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6 Gastroenterology
Barrett's oesophagus
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Barrett’s oesophagus is metaplasia of the normal stratified squamous epithelium
of the distal oesophagus to a columnar epithelium, as a result of chronic
Prevalence estimates vary widely;
in asymptomatic individuals. Population- based screening is not recommended, but
is advised in those with chronic
old, hiatus hernia, obesity, , white race, smoking, family history of Barrett's
or oesophageal adenocarcinoma).
columnarization, or the newly- developed Cytosponge® (encapsulated sponge
which is swallowed and retrieved). The length should be recorded (using the Prague
Management Focus on detecting and preventing the most significant
criteria).
associated morbidity: oesophageal adenocarcinoma. The relative risk of progres-
30
× that of the g eneral population, but the absolute risk is low (0.1– 0.4% per
sion is
patient per year). Risk factors for malignant transformation include age, , long
segment involved, and evidence of dysplasia. Daily
surveillance for dysplasia is recommended but supportive evidence is lacking. For
patients without intestinal metaplasia (
segment, encourage discharge.
3
cm segments every 2– 3 years. Low- grade dysplasia warrants repeat endoscopy
>
6
months and mucosal radiofrequency ablation (
in
≈
8
% in patients with symptomatic
GORD
sym ptoms and multiple ri sk fac tors ( >50 years
Diagnosis Biopsy of endoscopically visible
PPI
for all patients. Endoscopic
IM
7 For those with
) or dysplasia and with a short (<3cm)
IM,
survey every 3– 5 years, and
RFA
), if confirmed.
GORD,
RFA
GORD
≈6
or endo-
%
scopic resection for h igh- grade dysplasia or intramural carcinoma.
Hiatus hernia
Sliding hiatus hernia (95%) The gastro- oesophageal junction slides up into the
fig
6.20
chest— see
. Acid reflux often happens as the lower oesophageal sphincter
becomes less competent in many cases.
Paraoesophag eal hernia ( rolling hiatus h ernia) (5%) The gastric fundus her-
figs
6.20, 6.21
niates up into the chest alongside the oesophagus— see
jority of types where the gastro- oesophageal junction remains intact,
Clinical features: common: 30% of patients >50yrs, especially obese
common.
women. Although most small hernias are asymptomatic, patients with large hernias may develop
sophagitis) but cannot reliably exclude a hiatus hernia.
GORD
Tre at
therapy, complications (see
gulate the risk of this drops dramatically after
GORD
. Imaging: upper GI endoscopy visualizes the mucosa (?oe-
Tre at me nt : lose weight.
. Surgery indications: intractable symptoms despite aggressive medical
p
252
). Although paraoesophageal hernias may stran-
65
yrs. Prophylactic repair is only
undertaken in those considered at high risk, due to operative mortality (
. In the ma-
GORD
is less
≈
1– 2
%).
251
.
Fig 6.
20
Hiatus hernia— sliding and rolling.
Fig 6.
21
CT chest (IV contrast) showing the
rolling components of a hiatus hernia anterior
to the oesophagus. Between the oesophagus
and the vertebral column on the left- hand side
is the aorta.
© Dr S Golding.
6 Gastroenterology
Upper gastrointestinal bleeding
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252
Haematemesis is vomiting of blood. It may be bright red or look like coee
grounds. Melaena (Greek melas = black) means black stool, often like tar, and has
a characteristic smell of altered blood. Both indicate upper
Take a brief history and
examine to assess severity.
Ask about Past GI bleeds;
dyspepsia/ known ulcers;
known liver disease or oesophageal varices; dysphagia; prolonged vomiting/
retching (can cause an oesophageal mucosal 'MalloryWeiss' tear); weight loss.
Check drugs (
steroids, thrombolytics, anticoagulants) and alcohol use. Is there serious comor-
NSAID
S, aspirin,
bidity (bad prognosis), eg cardiovascular disease, respiratory disease, hepatic or
renal impairment, or malignancy?
PR
and do a
• Peripherally cool/ clammy; capillary refill time >2s; urine output <0.5mL/ kg/ h.
•
• Tachycardic (pulse >
• Systolic BP <
• Calculate the Rockall score (tables
to check for melaena. Is the patient shocked? Also:
GCS
(tricky to assess in decompensated liver disease) or encephalopathy (p
100
mmHg; postural drop >20
Acute management (p
Common causes Rare causes
• Peptic ulcers
• Severe gastritis/
oesophagitis/ duodenitis
• Oesophageal varices
• Portal hypertensive
gastropathy
• Mallory– Weiss tear
• Malignancy
• No obvious cause.
Look for signs of chronic liver disease (p
100
bpm).
mmHg.
6.7, 6.8
804
). Skill in resuscitation determines survival, so get good
).
GI
bleeding.
• Angiodysplasia
• Dieulafoy lesion
• Gastric antral vascular
ectasia
• Aorto- enteric fistula
• Haemobilia
• Bleeding disorders
• Osler– Weber– Rendu
syndrome.
at this! Endoscopy comes only after initial resuscitation.
Further management Anatomy is important in assessing risk of rebleeding.
DU
Posterior
• Re- examine after 4h and consider the need for
• Hourly pulse, BP,
• A restrictive transfusion strategy has better outcomes,8 transfuse only if Hb
• Check
• Keep nil by mouth if at high rebleed risk (see
are highest risk as they are nearest to the gastroduodenal artery.
FFP
CVP,
urine output (4hrly if haemodynamically stable may be OK).
80
g/ L; ensure a current valid group & save sample.
<
FBC, U&E, LFT,
bleeds’ and ‘Risk scoring for upper
and clotting daily.
GI
bleeds’)— ask the endoscopist.
if >4 units transfused.
BOX
‘Management of peptic ulcer
Gastro- oesophageal varices
Submucosal venous dilatation 2° to portal pressures (may not have documented
liver disease— suspect varices if alcohol history); bleeding can be brisk, particularly
if underlying coagulopathy
Causes of portal hypertension Pre- hepatic Thrombosis (portal or splenic vein).
Intra- hepatic Cirrhosis (80% in UK); schistosomiasis (commonest worldwide);
sarcoid; myeloproliferative diseases; congenital hepatic fibrosis.
Budd– Chiari syndrome (
occlusive disease.
endoscopic features of the variceal wall and advanced liver disease.
Management Endoscopic banding (oesophageal) or sclerotherapy (gastric).
Prophylaxis 1°: ~30% of cirrhotics with varices bleed vs ~15% with non- selective
- blockade (propranolol
after a
1
st variceal bleed, 60% rebleed within 1yr. Use banding and non- selective
- blockade; transjugular intrahepatic portosystemic shunt (
varices.
2
° to loss of hepatic synthesis of clotting factors.
p
686
); right heart failure; constrictive pericarditis; veno-
Risk factors for variceal bleeds Portal pressure, variceal size,
20– 40
mg/ 12h PO) or repeat endoscopic banding. 2°:
TIPS
10
11
12
272
272
).
Post- hepatic
) for resistant
)
10
A Dieulafoy lesion is the rupture of an unusually big arteriole, eg in the fundus of the stomach.
11
Also known as 'watermelon stomach', red bands of ectatic submucosal vessels radiate from the pylorus.
12
A patient with an aortic graft repair and upper GI bleeding is considered to have an aorto- enteric fistula
until proven otherwise:
CT
abdomen is usually required as well as endoscopy.
6 Gastroenterology
Risk- scoring for upper GI bleeds
https://t.me/med1917
Glasgow Blatchford score (GBS) Used pre- endoscopy, so can be calculated
0– 23
when the patient first presents. The score ranges from
predicting an increased risk of requiring endoscopic intervention. If
the likelihood ratio for needing urgent endoscopy is
can be avoided— ie Hb
100
/ min; urea <6.5mmol/ L; no melaena or syncope + no past/ present liver dis-
<
130
g/ L (or
120
g/ L if ); systolic BP
, with higher scores
0.02
, therefore admission
110
mmHg; pulse
GBS
≈ 0,
ease or heart failure.
Rockall score Initial Rockall score is based on pre- endoscopy criteria; these are
added to post- endoscopy criteria for final score which predicts risk of rebleeding
and death (
Table 6.
Pre- endoscopy
Age
Shock: systolic
BP
Comorbidity
Post- endoscopy
Diagnosis Mallory– Weiss tear;
Signs of recent
haemorrhage
on endoscopy
Table 6.
Score Mortality with initial scoring Mortality after endoscopy
table
6.8
).
7
Rockall score calculation
0
pts
60
yrs
<
BP
>
100
& pulse rate
8
GI bleed mortality by Rockall score
0 0.2
1 2.4
2 5.6
3 11.0
4 24.6
5 39.6
6 48.9
7 50.0
8
+
mmHg
100
/ min
Pulse <
Nil major Heart failure;
no lesion; no sign of
recent bl eeding
None, or dark red
spot
%
–
%
%
%
%
%
%
%
1
pt
60– 79
yrs ≥80yrs
BP
>
100
mmHg
100
/ min
Pulse >
ischaemic
heart disease
All other
diagnoses
2
pts
BP
<
100
mmHg
Renal failure
Liver failure
GI
Upper
malignancy
Blood in
GI
tract;
upper
adherent clot;
visible vessel
0
0
0.2
2.9
5.3
10.8
17.3
27.0
41.1
%
%
3
pts
Metastases
%
%
%
%
%
%
%
253
Management of peptic ulcer bleeds based on endoscopic findings
High- risk Active bleeding, adherent clot, or non- bleeding visible vessel: achieve
endoscopic haemostasis (
start
PPI
(eg omepra zole 40mg/ 12h
80
mg bolus then 8mg/ h not superior). If haemodynamically stable start oral intake of
6
clear liquids
Low- risk Flat, pigmented spot or clean base: no need for endoscopic haemo-
stasis. Consider early discharge if patient otherwise low risk. Give oral
Regular diet
h after endoscopy. Treat if positive for H. pylori ( p
6
h after endoscopy if stable. Treat if positive for H. pylori (p
2
of: clips, cautery, adrenaline). Admit to monitored bed;
IV/ PO
; meta- analyses show 72h
IVI
, eg omeprazole
248
).
PPI
248
(p
248
).
).
6 Gastroenterology
Diarrhoea
BNF
FBC
ESR/ CRP
U&E
TSH
MC&S
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254
Diarrhoea is characterized by increased stool frequency and volume and decreased
consistency relative to the usual habit of the individual.
History As ever, a careful history will help narrow myriad causes to just a few.
Acute or chronic? If acute (<2wks) suspect gastroenteritis— any risk factors: travel
p
425
)? Diet change? Contact with
(
of listeriosis)?
Chronic diarrhoea alternating with constipation suggests
HIV
; achlorhydria (eg PA, p
D&V
? Any fever/ pain? Pregnant (20× risk
330
), or on acid suppressants, eg
IBS
(p
nocturnal diarrhoea, or anaemia mandate close follow- up (coeliac/
4
wks (fig
6.22
Chronic is ≥
).
Inflammatory? Small volume, high frequency, urgency, pre- defecation lower ab-
dominal cramping, tenesmus. May be nocturnal, bloody, and associated with fever
and shock. (See
large volume, upper abdominal cramping.
Bloody? Campylobacter, Shigella/ Salmonella (p
Crohn’s, colorectal cancer (
chaemic colitis (
Mucus Occurs in
Frank pus Suggests
Explosive Eg cholera; Giardia; Yersinia (p
Steatorrhoea (See fig
Drugs? (Many potentially to blame, see
abuse, propranolol, digoxin,
with microscopic colitis.
fig
6.22
for causes.) Non- inflammatory diarrhoea is watery and
427
p
608
p
617
). Fresh PR bleeding: p
IBS
(p
IBD
), colonic polyps, pseudomembranous colitis, is-
264
), colorectal cancer, and polyps.
, diverticulitis, or a fistula/ abscess.
6.22
.)
14
PPI
S,
NSAID
S. The latter two are particularly associated
), E. coli, amoebiasis (p
621
.
427
); Rotavirus.
.
) Eg antibiotics,13 cytotoxics, laxative
Look for Dehydration— dry mucous membranes, skin turgor; capillary refill >2s;
p
242
shock. Any fever, weight, clubbing, anaemia, oral ulcers (
), rashes or abdominal mass or scars? Any goitre/ hyperthyroid signs? Do rectal exam for masses (eg
rectal cancer) or impacted faeces:
• Blood
:
MCV
B
or
12
infection, Crohn’s/
serology:
• Stool
‘Clostridium difficile’), viral
tory causes (
sorption, steatorrhoea).
• Lower GI endoscopy (Malignancy? Colitis?) If acutely unwell, limited flexible
sigmoidoscopy with biopsies. Full colonoscopy (including terminal ileum) can as-
/ Fe defi cien cy, eg coelia c or colon ca ;
absorption, eg in coeliac or Crohn’s; eosinophilia if parasites.
UC
, cancer.
p
262
.
:
K
+
≈ severe
D&V
: bacterial pathogens, ova cysts, parasites, C. diff toxin (
PCR
p
258
, p
. Faecal calprotectin: highly sensitive for inflamma-
260
). Faecal elastase: if suspect chronic pancreatitis (malab-
MCV
.
: thyrotoxicosis. Coeliac
sess for more proximal disease If normal, consider small bowel radiology or video
capsule.
Management Treat cause. Food handlers: no work until stool samples are – ve.
If a hospital outbreak, wards may need closing. Oral rehydration is better than
IV
, but if sustained diarrhoea or vomiting, IV fluids with appropriate electrolyte
replacement may be needed. Codeine phosphate
PO
after each loose stool (max 16mg/ day) stool frequency (avoid in colitis; both
30
mg/ 8h PO or loperamide 2mg
may precipitate toxic megacolon). Avoid antibiotics unless infective diarrhoea is
causing systemic upset, but consider metronidazole if C. diff is suspected (see
Antibiotic- associated diarrhoea
13
may respond to probiotics (eg lactobacilli).
). Weight,
UC
/ Crohn’s?).
428
PPI
), UC,
264
if alcohol abuse
CDT
, see
BOX
BOX
?
:
).
13
Erythromycin is prokinetic, others cause overgrowth of bowel organisms, or alter bile acids.
14
Think of this in any chronic watery diarrhoea; diagnosis by biopsy. Associated with a range of drugs in-
cluding
NSAID
S and
PPI
S. Stop the oending drug where possible. Treat with budesonide.
6 Gastroenterology
Fig 6.
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22
Chronic diarrhoea dierential diagnosis according to history and stool assessment.
* Non- absorbed carbohydrate; lab tested with stool electrolytes, pH, and osmotic gap in watery diarrhoea.
†
Vasoactive intestinal polypeptide- secreting tumour; suspect if K+ and acidosis; Ca
Clostridium difficile: the cause of pseudomembranous colitis
First isolated from stools of healthy neonates, C. difficile was named owing to difficulties in culture. Today, ‘difficile’ might better refer to challenges of containment.
Signs T°; colic; diarrhoea with systemic upset—
(with yellow adherent plaques on inflamed non- ulcerated mucosa— the pseudomembrane) progressing to toxic megacolon and multi- organ failure.
Asymptomatic carriage 2– 5% of all adults. Only problematic with gut ecology
disrupted by, eg antibiotics, leading to rapid proliferation and toxin expression.
Predictors of fulminant C. diff colitis >70yrs, past C. diff infection; use of
antiperistaltic drugs; severe leucocytosis; haemodynamic instability.
Detection Urgent testing of suspicious stool (characteristic smell— ask the
nurses). Two- stage process with rapid screening test for C. diff protein (or
followed by specific
ELISA
Stop causative antibiotic if possible. Mild disease: metronidazole
10– 14
d (vancomycin
vancomycin
Urgent colectomy may be needed if toxic megacolon,
Recurrent dise ase Comm on (≈20
≈
50
%. Fidaxomicin (
to
125
500
mg/ 6h PO is better in severe disease). Intensive regimens of
mg/ 6h with IV and PR van comyc in ma y be ne eded for n on- responders.
200
ated with lower relapse rates and is recommended. Faecal transplantation (introduction of a suspension prepared from the faeces of a screened donor via endoscopy or
NG/ NJ
tub e) is a highl y eective, if aesthetically unappealing, treatment.
via
Preventing spread Meticulous cleaning and appropriate bed management policies,
use of disposable gloves and aprons, hand- washing (not just gel— kill the spores).
CRP
,
WCC
, albumin, and colitis
for toxins.
AXR
for toxic megacolon.
400
LDH
, or if deteriorating.
%). After a first recurrence, the risk of another rises
mg/ 12h
PO)
, a minimally absorbed oral antibiotic, is associ-
2
+
; Mg
PCR
mg/ 8h PO for
)
2
.
255
6 Gastroenterology
Constipation
https://t.me/med1917
256
Constipation reflects pelvic dysfunction or transit time. Accepted definitions and
reported rates vary, but a place to start is the passage of ≤
often passed with diculty, straining, or pain, and a sense of incomplete evacu-
≈
2:1
ation. :
constipation + rectal bleeding ≈ cancer; constipation + distension + active bowel
sounds ≈ stricture/
. Doctors’ chief concerns are to find pointers to major pathology, eg
GI
The patient Ask about frequency, nature, and consistency of stools. Is there blood
or mucus in/ on the stools? Is there diarrhoea alternating with constipation (eg
p
264
)? Has there been recent change in bowel habit? Is she digitating the rectum or
vagina to pass stool?
when referring (refer if signs of colorectal ca, eg weight, pain, or anaemia).
Tests None in young, mildly aected patients. Threshold for investigation dimin-
ishes with age; triggers include:
ciency anaemia.
Blood
malignancy. Transit studies; anorectal physiology; biopsy for Hirschsprung’s are
occasionally needed.
Treatment Often reassurance, drinking more, and diet/ exercise advice (p
that is needed. Treat causes (
advised, but may cause bloating without helping constipation.
these measures fail, and try to use them for short periods only. Often, a stimulant
such as senna ± a bulking agent is more eective and cheaper than agents such as
Bulking agents Faecal mass, so stimulating peristalsis. They must be
lactulose.
taken with plenty of fluid and may take a few days to act.
GI
obstruction; colonic atony; faecal impaction. Bran powder 3.5g 2– 3 times/ d with
food (may hinder absorption of dietary trace elements if taken with every meal).
Ispaghula husk, eg
promptly (or else it becomes an unpleasant sludge). Methylcellulose, eg Celevac®
6
tablets/ 12h with ≥
on food daily.
1
300
Stimulant laxatives Increase intestinal motility, so do not use in intes-
tinal obstruction or acute colitis. Avoid prolonged use as it may cause colonic atony.
Abdominal cramps are an important
5– 10
tablets (
mg at night) or suppositories (10mg in the mornings) and senna (2– 4
tablets at night). Docusate sodium and dantron
tions. Glycerol suppositories act as a rectal stimulant. Sodium picosulfate (
at night) is a potent stimulant. Phosphate enemas are useful for rapid bowel evacuation prior to procedures.
painful anal conditions, eg fissure. Arachis oil enemas lubricate and soften impacted
faeces. Liquid paran should not be used for a prolonged period (
lipoid pneumonia, malabsorption of fat- soluble vitamins).
fluid in the bowel. Lactulose, a semisynthetic disaccharide, produces osmotic diarrhoea of low faecal pH that discourages growth of ammonia- producing organisms.
It is useful in hepatic encephalopathy (initial dose:
its role in treating constipation is limited. Macrogol (eg Movicol®) is a better tolerated example. Magnesium salts (eg magnesium hydroxide; magnesium sulfate)
are useful when rapid bowel evacuation is required. Sodium salts (eg Microlette®
and Micralax® enemas) should be avoided as they may cause sodium and water
retention.
If these don’t help Prucalopride is a selective
erties; lubiprostone is a chloride- channel activator that increases intestinal fluid
secretion; linaclotide is a guanylate cyclasetion and decreases visceral pain. Naloxegol (an opioid blocker bound to macrogol)
has recently been authorized for laxative- resistant opioid- induced constipation.
A multidisciplinary approach with behaviour therapy, habit training ± sphincter bio-
feedback may help.
15
Rectocele: front wall of the rectum bulges into the back wall of the vagina.
16
Dantron causes colon & liver tumours in animals, so reserve use for the very elderly or terminally ill.
2
bowel motions/ wk,
obstruction; constipation + menorrhagia ≈ hypothyroidism.
IBS
15
Ask about diet and drugs. PR examination is essential even
9 weight, abdominal mass, +
2
FBC, ESR, U&E
+
, Ca
,
TFT
. Colonoscopy If suspected colorectal
BOX
‘Causes of constipation’). A high- fibre diet is often
PR
blood, iron defi-
239
) is all
Only use drugs if
CI
: diculty in swallowing;
Fybogel® sachet after a meal, mixed in water and swallowed
mL water. Sterculia, eg Normacol® granules, 10mL sprinkled
SE
. Pure stimulant laxatives are bisacodyl
16
have stimulant and softening ac-
5– 10
mg
Stool softeners Particularly useful when managing
SE
: anal seepage,
Osmotic laxatives Retain
30– 50
mL/ 12h). SE: bloating, so
5HT
agonist with prokinetic prop-
4
C
agonist that also increases fluid secre-
,
3
–
6 Gastroenterology
Causes of constipation
https://t.me/med1917
General
• Poor die t ± lack o f exerci se.
• Poor fluid intak e/ dehydration.
• Irritable bowel syndrome.
• Old age.
• Post - operative pain.
• Hospital environment (privacy;
having to use a bed pan).
Anorectal disease (Esp. if painful.)
Anal or colorectal cancer.
• Fissures (p
• Rectal prolapse.
• Proctalgia fugax (p
• Mucosal ulceration/ neoplasia.
• Pelv ic muscle d ysfunc tion/ levator ani
Intestinal obstruction
• Strictures (eg Crohn’s disease).
• Pelv ic mass (eg fetus, fibroid s).
• Diverticulosis (rectal bleeding is a
• Pseudo- obstruction (p
Metabolic/ endocrine
• Hypercalcaemia (p
• Hypothyroidism (rarely presents
622
), strictures, herpes.
622
syndrome.
Colorectal carcinoma (p
commoner presentation).
with constipation).
668
603
).
).
608
).
).
• Hypokalaemia (p
• Porp hyria.
• Lead poisoning.
Drugs (Pre- empt by diet advice.)
• Opiates (eg morphine, codeine).
• Anticholinergics (eg tricyclics).
• Iron.
• Some antacids, eg with aluminium.
• Diuretics, eg furosemide.
• Calcium channel blockers.
Neuromuscular (Slow transit from
decreased propulsive activity.)
• Spinal or pelvic nerve injury (eg
trauma, surgery).
• Aganglionosis (Chagas’ disease,
Hirschsprung’s disease).
• Systemic sclerosis.
• Diabetic neuropathy.
Other causes
• Chronic laxative abuse (rare—
diarrhoea is commoner).
• Idio pathic s low trans it.
• Idio pathic m egarect um/ colon.
• Fun cti onal con stip ati on.
666
).
257
6 Gastroenterology
Ulcerative colitis (UC)
MC&S/ CDT
AXR
https://t.me/med1917
258
UC
is a relapsing and remitting inflammatory disorder of the colonic mucosa. It may
aect just the rectum (proctitis, as in ~
(left- sided colitis, in ~
proximal to the ileocaecal valve (except for backwash ileitis). Cause Inappropriate
immune response against (?abnormal) colonic flora in genetically susceptible in-
Patho logy Hyperaemic/ haemorrhagic colonic mucosa ± pseudopolyps
dividuals.
formed by inflammation. Punctate ulcers may extend deep into the lamina propria—
inflammation is normally not transmural. Continuous inflammation limited to the
mucosa dierentiates it from Crohn’s disease.
Incidence 10– 20/
100 000
as common in non- smokers (opposite is true for Crohn’s disease)— symptoms may
relapse on stopping smoking.
Symptoms Episodic or chronic diarrhoea (± blood & mucus); crampy abdominal dis-
comfort; bowel frequency relates to severity (
Systemic symptoms in attacks: fever, malaise, anorexia, weight.
Signs May b e non e. In acute , sev ere UC there may be fever, tachycardia, and a tender,
distended abdomen.
nodosum (
fig
6.23
, p
large joint arthritis; sacroiliitis; ankylosing spondylitis;
Complications Acute Toxic dilatation of colon (mucosal islands, colonic diameter
6
cm) with risk of perforation; venous thromboembolism: give prophylaxis to all in-
>
patients regardless of rectal bleeding (
disease extent and activity
occur in flat, normal- looking mucosa. To spot precursor areas of dysplasia, surveillance
colonoscopy, eg
guided by dierential uptake by abnormal mucosa of dye sprayed endoscopically.
Tests Blood
1– 5
yrs (depending on risk), with multiple random biopsies or biopsies
FBC, ESR, CRP, U&E, LFT
ment tests early (see
C. difficile, Salmonella, Shigella, E. coli, amoebae.
non- invasive test for GI inflammation with high sensitivity.
mucosal thickening/ islands (
Lower GI endoscopy Limited flexible sigmoidoscopy if acute to assess and biopsy;
full colonoscopy once controlled to define disease extent (see
Table 6.
9
Assessing severity in UC (Truelove & Witts criteria modified to include
Variable Mild
Motions/ day
Rectal bleeding Small Moderate Large
T°C
Resting pulse
Haemoglobin
ESR
(do
CRP
Data from Truelove et al., ‘Cortisone in ulcerative colitis’, BMJ; 2(
≤
Apyrexial
<
>
too) <
Treatment Goals are to induce, then maintain disease remission. Management is
based on the severity and anatomical extent of disease.
Inducing remission
Mild to moderate UC: • Fo r di sta l d isea se (pr octi tis an d pr octo sig moi diti s) top ical
eg mesalazine is the mainstay; suppositories or enemas, eg Pentasa®
sion is not achieved after a month, consider adding
daily) and/ or a topical steroid (eg hydrocortisone as Colifoam®, or prednisolone
retention enemas as Predsol®).
mission after
40
17 5
Alternatively, olsalazine is a dimer of
Rare hypersensitivity reactions: worsening colitis, pancreatitis, pericarditis, nephritis.
1
month stop the topical treatment and add a course of oral prednisolone
mg/ d for 1wk, then taper by 5mg/ week over following 7wks, then maintain on
- aminosalicylic acid (
5- ASA
30
40
%) or the entire colon (pancolitis, in ~30%). It ‘never’ spreads
%) or extend to involve part of the colon
Prevalence
200– 1000/ 100 000
/ yr; typically presents ~15– 40yrs. Associations UC is 3- fold
table
6.9
); urgency/ tenesmus ≈ proctitis.
Extra- intestinal signs Clubbing; aphthous oral ulcers; erythema
261
); pyoderma gangrenosum; conjunctivitis; episcleritis; iritis;
≈
p34); K+ Chronic Colonic cancer: risk related to
5– 10
% if uncontrolled pancolitis for 20yrs. Neoplasms may
PSC (
p
278
); nutritional deficits.
, blood culture. Consider performing pretreat-
BOX
). Stool
(See p
254
.) To exclude Campylobacter,
Faecal calprotectin A simple,
fig
16.9
, p
713
); colonic dilatation (see ‘Complications’).
UC
4 5
70
beats/ min
110
g/ L
30
Moderate
UC
37.1– 37.8
°C >37.8°C
70– 90
beats/ min >90 beats/ min
105– 110
g/ L <
4947
PO 5- ASA
• For ext ensi ve di seas e com bin e PR +
or mesalazine) must be stabilized in oral preparations to survive gastric pH.
5-ASA
or balsalazide is a prodrug, both of which are cleaved in the colon.
No faecal shadows;
p
245
, fig
6.12
).
CRP
Severe uc
≥
6
105
>30 (or
):
1041– 8
.
treatment (eg Pentasa® 2g
)
g/ L
CRP
>45mg/ L)
1
g daily. If remis-
PO 5- ASA.
If no re-
5- ASA,
20
5- ASA
mg
.
17
.
6 Gastroenterology
Severe UC: admit for: IV hydration/ electrolyte replacement; IV steroids, eg hydro-
JAK
https://t.me/med1917
100
cortisone
tisone
ensure multiple stool
• Monitor T°, pulse, and BP— and record stool frequency/ character on a stool chart.
• Twice- daily exam: document distension, bowel sounds, and tenderness.
• Daily
• If on day 3– 5
ciclosporin or infliximab, can avoid colectomy, but involve surgeons early in shared care.
• If improving, transfer to prednisolone PO (40mg/ 24h). Schedule maintenance
infliximab if used for rescue, or azathioprine if ciclosporin rescue.
• If failure to improve then refer for urgent colectomy by d7– 10— the challenge is
not to delay surgery so long as to accumulate significant steroid exposure and
mg/ 6h or methylprednisolone 40mg/ 12h; rectal steroids, eg hydrocor-
100
mg in
100
mL 0.9% saline/ 12h PR; thromboembolism prophylaxis (p
MC&S/ CDT
to exclude infection.
FBC, ESR, CRP, U&E
±
AXR
CRP
. Consider blood transfusion (eg if Hb <80g/ L).
>45 or >6 stools/ d, action is needed.18 Rescue therapy with
debilitation that will delay post- surgical recovery.
Maintaining remission
Mild to moderate: PO (and/ or PR if distal)
decreasing relapse rates from
fective as split dose and may improve adherence.
U&E
at the start, then after 2– 3 months, then annually.
80
Moderate to severe: consider maintenance treatment escalation with immunomodulation in patients who flare on steroid tapering or require ≥
eg azathioprine (
ment cessation including abdominal pain, nausea, pancreatitis, leucopenia, abnormal
LFT
S. Monitor
3
least
2– 2.5
mg/ kg/ d PO). 30% of patients will develop SE requiring treat-
FBC, U&E, LFT
weekly for 4wks, then every 4wks for 3 months, then at
- monthly. Biologics were once reserved for those intolerant of immunosup-
5- ASA
is first line maintenance therapy,
% to 20% at 1 year. Once- daily dosing is as ef-
Nephrotoxicity risk; monitor
2
courses of steroids/ year,
pressive therapy, but with the availability of agents with less risk of toxicity and high
ecacy they are being increasingly used both to induce and maintain remission (see
BOX
‘Therapies in Crohn’s disease’, p
261
). Monoclonal antibodies to
(infliximab,
adalimumab, golimumab), to gut- selective integrins (vedolizumab), to interleukin
(ustekinumab) play an important role. Small molecule drugs including Janus kinase
) inhibitors (tofacitinib, filgotinib, upadacitinib) oer eective oral options.
(
Surgery This is needed at some stage in ~20%, eg subtotal colectomy + terminal
ileostomy for failure of medical therapy or fulminant colitis with toxic dilatation/
perforation. Subsequently completion proctectomy (permanent stoma) vs ileo– anal
pouch. Pouches mean stoma reversal and the possibility of long- term continence
but pouch opening frequency may still be around
can be troublesome (give antibiotics, eg metronidazole + ciprofloxacin for
6
×/ day and recurrent pouchitis
2
wks).
346
12/ 23
259
);
Immunomodulator and biologics pretreatment screening
All newly diagnosed
IBD
preparation for immunosuppressive treatment and because of the overall increased risk.
• TB screening— ask about prior infection and exposures.
release assay (
• Vac cinat ion his tory— consider updating vaccinations in all patients prior to treat-
ment, at least
vaccin ation if immunosuppression planned.
• Serology— screen for
history of chickenpox, shingles, or vaccination.
• Azathioprine precautions— test for
activity), ensure cervical screening is up to date and provide skin cancer risk advice.
18
Day 3 stool frequency >8×/ day or frequency 3– 8×/ day &
admission.
19
Inherited thiopurine methyltransferase in <1% is associated with an increased risk of potentially
life- threatening bone marrow suppression.
IGRA
) (p
390
4
weeks before starting. Pneumococcal and annual flu vaccine.
patients should be screened for infection risk, both as
CXR
and interferon- gamma
) in those considered for biologic therapy.
HCV, HBV, HIV
. Varicella IgG testing in patients without a clear
TPMT
ac tiv ity19 ( dose if low activity; avoid if no
CRP
>45 = 85% chance of colectomy this
VZV
6 Gastroenterology
Crohn’s disease
MRI
US
https://t.me/med1917
260
A chronic inflammatory disease characterized by transmural granulomatous inflammation aecting any part of the gut from mouth to anus (esp. terminal ileum in ~
UC
, there may be unaected bowel between areas of active disease (skip le-
Unlike
sions). Cause As with
gut flora in a genetically susceptible individual.
Incidence 10– 20/
3– 4
risk ×
100 000
;
NSAID
S may exace rbate d iseas e.
Symptoms Diarrhoea, abdominal pain, weight loss/ failure to thrive. Systemic
symptoms: fatigue, fever, malaise, anorexia.
Signs Bowel ulceration (fig
tulae/ skin tags; anal strictures; aphthous ulcers (
Clubbing, skin, joint,
Complications Small bowel obstruction; toxic dilatation (colonic diameter >6cm,
toxic dilatation is rarer than in
fistulae (present in
~
anal, enterocutaneous; perforation; colon cancer;
Tests Blood
ment tests (see
Stool
calprotectin is a simple, non- invasive test for
Colonoscopy + biopsy Even if mucosa looks normal. Small bowel To detect isolated
FBC, ESR, CRP, U&E, LFT, INR
BOX
MC&S
‘Immunomodulator and biologics pretreatment screening’ p
and
CDT
(p
proximal disease by, eg capsule endoscopy (
that disintegrates if it gets stuck);
fistulae, small bowel disease activity and strictures;
small bowel imaging.
Tre at me nt Find out how your patient deals with what may be a brutal disease (no
intimacy... no sex... no hope... ‘I live with this alone and will die alone’). With a collaborative approach, courage, attention to detail, and psychological support, this can
change. Help quit smoking.
WCC, CRP
, + albumin may merit admission for IV steroids.
Inducing remission
Mild to moderate: symptomatic but systemically well. Prednisolone 40mg/ d PO for
1
wk, then taper by 5mg every wk for next 7wks. Budesonide (an enteric- coated
steroid with extensive
there are contraindications, but is less eective. Exclusive enteral nutrition (
is an alternative dietary approach based upon a liquid diet with polymeric (whole
protein) or semi- elemental (peptide)- based feeds (more palatable than the elemental diet), is eective in children but used less in adults.
Severe: consider admission for
and similar initial care to severe
40
mg/ d). A 'top- down' approach with the early introduction of biologics
olone (
may be considered in patients with an aggressive disease course or poor prognostic factors (see
complicating Crohn’s disease especially if abdominal pain (ultrasound,
BOX
often required to assess this). Seek surgical advice; laparoscopic resection should
be considered for those with relapsing localized ileocaecal disease.
Maintaining remission
Steroids are not eective in maintaining remission, regardless of how it is induced,
and expose patients to toxicity risk. Monotherapy with azathioprine is eective
BOX
‘Therapies in Crohn’s disease’). Methotrexate (at least 15mg weekly, sub-
(see
cutaneous dosing preferred) is an alternative. Combination therapy with infliximab
should be considered in more severe cases, but there are long- term safety issues
(eg increased lymphoma risk). Biologics may be considered in those refractory to
immunomodulators (see
20
Much of the genetic risk is shared with UC— small dierences in genetics combined with environmental
modifiers may explain the very dierent phenotypes.
UC
an inappropriate immune response against the (?abnormal)
20
Prevalence
200– 1000/ 100 000
/ yr; typically presents ~15– 40yrs. Associations Smoking
6.24
); abdominal tenderness/ mass; perianal abscess/ fis-
&
eye problems.
UC
10
); abscess formation (abdominal, pelvic, or perianal);
%), eg entero- enteric, colovesical (bladder), colovaginal, peri-
, ferritin,
254
) to exclude, eg C. difficile, Campylobacter, E. coli; faecal
increasingly used to assess pelvic disease and
p
242
). Beyond the gut (fig
PSC
(p
278
), malnutrition.
TIBC, B
, folate. Biologics pretreat-
12
GI
inflammation with high sensitivity.
p
244
, use dummy patency capsule 1st
in skilled hands can provide
Optimize nutrition. Assess severity: T°, pulse,
1
st- pass metabolism) has fewer side eects so is useful if
IV
hydration/ electrolyte replacement; IV steroids
UC
(p
259
). If improving switch to oral prednis-
‘Therapies in Crohn’s disease’). Consider abdominal sepsis
CT, & MRI
BOX
‘Therapies in Crohn’s disease’).
70
%).
6.23
259
ESR
EEN
are
.
)
)
,
)
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