IBS
Intro
Functional disorder
Chronic abdo pain and altered bowel habit
Prevalence
10 to 15% of people
Associations
Fibromyalgia
CFS
Reflux
Functional dyspepsia
Non-cardiac chest pain
Psychiatric disorders including depression, anxiety and somatisation
Symptoms
Chronic abdominal pain
Cramping, variable intensity, periodic exacerbations
Location and severity vary
Often associated defecation, worsens or improves
Emotional stress and meals exacerbate pain
Altered bowel habits
Diarrhoea
Small to moderate volume, loose, frequent
Waking hours, most often in the morning or after meals
Preceded by lower abdo pain, urgency, and sense of incomplete evacuation
50% of patients have mucous discharge with stools
Constipation
Hard, pellet-shaped, associated tenesmus
Diagnosis
Recurrent abdominal pain
At least one day per week in the last 2 months
Associated with two or more of
Related to defecation
Associated change in stool frequency
Associated with a change in stool appearance
Subtype
IBS with predominant constipation
IBS with predominant diarrhoea
IBS with mixed bowel habits
IBS unclassified
Evaluation
History
Exclude organic diseases
Identifying medication that can contribute
Some patients have viral or bacteria gastro prior to symptoms starting
Exam
OFten normal
Some mild tenderness
Investigations
FBC
If diarrhoea then
Faecal calprotectin.
FCP >50 = Sensitivity 81% and specificity 87% for IBD
Stool test for giardia
Serology for coeliac
CRP if faecal calprotectin is unavailable
If appropriate colorectal cancer screening
If constipation consider AXR
Red flags
Age of onset > 50
Rectal bleeding
Nocturnal diarrhoea
Progressive abdominal pain
Unexplained weight loss
Lab abnormalities
Low ferritin and Hb
High CRP
High FCP
If no red flags, the above investigations rule out organic disease in 95% of patients
If red flags, further workup including endoscopy, abdominal imaging
Ddx:
Diarrhoea
Coeliac
Microscopic colitis
SIBO
IBD
Constipation
Organic disease
Dyssynergic defecation
Slow colon transit
Disease course
Chronic symptoms that vary over time
6 years after the diagnosis
2 to 5% developed an alternative diagnosis
30 to 50% had unchanged symptoms
2 to 18% had worsening of symptoms
12 to 38% had improvement in symptoms
Pathophysiology
GIT motility
Motor abnormalities detected in some patients
Irregular luminal contractions
Exaggerated motor response to CCK
Visceral hypersensitivity
Increased sensation in response to stimuli
Stimulation of various receptors in the gut wall
Several studies show selective hyper sensitisation of visceral afferent nerves in the gut triggered by bowel distention or bloating as a possible cause
Distention - studies show awareness and pain caused by balloon distention in the intestine are experienced at lower balloon volumes compared with controls
Bloating - 50% of patients with IBS have a measurable increase in abdominal girth associated with bloating
Intestinal inflammation
Mucosal immune system activation characterised by alterations in particular immune cells and markers
Lymphocytes
Increased numbers in colon and small bowel
One study showed neuronal degeneration around myenteric plexus
Cells release NO, histamine, protease
Lead to abnormal motor and visceral responses
Stools have higher serine-protease activity
Stool taken from IBS patient put into mice increase cellular permeability and visceral pain in the mice
Mast Cells
Increased mast cells in ileum, jejunum, colon
Pro-inflammatory cytokines
Elevated in patients with IBS
Higher TNR
Post Infectious
6 x increased risk after acute gastroenteritis
Risk factors for this include
Young age
Female sex
Prolonged fever
Anxiety and depression
Post infective cause not known
Alteration in faecal microbiota
Needs more research
Bacterial overgrowth
SIBO not obviously linked to IBS, needs more research
Food sensitivity
Role of food in the cause of IBS is uncertain
Some patients report clear worsening of symptoms afting eating and perceive food intolerance to certain foods
Food allergy
Data re: skin prick testing is conflicting.
Great number of positive food skin prick test in IBS patients however didn’t seem to exacerbate symptoms
Carb malabsorption
Fructose, sorbitol, lactose possible
Gluten sensitivity
Overlap with IBS and coeliac
Genetics
Familial studies suggest genetic susceptibility
Psychosocial Dysfunction
Patients with more GIT symptoms reported more lifetime and daily stressful events than controls
Treatment
Establish rapport and continuity of care
Education and reassurance
Diet modification
Consider excluding gas-producing foods
Low FODMAP
Initial eliminate for 6 to 8 weeks then reintroduce
Lactose avoidance
Gluten avoidance
Possible gluten avoidance improves IBS due to concurrent fructan reduction
Fibre
Soluble fibre (psyllium = metamucil) but not insoluble fibre (bran) has a significant effect
Improve both constipation and diarrhoea
Food allergy testing
No evidence
Physical activity
Improves IBS symptoms and reduces the risk of worsening of symptoms in the future
Medication
Constipation
Psyllium husk first
If not enough then Movicol 1 daily
Movicol improves constipation but not abdominal pain
Diarrhoea
Loperamide 2mg taken 45 minutes before meals regularly
For patients with ongoing diarrhoea consider bile acid sequestrants (Questran)
Abdominal pain and bloating
Antispasmodics
Mebeverine (Colofac)
Antidepressants
Improve mood, slow intestinal transit time
Start low and titrate up
3 to 4 weeks of therapy before increasing
Endep, Nortriptyline, Imipramine
Less evidence for SSRI/SNRI
Antibiotics
If moderate to severe without constipation, and particularly if bloating, who failed the above treatments
Can consider a 2-week trial on Rifaximin 550mg TDS for 14 days
Probiotics
Associated with improvement in symptoms but the magnitude of benefit and most effective species and strain are uncertain
Refractory symptoms
Behaviour modification
CBT
Anxiolytics
Limited, short term
Faecal transplant
Reduces symptoms but not sustained at 12 months