
High-fibre diet ± fibre supplements Refer to dietician ± prescribe ispaghula
for constipation husk
Antidiarrhoeal drugs for bowel Loperamide
frequency
Codeine phosphate
Co-phenotrope
Central treatment Action
Explain physiology and symptoms At consultation (leaflets with diagrams
help)
psychotherapy Refer to clinical psychologist
Hypnotherapy.
Cognitive behavioural therapy Refer to psychiatrist
antidepressants Clomipramine in functional diarrhoea;
tricyclic group, e.g. amitriptyline in
diarrhoea-predominant IBS; selective
serotonin reuptake inhibitors in
constipation-predominant IBS, e.g.
paroxetine.
Pain/gas/bloat syndrome/midgut dysmotility
There exist a group of patients with functional bowel disease whose abdominal pain and other
clinical features are likely to occur as a consequence of disordered motility and visceral
sensation that predominantly affects the small intestine or midgut. The symptom-based
diagnostic criteria are abdominal pain, often exacerbated by eating and not relieved by
opening the bowels and not associated with the passage of more frequent or looser stools
than normal and not associated with constipation. Other symptoms include abdominal
distension (bloating). Abdominal distension that is not restricted to the upper abdomen
occurs, as well as postprandial fullness, nausea and, on occasions, anorexia and weight loss.

Some patients with pain/gas/bloat syndrome have particularly severe and chronic symptoms,
that may also be nocturnal. A subgroup of these have been shown to have manometric
features consistent with a diagnosis of chronic idiopathic intestinal pseudo-obstruction (CIIP),
and specifically of an enteric neuropathy. Full-thickness small intestinal biopsies have
confirmed the diagnosis in some patients, while in others a deficiency of α actin staining in the
inner circular layer of smooth muscle has been demonstrated. More appropriately these
patients should be considered to have a gastrointestinal neuromuscular disorder (GINMD) of
the gut. About 10% of these patients are subsequently found to have an underlying
autoimmune overlap disorder (see p. 548).

Treatment of patients with pain/gas/bloat syndrome is not easy; and in some, pain can be
chronic and severe. Narcotics should always be avoided. Central and end-organ targeted
treatment approaches should be combined, e.g. selective serotonin reuptake inhibitor
paroxetine combined with a prokinetic agent domperidone or smooth muscle relaxant, e.g.
Mebeverine. Treatment of patients with neuromuscular disorders of the gut requires a
multidisciplinary approach, with emphasis on management of pain, psychological state and
nutrition. Patients with underlying autoimmune inflammatory mixed connective tissue
disorders may benefit from primary treatment of these.

Functional diarrhoea
In this form of functional bowel disease, symptoms occur in the absence of abdominal pain
and commonly are:
  The passage of several stools in rapid succession usually first thing in the morning.
No further bowel action may occur that day or defecation only after meals.
 The first stool of the day is usually formed, the later ones mushy, looser or watery.
 Urgency of defecation.
 Anxiety, uncertainty about bowel function with restriction of movement (e.g.
travelling).
 Exhaustion after the 'morning rush'.

Chronic diarrhoea without pain is caused by many diseases indistinguishable by history from
functional diarrhoea. Features atypical for a functional disorder (e.g. large-volume stools,
rectal bleeding, nutritional deficiency and weight loss) call for more extensive studies of
intestinal structure and function. In cases where it proves difficult to distinguish between
functional and organic causes of diarrhoea, patients should be admitted to hospital for a
formal 3-day analysis of stool weights and faecal fat estimation, and a purgative screen
together with stool osmolality and creatinine contents to exclude factitious causes of
diarrhoea (see p. 308). Outpatient analysis of stool weights is unreliable as brain-gut
dysrhythmia may result in increased stool weights in the normal home environment.

Treatment of functional diarrhoea is with loperamide often combined with a tricyclic

antidepressant prescribed at night (e.g. Clomipramine 10-30 mg)