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CHAPTER12 Gastrointestinalmedicine
Inflammatory boweldisease
Ulcerative colitis (UC) and Crohn’s disease are collectively termed inammatory bowel disease.
Both are chronic, relapsing– remitting diseases characterized by acute, noninfectious inammation of the gut. In UC, inammation is limited to the
colorectal mucosa. Extent varies from disease limited to the rectum (proctitis) to disease aecting the whole colon (pancolitis). In Crohn’s, any part
of the gut from mouth to anus can be aected with normal bowel between
aected areas (skip lesions).
Cause Unknown. Both diseases are thought to result from an environ-
mental trigger on genetically susceptible individuals. Factors implicated
(none proven) include:
• Smoking— protective against UC (95% are non- smokers or ex- smokers)
but a causative factor in Crohn’s disease (⅔ are smokers and smoking
cessation halves the relapse rate)
• Gut ora or other infections, e.g. Mycobacterium paratuberculosis
• Food constituents
Features Table 12.15
Dierentialdiagnosis
• Irritable bowel syndrome
• Coeliac disease
• Anal ssure
• Gut infection, e.g. giardiasis
• Diverticulitis
Suspected diagnosis ~50% of severe attacks of UC are rst attacks
in patients who do not have a prior diagnosis. If bloody diarrhoea + fever
>37.5°C or tachycardia >90bpm, admit as an acute emergency. If persistent, unexplained diarrhoea lasting >4wk and/ or persistent abdominal
pain, refer for urgent further investigation to exclude GI malignancy and
establish diagnosis.
Assessing severity Table 12.14
• Colonic tumour
• Food sensitive colitis (infants)
• Pseudomembranous colitis
• Ischaemic colitis
• Microscopic colitis
Table12.14 Assessing theseverity ofulcerative colitis
Severity Symptoms Action
Mild <4 liquid stools/ d
Moderate 4– 6 liquid stools/ d
Severe >6 liquid stools/ d
Little/ no rectal bleeding
No signs of systemic disturbance
Moderate rectal bleeding
Some signs of systemic disturbance
Mild disease that does not respond to treatment
Severe rectal bleeding
Any systemic disturbance (i pulse rate >90bpm,
pyrexia >37.5°C, i ESR, i WCC, d Hb <10 g/ dL)
Signs of malnutrition (e.g. albumin <35g/ dL)
Weight loss >10%
Manage in primary
care
Consider
admission; contact
specialist team
for management
advice
Admit as an
emergency
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INFLAMMATORY BOWELDISEASE
Table12.15 Features ofinammatory bowel disease
UC Crohn’s disease
Incidence 10– 20/ 100,000/ y 5– 10/ 100,000/ y and increasing
Prevalence 100– 200/ 100,000 50– 100/ 100,000
Peak age 40– 60y (85% <60y)
Gender =
Risk factors Smoking is protective Smoking is a risk factor
GI symptoms Diarrhoea + blood/ mucus
Systemic
symptoms
Associated
conditions
Examination Abdominal + rectal examination— abdominal tenderness. Anal and
Investigation Blood— FBC (anaemia, i WCC), ESR (i when disease is active),
(stool may be solid if rectal
disease only)
Faecal urgency/ incontinence
Tenesmus
Lower abdominal pain
Tiredness and/ or malaise
Weight d or failure to thrive/ grow (children)
Fever
Joint disease— arthritis, sacroiliitis, ankylosing spondylitis
Eye disease— iritis or uveitis
Skin changes— erythema nodosum, pyoderma gangrenosum (UC >
Crohn’s)
Liver disease— autoimmune hepatitis (UC), gallstones (Crohn’s),
sclerosing cholangitis (UC > Crohn’s)
Miscellaneous— thromboembolism, osteoporosis (Crohn’s),
amyloidosis (Crohn’s)
perianal lesions (pendulous skin tags, abscesses, stulae) and/ or
mass in the right iliac fossa are characteristic of Crohn’s disease
General examination— clubbing, aphthous ulcers in the mouth
(Crohn’s), signs of weight loss, anaemia or hypoproteinaemia
eGFR, LFTs (including serum albumin). In severe UC, CRP >45g/ dL
after 3d steroid treatment indicates high (~85%) risk for colectomy
Stool— M,C&S (including Cl. dicile) to exclude infection
AXR— consider to clarify extent of disease, exclude toxic megacolon
(transverse colon diameter >5cm) or bowel obstruction and/ or
identify proximal constipation.
Proctoscopy— inammation and shallow ulceration extending
proximally from the anal margin suggests UC
Diarrhoea ± blood/ mucus
Malabsorption
Abdominal pain (crampy)
Mouth ulcers
Bowel obstruction due to strictures
Fistulae (often perianal)
Abscesses (perianal and
intra- abdominal)
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UC and Crohn’s disease are rare in childhood. Presentation is
variable and can be with non- specic features (e.g. failure to
thrive), GI symptoms (e.g. malabsorption, bloody diarrhoea,
acute abdomen), or complications (e.g. arthropathy or iritis).
If suspected refer for conrmation of diagnosis and specialist
management.
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CHAPTER12 Gastrointestinalmedicine
Management of ulcerative colitis
Activedisease
• Mesalazine 2– 4g daily. Topical 5- ASA derivatives are a useful adjunct if
troublesome rectal symptoms
• Add steroids (prednisolone 40mg od po + rectal preparation) if prompt
response is needed or mesalazine is unsuccessful. Review frequently and
d dose over 8wk. Rapid withdrawal i risk of relapse
• Azathioprine is added if the patient is having recurring attacks despite
mesalazine maintenance, frequent steroids (≥2 courses/ y), disease
relapses as dose of steroid is d, or relapse <6wk after stopping steroids.
Requires regular supervision
• Ciclosporin or iniximab (anti- TNF antibody)— consultant supervised—
may be eective as acute therapy for severe, steroid- refractory disease
• Admit acutelyif
• Severe abdominal pain (especially if associated with tenderness)
• Severe diarrhoea (>8×/ d) ± bleeding
• Dramatic weight loss
• Fever >37.5°C, tachycardia >90bpm or other signs of systemic disease
Maintenance treatment Follow- up in 2° care is routine. Most patients require lifelong therapy. Mainstays of treatment are 5- ASA derivatives (e.g.
mesalazine 1– 2g/ d or balsalazide 2.5g/ d). Use a rectal formulation (e.g.
mesalazine 1g/ d PR) if disease is conned to the rectum or descending
colon. Long- term treatment d risk of colonic cancer by 75%. 10% are intolerant to 5- ASA derivatives— alternative is azathioprine (see earlier in
topic). Treat proximal constipation with stool bulking agents or laxatives.
NSAIDs can precipitate relapse so avoid.
Surgery Last resort— but should not be delayed if severe colitis and failing
to respond to medical therapy. 20– 30% of patients with pancolitis require
colectomy— 1 in 3 develop pouchitis (non- specic inammation of the ileal
reservoir) within 5y of surgery.
Prognosis At any time 50% are asymptomatic, 30% have mild symptoms,
and 20% moderate/ severe symptoms. <5% are free from relapse after 10y.
Relapses usually aect the same part of the colon.
Complications Table 12.17
Management ofCrohn’sdisease
Active ileal and/ or colonicdisease
• Treat with mesalazine 4g daily. Less eective than for UC
• Add steroids (prednisolone 40mg od po or budesonide 9mg daily) if
unresponsive to mesalazine. Review frequently and d dose over 8wk.
Rapid withdrawal i risk of relapse. 0 steroids are associated with
irisk of severe sepsis and mortality in Crohn’s disease so alternatives
to steroid therapy are increasingly sought and steroid maintenance for
>3mo should always be avoided
• Elemental or polymeric diets for 4– 6wk can be a useful adjunct or
alternative to steroid treatment— take consultant advice
• Other treatments (consultant supervision) include metronidazole,
azathioprine, antitumour necrosis factor (iniximab or adalimumab)
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INFLAMMATORY BOWELDISEASE
• Surgery is an option if medical treatment has failed. 50% need surgery <10y
after onset. Surgery is not curative and 50% will require a further operation
at a later stage. After ileal resection check vitamin B12 levels annually
• Admit acutelyif
• Severe abdominal pain (especially if associated with tenderness)
• Severe diarrhoea (>8×/ d) ± bleeding
• Dramatic weight loss
• Bowel obstruction
• Fever/ other signs of systemic disease
0 For disease elsewhere, take specialist advice.
Maintenance treatment Follow- up in 2° care is routine. Treatment is aimed
at d impact of the disease. Mesalazine has limited benet. It is ineective
at doses <2g/ d. Other agents used include azathioprine, mercaptopurine,
methotrexate, and iniximab/ adalimumab. All require consultant supervision. Treat diarrhoea symptomatically with codeine phosphate or loperamide unless it is due to active colonic disease. Colestyramine (4g 1– 3 ×/ d)
d diarrhoea due to terminal ileal disease/ resection. NSAIDs can precipitate
relapse— so avoid.
Prognosis 75% are back to work after the rst year but 15% remain unable
to work long term. Complications— Table 12.16.
Table12.16 Complications ofinammatory bowel disease
UC Crohn’s
Toxic megacolon— colon distends and may
perforate
Colonic cancer— risk i if disease >8y,
onset in childhood/ adolescence,
age >45y, FH of colon cancer,
extensive colitis, sclerosing cholangitis.
Prevention:screening with colonoscopy.
Frequency depends on severity of the
disease and duration of symptoms
Sclerosing cholangitis— brosis and
stricture of intra- and extra- hepatic bile
ducts. Presents with obstructive jaundice
Psychological eects— chronic lifelong conditions which have major impact on
work and domestic life. Self- help groups can be useful.
Intra- abdominal abscess
Intestinal stricture— common— may
require surgery
Toxic megacolon— rare (see UC)
Bowel obstruction
Fistula formation
Perianal disease
Malignancy— large and small bowel
cancer— 5% 10y after diagnosis
Osteoporosis
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Further information
NICE (2019) Crohn’s disease:management. M www.nice.org.uk/ guid-
ance/ ng129
NICE (2019) Ulcerative colitis:management. M www.nice.org.uk/ guid-
ance/ ng130
Advice and support forpatients
Crohn’s and Colitis UK F 0300 222 5700 M www.crohnsandcolitis.
org.uk
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CHAPTER12 Gastrointestinalmedicine
Irritable bowelsyndrome
Irritable bowel syndrome (IBS) is a chronic (>6mo) relapsing and remitting
condition of unknown cause with symptoms including: abdominal pain or
discomfort; bloating; and change in bowel habit.
Diagnosis is clinical and there is no conrmatory test. Extremely common.
Lifetime prevalence ≥20%, although 750% never consult a GP. >
(2.5:1). Symptoms can appear at any age.
Diagnosis ofIBS Abdominal pain or discomfort that is:
• Relieved by defecation, or
• Associated with altered bowel frequency or stool form
And ≥2 of the following:
• Altered stool passage (straining, urgency, incomplete evacuation)
• Abdominal bloating ( > ), distension, tension or hardness
• Symptoms made worse by eating • Passage of mucus
Other commonly associated symptoms Include lethargy, nausea, backache
and bladder symptoms.
Dierentialdiagnosis
• Colonic carcinoma
• Coeliac disease
• Inammatory bowel disease
(Crohn’s disease or UC)
Investigation A diagnosis of exclusion. How far to investigate is a clin-
ical judgement weighing risks of investigation against possibility of serious
disease. Judgement is based on age of the patient, family history, length of
history, and symptom cluster.
• Patients <40y Check FBC, CRP, ESR, and antibody testing to exclude
coeliac disease (TTG/ EMA)
• Patients >40y Colonic cancer must be excluded for any patient with
a persistent, unexplained change in bowel habit— particularly towards
looser stools (E p. 370)
• Other investigations to consider
• Faecal calprotectin stool test ± referral for colonoscopy to exclude
inammatory bowel disease (as per local guidelines)
• Thyroid function tests if other symptoms/ signs of thyroid disease
• Stool samples to exclude GI infection if diarrhoea
• Endocervical swabs for Chlamydia
• Laparoscopy to exclude endometriosis
Referral To gastroenterology/ general surgery if (U=urgent; S= soon;
R=routine):
• Passing blood (except if from an anal ssure or haemorrhoids)— U
• Abdominal, rectal or pelvic mass— U
• Unintentional/ unexplained weight loss— U/ S
• +ve faecal calprotectin, inammatory markers, and/ or anaemia— U/ S
• >40y with new symptoms— U (if age >60y)/ S/ R
• Change in symptoms— especially if >40y— U (if age >60y)/ S/ R
• Atypical features (i.e. not those listed above)— U/ S/ R
• Pelvic inammatory disease
• Endometriosis
• GI infection
• Thyrotoxicosis
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IRRITABLE BOWELSYNDROME
• Family history of bowel or ovarian cancer— R
• Patient is unhappy to accept a diagnosis of IBS despite explanation— R
Treatment Reassure. Information leaets are helpful. Encourage lifestyle
measures, stress d, leisure time and regular physical exercise.
Diet Encourage patients to have regular meals and take time to eat. Avoid
missing meals or leaving long gaps between eating.
• Drink ≤8 cups of uid/ d, especially water. Restrict tea/ coee to 3
cups/ d. d intake of alcohol and zzy drinks
• d intake of high- bre foods (e.g. wholemeal/ high- bre our and breads,
cereals high in bran, and whole grains such as brown rice)
• d intake of ‘resistant starch’ found in processed or re- cooked foods
• Limit fresh fruit to 3 × 80g portions/ d
• For diarrhoea, avoid sorbitol, an articial sweetener
• For wind and bloating consider i intake of oats (e.g. oat- based breakfast
cereal or porridge) and linseeds (≤1 tablespoon/ d)
• Up to 50% may be helped by exclusion of certain foods. Diaries may
help identify foods that provoke symptoms, e.g. dairy products, citrus
fruits, caeine, alcohol, tomatoes, gluten, and eggs. Refer to dietician
Specicmeasures
• Fibre/ bulking agents Constipation- predominant IBS. Bran can make
some patients worse. Oats and ispaghula husk are better tolerated.
Laxatives are an alternative but avoid use of lactulose
• Antispasmodics e.g. mebeverine, peppermint oil. Limited eectiveness.
If no response in a few days, switch to another— dierent agents suit
dierent individuals. Once symptoms are controlled use prn
• Antidiarrhoeal preparations e.g. loperamide. Avoid codeine phosphate
as may cause dependence. Use prn for patients with diarrhoeapredominant disease. Use pre- emptive doses to cover dicult situations
(e.g. air travel)
• Antidepressants There is some evidence that low- dose amitriptyline,
e.g. 10mg nocte or SSRIs may help symptoms
• Probiotics Some evidence of eectiveness. Consider a 4wk trial
• Psychotherapy and hypnosis Evidence of eectiveness but limited
availability. Consider for cases that have failed to respond to rst- line
treatment after >1y
• FODMAPs diet Some evidence of eectiveness. Refer to dietician
Failure torespond totreatment Consider another diagnosis— review history
and examination ± refer for further investigation.
Prognosis >50% still have symptoms after 5y.
Further information
NICE (2013) Faecal calprotectin diagnostic tests for inammatory bowel
disease. M www.nice.org.uk/ guidance/ dg11
NICE (2008, updated 2017)Irritable bowel syndrome in adults:diagnosis
and management of irritable bowel syndrome in primary care. M www.
nice.org.uk/ guidance/ cg61
Advice and support forpatients
The IBS Network M www.theibsnetwork.org
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CHAPTER12 Gastrointestinalmedicine
Jaundice and abnormal liverfunction
Jaundice Yellow pigmentation of the tissues due to excessive bile pig-
ment. Clinical jaundice appears when serum bilirubin >35 micromol/ L.
Causes
• i production of bilirubin (pre- hepatic) Haemolytic anaemia, drug-
induced haemolysis, malaria, Gilbert’s/ Crigler- Najjar syndrome
• Defective processing (hepatic) Hepatitis, cirrhosis
• Blocked excretion (obstructive) Gallstones, pancreatic cancer, primary
biliary cholangitis, primary sclerosing cholangitis, cholangiocarcinoma,
sepsis, enlarged porta hepatis (e.g. 2° to lymphoma)
History Patients presenting with jaundice may have no other symptoms.
General symptoms include tiredness, nausea, and pruritus. Ask about colour
of the stools and urine (dark urine suggests conjugated hyperbilirubinaemia
and hepatobiliary disease). Check alcohol consumption.
Examination Mild jaundice is best seen by examining the sclerae in natural
light. Look for signs of chronic liver disease and examine the abdomen for
masses and hepatomegaly.
Investigations Initially check FBC and liver function tests— Table 12.17.
Further investigations depend on the results.
Management Treat the cause of the jaundice. Most patients (except those
with Gilbert’s syndrome or self- limiting viral hepatitis) will require specialist
referral. Refer patients with pre- hepatic/ hepatic jaundice to a hepatologist;
refer patients with post- hepatic jaundice to a hepatobiliary surgeon. If aged
≥40y + jaundice— refer urgently to be seen in <2wk.
Neonatal jaundice E p. 846
Abnormal liverfunction
Raised AST/ ALT/ GGT inisolation Liver enzymes can i transiently as a result
of viral infection, drugs, or alcohol. ALT tends to be more raised in viral and
autoimmune hepatitis; AST tends to be more raised in patients with fatty
liver; raised GGT is associated with alcohol excess.
• Check medication including herbal medicines
• Stop alcohol
• Repeat LFTs:
• In 1mo if AST/ ALT are <3× upper limit of normal
• In 1wk if AST/ ALT are ≥3× upper limit of normal
• If still raised request hepatitis screen and USS, or refer to hepatology or
gastroenterology depending on clinical state
• If ALT is <2× upper limit of normal and hepatitis screen is negative:
• If USS is normal, repeat LFTs every 3– 6mo to see if abnormalities
settle— may be due to drugs, alcohol, or early fatty liver disease
• If USS shows fatty liver and consuming excess alcohol— advise
abstinence from alcohol and recheck LFTs every 3– 6mo
• If USS shows fatty liver and alcohol consumption is within normal
limits, advise weight d and low- fat diet, treat metabolic syndrome, and
recheck LFTs every 3– 6mo
• In all other cases, refer for specialist opinion
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JAUNDICE AND ABNORMAL LIVERFUNCTION
Table12.17 Distinguishing dierent types ofjaundice
Type of jaundice
Pre- hepatic Hepatic Cholestatic
Tests
Bilirubin ii ii ii
AST/ ALT Normal ii i
Alkaline phosphatase Normal i iii
Hb d Normal Normal
Jaundice Mild, lemon
Other symptoms Urine is not
0 Amixed picture is common and can be confusing.
yellow
darkened
May be marked
jaundice
Tender, enlarged
liver
May be marked
jaundice
Enlarged liver, itching
skin, pale stools
Raised bilirubin Possible causes include:
• Hepatitis/ biliary obstruction— if ALT/ AST are i, refer for liver USS and
do a hepatitis screen or refer as for jaundice
• Haemolysis— check FBC/ reticulocyte count— refer to haematology if
abnormal
• Gilbert’s disease— likely if serum bilirubin is <40mmol/ L and ALT/ AST
and RBC/ reticulocytes are normal. Bilirubin levels i after a fast
• If isolated i bilirubin >40mmol/ L— probably still Gilbert’s syndrome
but refer
Raised alkaline phosphatase Usually originates from liver or bone. Bone is
more likely if serum Ca2+ and phosphate are raised and GGT is normal. i
may be associated with any liver disease but is particularly marked in patients with biliary obstruction and primary biliary cholangitis.
Medications that cause raised AST/ ALT
• Most penicillins (especially co- amoxiclav)
and minocycline
• Antifungals
• Statins
• Antiepileptics
• NSAIDs
• Some herbal medicines
• Some recreational drugs
Statins and abnormal liver function Statins cause a biochemical
abnormality, but do not cause liver failure and are not contraindicated in
compensated liver disease. May improve fatty liver disease. Measure liver
function tests pre- treatment and after 1– 3mo. Thereafter measure each
6mo for 1y. Discontinue if AST/ ALT i and stays at >3× normal.
Hepatitis screen Check as appropriate:
• Hepatitis A, B, and C serology
• EBV serology
• Liver autoantibodies
• Iron studies and transferrin
saturation to exclude
haemochromatosis
• α1 antitrypsin level
• Serum copper and caerulo-
plasmin levels (if <40y)
• AFP
• Fasting blood glucose and lipids
• HbA1c
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CHAPTER12 Gastrointestinalmedicine
Fatty liverdisease
Fatty liver describes the pathological process where fat is deposited in liver
cells, but there is no inammation or scarring. Common condition aecting
up to 1:4 adults in the UK.
Presentation
• Usually asymptomatic. >50% present after investigation for abnormal
LFTs (E p.390). Characteristic ‘bright’ appearance on liver USS
• Less frequently presents with a smoothly enlarged liver or symptoms—
nausea, vomiting, abdominal pain, fat embolus (may be fatal)
Broadly divides into 2 forms:
Alcohol- associated fatty liver disease (AFLD) Dened as fatty
liver disease associated with daily ethanol consumption >20g () or
30g (). Earliest stage of alcohol- related liver disease. Aects 890% of
people who drink more than recommended limits. Can develop in weeks.
Blood markers (may be normal)
• Typically serum AST and ALT are i, but serum AST >serum ALT
• GGT may be i
• Alkaline phosphatase may also be i but usually <2× upper limit of normal
Primary caremanagement
• Identication of hazardous/ harmful drinking + brief interventions to
dconsumption— E p. 158
• Referral to specialist alcohol addiction service if needed
• If persistent heavy drinker ( >35U/ wk; >50U/ wk) refer for
transient elastography (TE) to assess for brosis/ cirrhosis. Refer
for specialist management if advanced brosis/ cirrhosis. If TE is not
available, follow local protocols for assessment of brosis, Alternatives
include:serum brosis markers, FIB- 4 test, brotest, AST:ALT ratio, and
AST to Platelet Ratio Index (APRI). Repeat every 2y
• Consider thiamine supplements if chronic alcohol dependence:if
severe, 200– 300mg/ d; if mild, 10– 25mg/ d
Prognosis AFLD is fully reversible and can resolve in <6wk with complete
abstinence from alcohol. If excessive alcohol use continues, predisposes to
alcoholic hepatitis and cirrhosis (irreversible).
Alcohol misuse E p. 158
Chronic hepatitis E p. 394–5
Cirrhosis E p. 396
Non- alcoholic fatty liver disease (NAFLD)N Very common.
Aects 20– 30% of the UK population. Prevalence has i ×2 over the past
20y. Associated with obesity, insulin resistance and metabolic syndrome
(E p. 313).
Screening With liver USS is not recommended except for children/ young
people with metabolic syndrome/ type 2 DM— repeat every 3y.
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FATTY LIVERDISEASE
Blood markers (may be normal)
• Typically, serum AST and ALT are i but serum ALT >serum AST
• GGT may be i
• Alkaline phosphatase may be i but usually <2× upper limit of normal
Complications
• Ahigh proportion develop DM long term
• More severe disease results in non- alcoholic steato- hepatitis (NASH)—
12% with NASH develop cirrhosis
Assessment forbrosis Once NAFLD has been diagnosed, assess for brosis
risk using the Enhanced Liver Fibrosis (ELF) test, if available. Alternatives
include:FIB- 4 test, NAFLD score, or TE.
Referral forspecialistassessment
• Child/ young person with suspected NAFLD on USS
• Any age with signicant liver brosis risk (e.g. ELF score >10.51)
Management inprimarycare
• Lifestyle advice— low- fat diet, weight d, i exercise, d alcohol
• Consider referral for bariatric surgery if meets local referral criteria
• Repeat ELF or other brosis score every 3y
Drugtreatment
• Not usually indicated in primary care— in secondary care, treatment
(unlicensed) with metformin, pioglitazone and/ or vitamin E may be
considered
• Treatment with statins is ineective
Other rarer causes offatty liverdisease
• Drugs, e.g. amiodarone, tamoxifen, valproate
• Inammatory bowel disease
• Malnutrition
• Pregnancy
Further information
NICE (2016) Cirrhosis in over 16s. M www.nice.org.uk/ guidance/ ng50
NICE (2016) Non- alcoholic fatty liver disease:assessment and manage-
ment. M www.nice.org.uk/ guidance/ ng49
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