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CHAPTER12 Gastrointestinalmedicine
Hepatitis
Acute hepatitis May be asymptomatic or present with fatigue, u- like
symptoms, fever, light stools, dark urine, and/ or jaundice. Causes:
• Viral hepatitis (e.g. HBV, HAV, EBV)
• Alcohol (E p. 158)
• Drugs (e.g. diclofenac, co- amoxiclav)
• Toxins
Management Check LFTs, FBC, U&E, eGFR, hepatitis serology. Treat the
cause. Admit if condition is poor or rapidly deteriorating; refer for investigation if sustained abnormalities in liver function with unclear cause (Ep.
390). Complications:chronic hepatitis, acute liver failure.
Hepatitis A(HAV) Common. Spread:faecal– oral route. Patients are in-
fectious 2wk before feeling ill. Incubation is 2– 7wk (average 4wk). High- risk
groups:travellers to high- risk areas, institutional inhabitants and workers, IV
drug abusers, patients with high- risk sexual practices. May be asymptomatic
(especially young children) or present with fever, malaise, fatigue, anorexia,
nausea/ vomiting, abdominal pain, diarrhoea, tender hepatomegaly, pale
stools, dark urine, and/ or jaundice (70– 80% adults).
Management Check LFTs (hepatic jaundice— Table 12.17, E p. 391) and
hepatitis serology. IgM antibodies signify recent infection. Immunity follows
infection, and IgG remains detectable lifelong. Management is supportive.
Avoid alcohol until LFTs are normal. Most recover in <2mo. Hepatitis
Adoes not cause chronic liver disease; there is no carrier state.
Prevention Vaccination is indicated for travellers to high- risk areas,
people with chronic liver disease, or those working in high- risk situations.
Preparations available include monovalent vaccine (e.g. Havrix®), hepatitis
Aand B combined vaccine (Twinrix®), and hepatitis Aand typhoid combined vaccine (e.g. Hepatyrix®). Passive immunization with human immunoglobulin gives protection for ≤3mo and is used for short- term travel or
protecting household contacts of suerers.
Hepatitis E (HEV) Similar to HAV infection. Usually acquired in
developing countries. Incubation is 2– 9wk (average 40d). Diagnosis is made
with serology. Treatment is supportive. There is no chronic state. Mortality
in pregnancy can be as high as 20%. No vaccine exists.
Hepatitis B (HBV) E p. 718
Hepatitis C (HCV) E p. 718
Chronic hepatitis Hepatitis lasting >6mo. May be asymptomatic
or present with fatigue; RUQ pain; jaundice; arthralgia; signs of chronic
liver disease— gynaecomastia, testicular atrophy, clubbing, palmar erythema, leuconychia, peripheral oedema, spider naevi, portal hypertension,
• Obstructive jaundice
• Other infections— malaria, Q
fever, leptospirosis, yellow fever
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HEPATITIS
recurrent infection; and/ or complications— acute liver failure, cirrhosis,
hepatocellular carcinoma. Causes:
• Viral hepatitis
• Alcohol— E p. 158
• Drugs (e.g. nitrofurantoin, methyldopa,
isoniazid)
• Chronic autoimmune hepatitis
Management Check LFTs; FBC; U&E; eGFR; and hepatitis screen
(Ep.391). Refer for specialist care.
• Primary biliary cholangitis
• Wilson’s disease
• Haemochromatosis
• α1- antitrypsin deciency
• Sarcoidosis
Chronic autoimmune hepatitis Also known as ‘chronic active hepa-
titis’. Typically young women. Associated with personal/ family history of
autoimmune disease (e.g. RA, vitiligo). Diagnosis is conrmed with liver biopsy and autoimmune markers. Specialist management is with steroids ±
immunosuppressants.
Primary biliary cholangitis Slow progressive cholangio- hepatitis
eventually resulting in cirrhosis. : 89:1. Peak age at presentation:45y.
Cause:probably autoimmune. Associations:
• Thyroid disease
• Sjögren’s syndrome
• CREST syndrome
Presentation 50% are asymptomatic at presentation. Symptoms/ signs:
• Fatigue
• Pruritus
• Arthralgia
Investigation and management Blood:LFTs (i alk phos, iALT, iGGT). Liver
biopsy is diagnostic. Refer for specialist care. If asymptomatic, 1:3 remain
symptom free— the rest develop symptoms in 2– 4y. Median survival is 7–
10y. Liver transplant is an option. Prognosis following transplant is good but
recurrence may occur in the transplanted liver.
• Osteoporosis/
• Hirsutism
• Coeliac disease
• Hepatic and extra- hepatic malignancy
• Pancreatic hyposecretion
osteomalacia
• Obstructive jaundice (late)
• Symptoms/ signs of cirrhosis
or liver failure
Information and support forpatients
British Liver Trust F 0800 652 7330 M www.britishlivertrust.org.uk
PBCers Organization M www.pbcers.org
Wilson’s Disease Association M www.wilsonsdisease.org
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CHAPTER12 Gastrointestinalmedicine
Liver failure and portalhypertension
• Acute liver failure Presents withsudden onset ofsevere illness.
• Jaundice
• Hypoglycaemia
• Hepatic encephalopathy— ranges from mild confusion and irritability
through drowsiness and i confusion to coma
• Haemorrhage— due to deranged clotting factors
• Ascites— hepatosplenomegaly and ascites are not usually prominent
• Infection
• Nausea ± vomiting
• i BP
• Fetor hepaticus (sweet smell on the breath)
Causes
In previously healthy patients:
• Viral hepatitis
• Weil’s disease
• Paracetamol overdose
• Halothane
• Idiosyncratic drug reactions
• Fungal/ plant toxins
• Malignant inltration
In patients withchronic liver disease:
• Infection
• GI bleeding
• Sedation
Management Admit as emergency unless an expected terminal event.
Prognosis is poor (<60% survive).
• Chemical exposure (e.g. carbon
tetrachloride)
• Heatstroke
• Budd– Chiari syndrome
• Pregnancy
• Wilson’s disease
• Reye’s syndrome
• Diuretics and/ or electrolyte imbalance
• Alcohol binges
• Constipation
Cirrhosis The liver is replaced by brotic tissue and regenerating nodules
of hepatocytes.
Common causes/ riskfactors
• Hepatitis B infection E p. 718
• Alcohol misuse E p. 158
Screening high- risk groups Oer transient elastography (TE) if:
• Chronic hepatitis B/ C infection— retest every 2y or more frequently
according to specialist advice
• Persistent heavy drinker ( >35U/ wk; >50U/ wk) or conrmed
alcohol- related liver disease— retest every 2y
• Non- alcoholic fatty liver disease + advanced liver brosis (Enhanced
Liver Fibrosis test score ≥10.51)— retest every 3y
• Liver biopsy is an alternative if TE is not suitable
0 Do not use liver function blood tests to rule out cirrhosis.
• Hepatitis C infection E p. 718
• Type 2 DM or BMI ≥30kg/ m
Rarercauses
• Chronic active hepatitis E pp. 394–5 • Wilson’s disease E p. 398
• Primary biliary cholangitis
E p. 395
• α1- antitrypsin deciency E p. 398
• Budd– Chiari syndrome
Ep.399
• Haemochromatosis E p. 398
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LIVER FAILURE AND PORTALHYPERTENSION
Presentation Variable. May be an incidental nding with no symptoms or
may present with non- specic symptoms, e.g. weakness, fatigue, lethargy.
Specic symptoms/ signs include:
• Hepatomegaly (but liver becomes small
and hard in late stages)
• Spider naevi
• Dupuytren’s contracture
• Palmar erythema
• Gynaecomastia
Late signs Occur when the liver can no longer compensate for the damage
to it— jaundice, hepatic encephalopathy, leuconychia, and oedema (due to
hypoalbuminaemia).
Management
• Refer to gastroenterology/ hepatology for expert advice
• Avoid alcohol completely and refer to dietician for advice on nutrition
• Pruritus 2° to jaundice may respond to cholestyramine
• Give pneumococcal vaccination and annual inuenza vaccination
Complications
• Portal hypertension (± bleeding
oesophageal varices)
• Encephalopathy
• Hepatocellular carcinoma
Prognosis Very variable— depending on age, cause, and willingness to
modify contributing lifestyle factors.
• Testicular atrophy
• Clubbing
• Xanthelasma/ xanthomata
• Portal hypertension
• Splenomegaly
• Ascites (bacterial peritonitis
complicates 1 in 4 cases— consider
prophylaxis with ciprooxacin)
• Renal failure
Portal hypertension Portal venous pressure is raised due to obstruc-
tion of the portal system before, within, or after the liver. In Western countries the most common cause is cirrhosis.
• Elevated portal venous pressure l collaterals between the portal and
systemic circulation (including oesophageal varices). Usually presents
with haematemesis and/ or melaena from bleeding varices
• Ascites develops if there is coexistent liver failure with
hypoproteinaemia and hyperaldosteronism
• Splenomegaly is common l thrombocytopenia and leucopenia
• Signs:splenomegaly (80– 90%), ascites, dilated veins around the
umbilicus (rare), purpura, signs of chronic liver disease
• After a diagnosis of cirrhosis, oer upper GI endoscopy to detect
oesophageal varices— repeat every 3y if– ve
• Refer to gastroenterology/ hepatology. Specialist management is
essential. If GI bleeding, refer as a ‘blue light’ emergency
Hepatocellular carcinoma E p. 398
Further information
NICE (2016) Cirrhosis in over 16s. M www.nice.org.uk/ guidance/ ng50
Information and support forpatients
British Liver Trust F 0800 652 7330 M www.britishlivertrust.org.uk
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CHAPTER12 Gastrointestinalmedicine
Other liverdisease
Gilbert’s syndrome Inherited metabolic disorder causing unconjugated
hyperbilirubinaemia. Prevalence: 71– 2%. Onset is shortly after birth— but
the condition may go unnoticed for years. Jaundice occurs during intercurrent illness. i bilirubin on fasting can conrm the diagnosis. Liver biopsy is
normal. No treatment is required and prognosis is excellent.
Primary haemochromatosis Autosomal recessive condition of ex-
cess gut absorption of iron l iron deposition and damage to heart, liver,
pancreas, joints, and pituitary. 71:400 people are homozygous for the condition but expression is highly variable. > ( present 710y later). Often
an incidental nding, or found by screening relatives of aected individuals
(genetic testing or serum ferritin). Symptoms/ signs:
• Tiredness
• Arthralgia/ arthritis
• Skin pigmentation
Investigation and management Blood:i ferritin; i iron; transferrin satur-
ation >70%; total iron binding capacity d. Refer. Liver biopsy is diagnostic.
Venesection returns life expectancy to normal.
Secondary haemochromatosis Iron overload from frequent
transfusions, e.g. for haemolysis. Specialist management with chelation
therapy to i iron excretion is required.
α1- antitrypsin deciency Autosomal recessive disorder. Defective
α1- antitrypsin production l lung, and more rarely liver damage.
Treatment with IV α1- antitrypsin d progression of COPD. Paracetamol
may protect the liver. Encourage use for minor illness. Liver transplantation
may eventually be needed.
Wilson’s disease (hepatolenticular degeneration) Rare, auto-
somal recessive disorder. Defective biliary copper excretion l accumulation of copper in the liver, brain, kidney, and cornea. Treatment is with
penicillamine. Liver transplantation is the only treatment if presentation is
with acute liver failure.
Benign tumours Hepatomegaly ± RUQ pain or an incidental nding.
Common types Hepatic adenoma, broma, leiomyoma, lipoma, haemangioma, focal nodular hyperplasia (e.g. with cirrhosis).
Management Refer to gastroenterology to exclude malignancy and conrm
diagnosis. Urgency depends on clinical picture and USS ndings.
Hepatocellular cancer (HCC) Rare in the UK (100 new cases and
100 deaths/ y). Much more common in areas of the world where hepatitis
B is endemic (e.g. China, India). Usually arises from regenerating nodules in
a cirrhotic liver. Peak age:60– 70y. Intra- and extrahepatic spread is common
and occurs early.
Surveillance All patients with conrmed cirrhosis should have regular USS
surveillanceN. Usually this is specialist led.
• Hepatomegaly ±
signs of cirrhosis
• DM
• Impotence/ testicular
atrophy
• Cardiomyopathy
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OTHER LIVERDISEASE
Presentation In a patient with known cirrhosis:
• Fatigue
• Fever
• Rapid deterioration in liver function
• Haemorrhage into the peritoneal cavity (often fatal)
• Budd– Chiari syndrome (occlusion of the hepatic vein resulting in jaundice,
epigastric pain, and shock)
• Examination— may reveal an abdominal mass, hepatomegaly ± an
arterial bruit over the tumour
Management If suspected, check AFP and refer for urgent assessment. AFP
>500ng/ mL in a patient with known cirrhosis is almost certainly diagnostic.
The most important prognostic factors are the number and size of the liver
lesions and the presence of vascular involvement. 95% of patients with cirrhosis have disease too extensive for curative surgery, or their severely
compromised liver function makes radical surgery inappropriate. 50% of
patients without cirrhosis have resectable tumours. Surgery may be combined with liver transplantation. Inoperable tumours may be treated with
hepatic artery ligation or embolization. Tumours respond poorly to chemo-
or radiotherapy.
Overall prognosis Patients with cirrhosis— median survival 3mo; patients
without cirrhosis— median survival 1y.
• Anorexia and/ or weight d
• Ascites
Cholangiocarcinoma Rare adenocarcinoma of the biliary tract. May
be associated with UC. Typically presents in patients >60y with jaundice,
RUQ pain and weight loss. The only eective treatment is surgery, which is
only possible in ~10– 20% of patients. Selected t patients with unresectable
disease may be oered palliative chemotherapy or enrolment in a clinical
trial. Median survival 4– 6mo.
Secondary tumours The most common type of liver tumours—
usually signalling late disease. Presentation:hard, enlarged, knobbly liver ±
RUQ pain ± jaundice (late). If found and no history of malignancy refer to
oncology/ general surgery for urgent referral to nd the primary.
Primary tumours commonly metastasizing to the liver Lung, breast, large
bowel, stomach, uterus, pancreas, carcinoid, lymphoma, leukaemia.
Further information
British Society for Haematology M www.b- s- h.org.uk/ guidelines/
• Investigation and management of a raised serum ferritin (2018).
• Diagnosis and therapy of genetic haemochromatosis (2018).
NICE (2015, updated 2017)Suspected cancer:recognition and referral
Mwww.nice.org.uk/ guidance/ ng12
Advice and support forpatients
Alpha- 1 Support for people with α1- antitrypsin deciency. M www.
alpha1.org.uk
British Liver Trust F 0800 652 7330 M www.britishlivertrust.org.uk
Cancer Research UK F 0808 800 4040 M www.cancerhelp.org.uk
Macmillan Cancer Support F 0808 808 0000 M www.macmillan.org.uk
Wilson’s Disease Association M www.wilsonsdisease.org
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CHAPTER12 Gastrointestinalmedicine
Gallbladderdisease
Gallstones Gallstones are increasingly common. 9% of 60y- olds have
them and prevalence i with age.
Other riskfactors
• Gender ( > )
• Body weight— prevalence i with weight; also associated with rapid
weight d
• Race— in the USA Native American > Hispanic > white > black
• Auency
• Pregnancy (and possibly HRT but not COC pill)
• Alcohol is protective
• Diet— vegetarian diet is protective
Associatedconditions
• Haemolysis
• DM
• Hypertriglyceridaemia
Drugs which cause gallstones Clobrate (and other bric acid derivatives);
octreotide (somatostatin analogue).
Presentation Gallstones are blamed for many digestive symptoms— they are
probably innocent in most cases. 70% of stones in the gallbladder do not
cause symptoms. Common presentations— Table 12.18.
Management ofgallstones
• Advise the patient to stick to a low- fat diet
• Refer for surgical review ± further evaluation (e.g. ERCP— endoscopic
retrograde cholangiopancreatography)
• Gallstones can be removed by cholecystectomy (laparoscopic or open)
or ERCP or may be dissolved with ursodeoxycholic acid (stones <5mm
diameter— 40% recur in <5y) or shattered with lithotripsy (1 in 3
develop biliary colic afterwards)
• Persistent digestive symptoms after surgery are common (50% after
cholecystectomy) and dicult to treat
Gallbladder cancer Rare. > . Gallstones are a predisposing factor.
Typically presents in patients >40y with RUQ pain, anorexia, weight d, and
jaundice. Refer for specialist upper GI assessment (to be seen in <2wk)
if suspected. Surgical resection oers the only hope of cure but disease
is usually advanced at presentation. Selected t patients with unresectable
disease may be oered palliative chemotherapy or enrolment in a clinical
trial. Prognosis is poor.
Further information
NICE (2015, updated 2017)Suspected cancer:recognition and referral. M
www.nice.org.uk/ guidance/ ng12
Information and support forpatients
British Liver Trust F 0800 652 7330 M www.britishlivertrust.org.uk
• Cirrhosis
• Crohn's disease
• Partial gastrectomy
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GALLBLADDERDISEASE
Table12.18 Presentation and management ofgallstone disease
Presentation Management
Biliary colic Clear- cut attacks of
Acute
cholecystitis/
cholangitis
Pancreatitis E p. 402 E p. 402
Gallstone
ileus
Chronic
cholecystitis
Jaundice Cholestatic jaundice— E
severe upper abdominal
pain which may radiate
l back/ shoulder tip,
lasting ≥½ h and causing
restlessness ± jaundice ±
nausea or vomiting.
Examination:tenderness
±guarding in the right
upper quadrant (i on
deep inspiration—
Murphy’s sign)
Pain and tenderness in
the right upper quadrant/
epigastrium ± vomiting
Examination:tenderness
± guarding in the right
upper quadrant ± fever ±
jaundice
Occurs usually after an
attack of cholecystitis.
Astone perforates from
the gallbladder into the
duodenum and impacts in
the terminal ileum causing
bowel obstruction
Vague intermittent
abdominal discomfort,
nausea, atulence and
intolerance of f ats
p. 390 ± right upper
quadrant pain
Treat acute attacks with pethidine
(50mg IM/ po) or diclofenac (50– 100mg
IM/ PO/ PR) + prochlorperazine
12.5mg IM or domperidone 10mg po/
PR for nausea
Admit if:uncertain of diagnosis,
inadequate social support, persistent
symptoms despite analgesia, suspicion
of complications, and/ or concomitant
medical problems (e.g. dehydration,
pregnant, DM, Addison’s)
Investigate for gallstones with abdominal
USS to prove diagnosis when settled
Dierential diagnosis:any cause of acute
abdomen
Treat gallstones to prevent recurrence
Treatment:broad- spectrum antibiotic
(e.g. ciprooxacin) and analgesia as for
biliary colic
Admit if:generalized peritonism,
diagnosis uncertain, very toxic,
concomitant medical problems
(e.g. dehydration, DM, Addison’s,
pregnancy), inadequate social support,
or not responding to medication
Empyema occurs when the obstructed
gallbladder lls with pus. Presents with
persistent swinging fever and pain.
Usually requires cholecystectomy ±
surgical drainage
Investigate and follow- up to prevent
recurrence as for biliary colic
E p. 372
Investigate for gallstones with abdominal
USS to prove the diagnosis
Dierential diagnosis:reux, IBS, upper
GI tumour, PU
Refer for treatment of gallstones
E p. 390
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CHAPTER12 Gastrointestinalmedicine
Pancreatitis
Acute pancreatitis Premature activation of pancreatic enzymes results
in autodigestion and tissue damage. Most episodes are mild and self- limiting
but 1:5 patients have a severe attack. Overall mortality 85– 10%. May be
recurrent.
Causes In 10% patients no cause is identied.
• Common causes (80%) Gallstones, alcohol
• Rarer causes
• Drugs (e.g. azathioprine)
• Trauma
• Pancreatic tumours
• Post- ERCP
• Viral infection (mumps, HIV,
Coxsackie B)
• Mycoplasma infection
• Hypercalcaemia
Presentation
• Poorly localized, continuous, boring epigastric pain which i over 71h—
often worse lying down ± radiation to the back (50%)
• Nausea ± vomiting
Examination
• General Tachycardia, fever, shock, jaundice
• Abdominal Localized epigastric tenderness or generalized abdominal
tenderness; abdominal distension ± d bowel sounds; evidence of
retroperitoneal haemorrhage (periumbilical and ank bruising— rare)
Management Admit as an acute surgical emergency. Prior to transfer give
analgesia with pethidine (morphine may induce spasm of the sphincter
of Oddi).
Complications Delayed complications may present in general practice—
suspect if persistent pain or failure to regain weight or appetite.
Complications include:
• Pancreatic necrosis
• Pseudocyst— localized collection of pancreatic secretions
• Fistula/ abscess formation
• Bleeding or thrombosis
Prevention offurtherattacks
• Avoid factors that may have caused pancreatitis, e.g. alcohol, drugs
• Advise patients to follow a low- fat diet
• Treat reversible causes e.g. hyperlipidaemia, gallstones
Chronic pancreatitis Chronic inammation of the pancreas results in
gradual destruction and brosis of the gland ± loss of pancreatic function
l malabsorption and DM.
Cause Alcohol is responsible for most cases. More rarely: familial; CF;
haemochromatosis; pancreatic duct obstruction (gallstones/ pancreatic
cancer); hyperparathyroidism.
• Hyperlipidaemia
• Pancreas divisum (normal variant in
7– 8% of the white population)
• Familial pancreatitis
• Vasculitis
• Ischaemia or embolism
• Pregnancy
• End- stage renal failure
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PANCREATITIS
Presentation
• Constant or episodic epigastric pain radiating to the back and relieved
by sitting forwards
• Vomiting
• Weakness
• Jaundice
• Steatorrhoea
Management Refer to gastroenterology. Treatment:
• Diet Low- fat, high- protein, high- calorie diet with fat- soluble vitamin
supplements. Refer to dietician
• Pancreatic enzyme supplementation e.g. Creon® capsules pre- meals.
May improve diarrhoea
• Alcohol abstinence
• Pain control Provide analgesia— beware of opioid abuse. Consider
referral for coeliac plexus block
• Surgery Pancreatectomy or pancreaticojejunostomy for pancreatic duct
stricture, obstructive jaundice, unremitting pain, or weight loss
• Diabetes management
• Weight d
• DM
• Chronic poor health
Pancreatic insuciency Global d function of the pancreas. Causes:
• Child Cystic brosis
• Adult Chronic pancreatitis, pancreatic tumour, pancreatectomy, total
gastrectomy
Presentation Malabsorption (frequent loose, odorous stools ± abdominal
pain), weight loss or failure to thrive, DM.
Management Take specialist advice. Treat the underlying cause. Treat associated DM. Supplement digestive enzymes (e.g. with Creon).
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