Abdominal pain

The table below gives characteristic exam question features for conditions causing abdominal
pain. Unusual and 'medical' causes of abdominal pain should also be remembered:

 myocardial infarction
 diabetic ketoacidosis
 pneumonia
 acute intermittent porphyria
 lead poisoning

Condition Characteristic exam feature

Peptic ulcer disease Duodenal ulcers: more common than gastric
ulcers, epigastric pain relieved by eating
Gastric ulcers: epigastric pain worsened by eating
Features of upper gastrointestinal haemorrhage
may be seen (haematemesis, melena etc)
Appendicitis Pain initial in the central abdomen before
localising to the right iliac fossa
Anorexia is common
Tachycardia, low-grade pyrexia, tenderness in RIF
Rovsing's sign: more pain in RIF than LIF when
palpating LIF
Acute pancreatitis Usually due to alcohol or gallstones
Severe epigastric pain
Vomiting is common
Examination may reveal tenderness, ileus and
low-grade fever
Periumbilical discolouration (Cullen's sign) and
flank discolouration (Grey-Turner's sign) is
described but rare
Biliary colic Pain in the RUQ radiating to the back and
interscapular region, may be following a fatty
meal. Slight misnomer as the pain may persist for
hours
Obstructive jaundice may cause pale stools and
dark urine
It is sometimes taught that patients are female,
forties, fat and fair although this is obviously a
generalisation
Acute cholecystitis History of gallstones symptoms (see above)
 Continuous RUQ pain
Fever, raised inflammatory markers and white
cells
Murphy's sign positive (arrest of inspiration on
palpation of the RUQ)
Diverticulitis Colicky pain typically in the LLQ
Fever, raised inflammatory markers and white
cells
Abdominal aortic aneurysm Severe central abdominal pain radiating to the
back
Presentation may be catastrophic (e.g. Sudden
collapse) or sub-acute (persistent severe central
abdominal pain with developing shock)
Patients may have a history of cardiovascular
disease
Intestinal obstruction History of malignancy/previous operations
Vomiting
Not opened bowels recently
'Tinkling' bowel sounds

Diagram showing stereotypical areas

where particular conditions present. The diagram is not exhaustive and only lists the more common conditions
seen in clinical practice. Note how pain from renal causes such as renal/ureteric colic and pyelonephritis may
radiate and move from the loins towards the suprapubic area.
Failure of oesophageal peristalsis and of relaxation of lower oesophageal sphincter (LOS) due to
degenerative loss of ganglia from Auerbach's plexus i.e. LOS contracted, oesophagus above
dilated. Achalasia typically presents in middle-age and is equally common in men and women.

Clinical features

 dysphagia of BOTH liquids and solids

 typically variation in severity of symptoms
 heartburn
 regurgitation of food - may lead to cough, aspiration pneumonia etc
 malignant change in small number of patients

Investigations

 manometry: excessive LOS tone which doesn't relax on swallowing - considered most
important diagnostic test
 barium swallow shows grossly expanded oesophagus, fluid level, 'bird's beak'
appearance
 CXR: wide mediastinum, fluid level

Treatment

 intra-sphincteric injection of botulinum toxin

 Heller cardiomyotomy
 pneumatic (balloon) dilation
 drug therapy has a role but is limited by side-effects
 © Image used on license from Radiopaedia

This film demonstrates the classical 'bird's beak' appearance of the lower oesophagus that is seen in achalasia. An
air-fluid level is also seen due to a lack of peristalsis
 © Image used on license from Radiopaedia

Mediastinal widening secondary to achalasia. An air-fluid level can sometimes be seen on CXR but it is not visible
on this film
 © Image used on license from Radiopaedia

Barium swallow - grossly dilated filled oesophagus with a tight stricture at the gastroesophageal junction resulting
in a 'bird's beak' appearance. Tertiary contractions give rise to a corkscrew appearance of the oesophagus

Acute appendicitis

Acute appendicitis is the most common acute abdominal condition requiring surgery. It can
occur at any age but is most common in young people aged 10-20 years.

Abdominal pain is seen in the vast majority of patients:

 peri-umbilical abdominal pain (visceral stretching of appendix lumen and appendix is

midgut structure) radiating to the right iliac fossa (RIF) due to localised parietal
peritoneal inflammation.
 the migration of the pain from the centre to the RIF has been shown to be one of the
strongest indicators of appendicitis
 patients often report the pain being worse on coughing or going over speed bumps.
Children typically can't hop on the right leg due to the pain.
Other features:

 vomit once or twice but marked and persistent vomiting is unusual

 diarrhoea is rare. However, pelvic appendicitis may cause localised rectal irritation of
some loose stools. A pelvic abscess may also cause diarrhoea
 mild pyrexia is common - temperature is usually 37.5-38oC. Higher temperatures are
more typical of conditions like mesenteric adenitis
 anorexia is very common. It is very unusual for patients with appendicitis to be hungry
 around 50% of patients have the typical symptoms of anorexia, peri-umbilical pain and
nausea followed by more localised right lower quadrant pain

Examination

 generalised peritonitis if perforation has occurred or localised peritonism

 retrocaecal appendicitis may have relatively few signs
 digital rectal examination may reveal boggy sensation if pelvic abscess is present, or
even right-sided tenderness with a pelvic appendix
 Rovsing's sign (palpation in the LIF causes pain in the RIF) is now thought to be of limited
value

Diagnosis

 typically raised inflammatory markers coupled with compatible history and examination
findings should be enough to justify appendicectomy
 a neutrophil-predominant leucocytosis is seen in 80-90%
 urine analysis: useful to exclude pregnancy in women, renal colic and urinary tract
infection. In patients with appendicitis, urinalysis may show mild leucocytosis but no
nitrites
 ultrasound is useful in females where pelvic organ pathology is suspected. Although it is
not always possible to visualise the appendix on ultrasound, the presence of free fluid
(always pathological in males) should raise suspicion
 CT scans are widely used in patients with suspected appendicitis in the US but this
practice has not currently reached the UK, due to the concerns regarding excessive
ionising radiation and resource limitations

Management
  appendicectomy which can be performed via either an open or laparoscopic approach.
Laparoscopic appendicectomy is now the treatment of choice
 administration of prophylactic intravenous antibiotics reduces wound infection rates
 patients with perforated appendicitis (typical around 15-20%) require copious
abdominal lavage.
 patients without peritonitis who have an appendix mass should receive broad-spectrum
antibiotics and consideration given to performing an interval appendicectomy.
 be wary in the older patients who may have either an underlying caecal malignancy or
perforated sigmoid diverticular disease.
 trials have looked at the use of intravenous antibiotics alone in the treatment of
appendicitis. The evidence currently suggests that whilst this is successful in the
majority of patients, it is associated with a longer hospital stay and up to 20% of patients
go on to have an appendicectomy within 12 months.

Ultrasound examination may show

evidence of lumenal obstruction and thickening of the appendiceal wall as shown below
 Laparoscopic appendicectomy is
becoming increasing popular as demonstrated below

Acute liver failure

Acute liver failure describes the rapid onset of hepatocellular dysfunction leading to a variety of
systemic complications.

Causes

 paracetamol overdose
 alcohol
 viral hepatitis (usually A or B)
 acute fatty liver of pregnancy

Features*

 jaundice
 coagulopathy: raised prothrombin time
 hypoalbuminaemia
 hepatic encephalopathy
 renal failure is common ('hepatorenal syndrome')
*remember that 'liver function tests' do not always accurately reflect the synthetic function of
the liver. This is best assessed by looking at the prothrombin time and albumin level.

Acute pancreatitis

Acute pancreatitis is usually due to alcohol or gallstones.

Pathophysiology:
- autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis

Features:

 Severe epigastric pain that may radiate through to the back

 Vomiting is common
 Examination may reveal tenderness, ileus and low-grade fever
 Periumbilical discolouration (Cullen's sign) and flank discolouration (Grey-Turner's sign)
is described but rare

Rare features associated with pancreatitis include:

 ischaemic (Purtscher) retinopathy - may cause temporary or permanent blindness

Investigations:

 raised amylase is seen in 75% of patients.

Scoring systems

There are several scoring systems used to identify cases of severe pancreatitis which may
require intensive care management. These include the Ranson score, Glasgow score and
APACHE II.

Some common factors indicating severe pancreatitis include:

  age > 55 years
 hypocalcaemia
 hyperglycaemia
 hypoxia
 neutrophilia
 elevated LDH and AST

Note that the actual amylase level is not of prognostic value.

Acute pancreatitis
Armando Hasudungan -

Acute pancreatitis: causes

The vast majority of cases in the UK are caused by gallstones and alcohol

Popular mnemonic is GET SMASHED

 Gallstones
 Ethanol
 Trauma
 Steroids
 Mumps (other viruses include Coxsackie B)
 Autoimmune (e.g. polyarteritis nodosa), Ascaris infection
 Scorpion venom
 Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
 ERCP
 Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide,
pentamidine, steroids, sodium valproate)
 © Image used on license from Radiopaedia

CT from a patient with acute pancreatitis. Note the diffuse parenchymal enlargement with oedema and indistinct
margins.

*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine

Acute pancreatitis: complications

Local complications
Peripancreatic fluid collections

 Occur in 25% cases

 Located in or near the pancreas and lack a wall of granulation or fibrous tissue
 May resolve or develop into pseudocysts or abscesses
 Since most resolve aspiration and drainage is best avoided as it may precipitate
infection

Pseudocysts

 In acute pancreatitis result from organisation of peripancreatic fluid collection. They

may or may not communicate with the ductal system.
 The collection is walled by fibrous or granulation tissue and typically occurs 4 weeks or
more after an attack of acute pancreatitis
 Most are retrogastric
 75% are associated with persistent mild elevation of amylase
 Investigation is with CT, ERCP and MRI or endoscopic USS
 Symptomatic cases may be observed for 12 weeks as up to 50% resolve
 Treatment is either with endoscopic or surgical cystogastrostomy or aspiration

Pancreatic necrosis

 Pancreatic necrosis may involve both the pancreatic parenchyma and surrounding fat
 Complications are directly linked to extent of parenchymal necrosis and extent of
necrosis overall
 Early necrosectomy is associated with a high mortality rate (and should be avoided
unless compelling indications for surgery exist)
 Sterile necrosis should be managed conservatively (at least initially)
 Some centres will perform fine-needle aspiration sampling of necrotic tissue if infection
is suspected. False negatives may occur and the extent of sepsis and organ dysfunction
may be a better guide to surgery

Pancreatic abscess

 Intraabdominal collection of pus associated with pancreas but in the absence of necrosis
 Typically occur as a result of infected pseudocyst
 Transgastric drainage is one method of treatment, endoscopic drainage is an alternative
Haemorrhage

 Infected necrosis may involve vascular structures with resultant haemorrhage that may
occur de novo or as a result of surgical necrosectomy.
 When retroperitoneal haemorrhage occurs Grey Turner's sign may be identified

Systemic complications

Acute respiratory distress syndrome

 associated with a high-mortality rate of around 20%

Acute pancreatitis: management

Management of Acute Pancreatitis in the UK

Diagnosis

 Traditionally hyperamylasaemia has been utlilised with amylase being elevated three
times the normal range.
 However, amylase may give both false positive and negative results.
 Serum lipase is both more sensitive and specific than serum amylase. It also has a longer
half life.
 Serum amylase levels do not correlate with disease severity.

Differential causes of hyperamylasaemia

Acute pancreatitis
Pancreatic pseudocyst
Mesenteric infarct
Perforated viscus
Acute cholecystitis
Diabetic ketoacidosis
Assessment of severity

 Glasgow, Ranson scoring systems and APACHE II

 Biochemical scoring e.g. using CRP

Features that may predict a severe attack within 48 hours of admission to hospital

Initial assessment  Clinical impression of severity

 Body mass index >30
 Pleural effusion
 APACHE score >8
24 hours after admission  Clinical impression of severity
 APACHE II >8
 Glasgow score of 3 or more
 Persisting multiple organ failure
 CRP>150
48 hours after admission  Glasgow Score of >3
 CRP >150
 Persisting or progressive organ failure
Table adapted from UK guidelines for management of acute pancreatitis. GUT 2005, 54 suppl III

Management

Nutrition

 There is reasonable evidence to suggest that the use of enteral nutrition does not
worsen the outcome in pancreatitis
 Most trials to date were underpowered to demonstrate a conclusive benefit.
 The rationale behind feeding is that it helps to prevent bacterial translocation from the
gut, thereby contributing to the development of infected pancreatic necrosis.

Use of antibiotic therapy

 Many UK surgeons administer antibiotics to patients with acute pancreatitis.

 A recent Cochrane review highlights the potential benefits of administering Imipenem to
patients with established pancreatic necrosis in the hope of averting the progression to
infection.
  There are concerns that the administration of antibiotics in mild attacks of pancreatitis
will not affect outcome and may contribute to antibiotic resistance and increase the
risks of antibiotic associated diarrhoea.

Surgery

 Patients with acute pancreatitis due to gallstones should undergo early

cholecystectomy.
 Patients with obstructed biliary system due to stones should undergo early ERCP.
 Patients who fail to settle with necrosis and have worsening organ dysfunction may
require debridement, fine needle aspiration is still used by some.
 Patients with infected necrosis should undergo either radiological drainage or surgical
necrosectomy. The choice of procedure depends upon local expertise.

References
www.bsg.org.uk/pdfworddocs/pancreatic.pdf

Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis
Villatoro et al Cochrane Library DOI: 10.1002/14651858.CD002941.pub3. 2010 version.

Acute upper gastrointestinal bleeding

NICE published guidelines in 2012 on the management of acute upper gastrointestinal bleeding
which is most commonly due to either peptic ulcer disease or oesophageal varices. Some of the
key points are detailed below.

Risk assessment

 use the Blatchford score at first assessment, and

 the full Rockall score after endoscopy

Blatchford score
 Admission risk marker Score
Urea (mmol/l) 6·5 - 8 = 2
8 - 10 = 3
10 - 25 = 4
> 25 = 6
Haemoglobin (g/l) Men

 12 - 13 = 1
 10 - 12 = 3
 < 10 = 6

Women

 10 - 12 = 1
 < 10 = 6
Systolic blood pressure (mmHg) 100 - 109 = 1
90 - 99 = 2
< 90 = 3
Other markers Pulse >=100/min = 1
Presentation with melaena = 1
Presentation with syncope = 2
Hepatic disease = 2
Cardiac failure = 2

Patients with a Blatchford score of 0 may be considered for early discharge.

Resuscitation

 ABC, wide-bore intravenous access * 2

 platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre
 fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre,
or a prothrombin time (international normalised ratio) or activated partial
thromboplastin time greater than 1.5 times normal
 prothrombin complex concentrate to patients who are taking warfarin and actively
bleeding

Endoscopy

 should be offered immediately after resuscitation in patients with a severe bleed

 all patients should have endoscopy within 24 hours
Management of non-variceal bleeding

 NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to
patients with suspected non-variceal upper gastrointestinal bleeding although PPIs
should be given to patients with non-variceal upper gastrointestinal bleeding and
stigmata of recent haemorrhage shown at endoscopy
 if further bleeding then options include repeat endoscopy, interventional radiology and
surgery

Management of variceal bleeding

 terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e.

before endoscopy)
 band ligation should be used for oesophageal varices and injections of N-butyl-2-
cyanoacrylate for patients with gastric varices
 transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from
varices is not controlled with the above measures

Royal College of Physicians Edinburgh 10

2017 Management of acute upper
gastrointestinal bleeding: an update for the
general physician

NICE 32
2012 Acute upper gastrointestinal bleeding:
management

Royal College of Physicians 02

2012 Managing acute upper gastrointestinal
bleeding in the acute assessment unit

Alcoholic ketoacidosis
Alcoholic ketoacidosis is a non-diabetic euglycaemic form of ketoacidosis. It occurs in people
who regularly drink large amounts of alcohol. Often alcoholics will not eat regularly and may
vomit food that they do eat, leading to episodes of starvation. Once the person becomes
malnourished, after an alcohol binge the body can start to break down body fat, producing
ketones. Hence the patient develops a ketoacidosis.

It typically presents with a pattern of:

 Metabolic acidosis
 Elevated anion gap
 Elevated serum ketone levels
 Normal or low glucose concentration

The most appropriate treatment is an infusion of saline & thiamine. Thiamine is required to
avoid Wernicke encephalopathy or Korsakoff psychosis.

Alcoholic liver disease

The STOPAH study (see reference) compared the two common treatments for alcoholic
hepatitis, pentoxyphylline and prednisolone. It showed that prednisolone improved survival at
28 days and that pentoxyphylline did not improve outcomes.

Reference:
Thursz et al. Prednisolone or Pentoxifylline for Alcoholic Hepatitis. NEJM. 2015.
statMed.org 00
Alcoholic liver disease
 Alcohol-related liver disease
Osmosis - YouTube 30

Liver cirrhosis
Osmosis - YouTube

Aminosalicylate drugs

5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts locally as an
anti-inflammatory. The mechanism of action is not fully understood but 5-ASA may inhibit
prostaglandin synthesis

Sulphasalazine

 a combination of sulphapyridine (a sulphonamide) and 5-ASA

 many side-effects are due to the sulphapyridine moiety: rashes, oligospermia, headache,
Heinz body anaemia, megaloblastic anaemia, lung fibrosis
 other side-effects are common to 5-ASA drugs (see mesalazine)
Mesalazine

 a delayed release form of 5-ASA

 sulphapyridine side-effects seen in patients taking sulphasalazine are avoided
 mesalazine is still however associated with side-effects such as GI upset, headache,
agranulocytosis, pancreatitis*, interstitial nephritis

Olsalazine

 two molecules of 5-ASA linked by a diazo bond, which is broken by colonic bacteria

*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine

Gut 10
Adverse effects of sulfasalazine and
mesalazine

BNF 00
Sulfasalazine

Anal cancer

Anal cancer is defined as a malignancy which lies exclusively in the anal canal, the borders of
which are the anorectal junction and the anal margin (area of pigmented skin surrounding the
anal orifice). 80% of anal cancers are squamous cell carcinomas (SSCs). Other types include
melanomas, lymphomas, and adenocarcinomas. The lymphatic drainage, and therefore, tumour
spread, varies in different parts of the canal: anal margin tumours spread to the inguinal lymph
nodes and those which are more proximal spread to the pelvic lymph nodes.

Epidemiology
  Anal cancer is relatively rare, with an annual incidence in the UK of about 1.5 in 100,000.
However, its incidence is rising, especially amongst men who have sex with men, due to
widespread infection by human papillomavirus (HPV).2
 1:2 male:female ratio.3
 The average age of presentation in the UK is 85-89 years.
 30-40% of patients present with lymph node involvement at diagnosis, however, distant
spread is uncommon, with 5-8% of cases presenting with extrapelvic metastases at time
of diagnosis.1

Risk factors

 HPV infection causes 80-85% of SSCs of the anus (usually HPV16 or HPV18 subtypes).
 Anal intercourse and a high lifetime number of sexual partners increases the risk of HPV
infection.
 Men who have sex with men have a higher risk of anal cancer.
 Those with HIV and those taking immunosuppressive medication for HIV are at a greater
risk of anal carcinoma.
 Women with a history of cervical cancer or cervical intraepithelial neoplasia (CIN) are
also at greater risk of anal cancer.
 Immunosuppressive drugs used in transplant recipients increase the risk of anal cancer.
 Smoking is also a risk factor.

Patients typically present with a subacute onset of:

 Perianal pain, perianal bleeding

 A palpable lesion
 Faecal incontinence
 A neglected tumour in a female may present with a rectovaginal fistula.

Investigations

 T stage assessment: examination, including a digital rectal examination, anoscopic

examination with biopsy, and palpation of the inguinal nodes.
 Imaging modalities: CT, MRI, endo-anal ultrasound and PET.
 The patient should be tested for relevant infections, including HIV.

T staging
The following is a T stage system for anal cancer described by the American Joint Committee on
Cancer and the International Union Against Cancer:

TX primary tumour cannot be assessed

T0 no evidence of primary tumour
Tis carcinoma in situ
T1 tumour 2 cm or less in greatest dimension
T2 tumour more than 2 cm but not more than 5 cm
in greatest dimension
T3 tumour more than 5 cm in greatest dimension
T4 tumour of any size that invades adjacent organ(s)
- for example, vagina, urethra, bladder (direct
invasion of the rectal wall, perirectal skin,
subcutaneous tissue, or the sphincter muscle(s) -
is not classified as T4)

Anal fissure

Anal fissures are longitudinal or elliptical tears of the squamous lining of the distal anal canal. If
present for less than 6 weeks they are defined as acute, and chronic if present for more than 6
weeks. Around 90% of anal fissures occur on the posterior midline.

Risk factors

 constipation
 inflammatory bowel disease
 sexually transmitted infections e.g. HIV, syphilis, herpes

Features

 painful, bright red, rectal bleeding

Management of an acute anal fissure (< 6 weeks)

  dietary advice: high-fibre diet with high fluid intake
 bulk-forming laxatives are first-line - if not tolerated then lactulose should be tried
 lubricants such as petroleum jelly may be tried before defecation
 topical anaesthetics
 analgesia
 topical steroids do not provide significant relief

Management of a chronic anal fissure (> 6 weeks)

 the above techniques should be continued

 topical glyceryl trinitrate (GTN) is first-line treatment for a chronic anal fissure
 if topical GTN is not effective after 8 weeks then secondary care referral should be
considered for surgery or botulinum toxin

Clinical Knowledge Summaries 70

Anal fissure guidelines

Angiodysplasia

Angiodysplasia is a vascular deformity of the gastrointestinal tract which predisposes to

bleeding and iron deficiency anaemia. There is thought to be an association with aortic stenosis,
although this is debated. Angiodysplasia is generally seen in elderly patients

Diagnosis

 colonoscopy
 mesenteric angiography if acutely bleeding

Management

 endoscopic cautery or argon plasma coagulation

 antifibrinolytics e.g. Tranexamic acid
 oestrogens may also be used
Ascending cholangitis

Ascending cholangitis is a bacterial infection (typically E. coli) of the biliary tree. The most
common predisposing factor is gallstones.

Charcot's triad of right upper quadrant (RUQ) pain, fever and jaundice occurs in about 20-50%
of patients

 fever is the most common feature, seen in 90% of patients

 RUQ pain 70%
 jaundice 60%
 hypotension and confusion are also common (the additional 2 factors in addition to the
3 above make Reynolds' pentad)

Other features

 raised inflammatory markers

Management

 intravenous antibiotics
 endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve
any obstruction

Ascending cholangitis
Osmosis - YouTube
Ascites

The causes of ascites can be grouped into those with a serum-ascites albumin gradient (SAAG)
<11 g/L or a gradient >11g/L as per the table below:

SAAG > 11g/L SAAG <11g/L

Indicates portal hypertension Peritoneal carcinomatosis
Tuberculous peritonitis
Cirrhosis Pancreatic ascites
Alcoholic hepatitis Bowel obstruction
Cardiac ascites Biliary ascites
Mixed ascites Postoperative lymphatic leak
Massive liver metastases Serositis in connective tissue diseases
Fulminant hepatic failure
Budd-Chiari syndrome
Portal vein thrombosis
Veno-occlusive disease
Myxoedema
Fatty liver of pregnancy

Management

 reducing dietary sodium

 fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
 aldosterone antagonists: e.g. spironolactone
o loop diuretics are often added. Some authorities only add loop diuretics in
patients who don't respond to aldosterone agonists whereas other authorities
suggest starting both types of diuretic on the first presentation of ascites
 drainage if tense ascites (therapeutic abdominal paracentesis)
o large-volume paracentesis for the treatment of ascites requires albumin 'cover'.
Evidence suggests this reduces paracentesis-induced circulatory dysfunction and
mortality
o paracentesis induced circulatory dysfunction can occur due to large volume
paracentesis (> 5 litres). It is associated with a high rate of ascites recurrence,
development of hepatorenal syndrome, dilutional hyponatraemia, and high
mortality rate
 prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis. NICE
recommend: 'Offer prophylactic oral ciprofloxacin or norfloxacin for people with
cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has
resolved'
  a transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some
patients

NICE 00
2016 Liver cirrhosis guidelines

Royal College of Physicians 00

Portal vein thrombosis – a primer for the
general physician

European Association for the Study of the 00

Liver
2010 EASL clinical practice guidelines on the
management of ascites, spontaneous
bacterial peritonitis, and hepatorenal
syndrome in cirrhosis

Autoimmune hepatitis

Autoimmune hepatitis is condition of unknown aetiology which is most commonly seen in

young females. Recognised associations include other autoimmune disorders,
hypergammaglobulinaemia and HLA B8, DR3. Three types of autoimmune hepatitis have been
characterised according to the types of circulating antibodies present

Type I Type II Type III

Anti-nuclear antibodies (ANA) Anti-liver/kidney microsomal Soluble liver-kidney antigen
and/or anti-smooth muscle type 1 antibodies (LKM1)
antibodies (SMA) Affects adults in middle-age
Affects children only
Affects both adults and children

Features

 may present with signs of chronic liver disease

  acute hepatitis: fever, jaundice etc (only 25% present in this way)
 amenorrhoea (common)
 ANA/SMA/LKM1 antibodies, raised IgG levels
 liver biopsy: inflammation extending beyond limiting plate 'piecemeal necrosis', bridging
necrosis

Management

 steroids, other immunosuppressants e.g. azathioprine

 liver transplantation

Autoimmune hepatitis
Osmosis - YouTube