Gastroenterology

Gastroduodenal disease

Helicobacter pylori

Introduction

  • Who would have thought that we would be treating Peptic ulcer disease with antibiotics 20 years ago rather than complex surgery with a high rate of complications
  • Anyone foolish enough to have blamed an infectious cause would have been rapidly dismissed as a fool unless they satisfied Koch's postulates as did Dr Marshall

Aetiology

  • HP is now reckoned to be the commonest cause of peptic ulceration.
  • Carriage is often asymptomatic and ongoing studies are looking at the link to other diseases.
  • The almost complete medicalisation of peptic ulcer disease has spared countless patients the significant morbidity and long term complications from gastric surgical procedures. Gastric surgery for peptic ulcer disease is almost unheard of now.

Microbiology

  • HP is likely spread person to person through touch or oral to oral or Faeco oral spread.
  • It is commoner in older patients and in poor socioeconomic environments and the reservoir is humans with faeco-oral and oral oral routes but also it is also found in domestic pets - cats.
  • Its characteristics are that it is a slow growing spiral-shaped gram-negative highly motile bacillus which possesses 4 to 6 unipolar flagella.
  • It produces Urease which is often used as a test for its presence. HP attaches to human gastric epithelial cells and exists below mucous layer and sets off a localised neutrophilic gastritis.
  • The presence of cytotoxin associated gene (cAgA gene+ strain) is associated with disease.

Pathogenicity of HP

  • Antral gastritis - achlorhydria + raised gastrin ? increased acid secretion
  • Chronic duodenal ulcer > 95%
  • Gastric ulcer > 80%
  • Gastric adenocarcinoma > 80%
  • Mucosal associated lymphoid tissue (MALT) lymphoma - regression with eradication

Investigations - there are several different tests and local policies depend on what is available.

  • Serology to IgG is cheap and sensitive but gives no timing as to the infection whether it was recent or longstanding
  • Carbon urea breath test using 13C or 14C - urease is present in the stomach causes formation of labeled carbon dioxide when urea is split which is absorbed into the circulation, where its presence can be determined by analysis of expired breath [overall best test] [14 C - radioactivity, 13C needs expensive mass spectrometer]
  • Histology - high sensitivity and specificity
  • Rapid urease tests - done at endoscopy. CLO test. Cheap and quick and specific
  • Culture - highly specific - slow and laborious but gold standard
  • Acute H. pylori is diagnosed by a positive urea breath test and negative IgG anti?H. pylori antibodies

Management is with a 1 week course of 2 antibiotics + a PPI in an attempt to eradicate the organism

  • PAC regimen: (PPI) omeprazole 20 mg bd,amoxicillin 1 g bd and clarithromycin 500 mg bd for 1 week
  • PMC regimen: (PPI) omeprazole 20 mg bd,metronidazole 400 mg bd and clarithromycin 500 mg bd for 1 week
  • Those where symptoms do not resolve or "red flags" should have endoscopy
  • Treatment indicated for peptic ulcer disease and MALT lymphoma
  • Routine screening for H. pylori in asymptomatic individuals is not indicated in low-risk patients

Dyspepsia

Introduction

  • Dyspepsia is rather a loose term meaning abdominal pain, fullness in the stomach, with nausea, bloating, belching,wind.
  • It is a common complaint mostly managed by GPs. Some are referred for further assessment/endoscopy.
  • Malignancy is always a prime concern as well as other pathologies.
  • Look for "red flags" and see those patients soonest
  • In low risk patients testing and treating HP infection as a first line measure is useful.

Causes of dyspepsia include

  • GORD
  • Peptic ulcer disease
  • Oesophagitis
  • Stomach cancer
  • Non ulcer dyspepsia

"Red flag" symptoms requiring endoscopy/further investigations

  • Haematemesis or melaena (admit) (usually as part of 2 week cancer pathway)
  • Iron deficiency anaemia
  • Unplanned weight loss
  • Dysphagia especially progressive
  • Epigastric mass
  • Hepatomegaly
  • Persisting vomiting
  • Age > 55
  • Previous gastric surgery

Appropriate First line measures

  • Sensible alcohol intake
  • Stopping smoking
  • Weight reduction
  • Avoiding NSAIDs/Aspirin if possible

Duodenal Ulcer

Introduction

  • A duodenal ulcer is defined as a break in the mucous membrane lining the duodenum
  • Commoner than GU

Aetiology

  • Duodenal Ulcer are much commoner than GU and are commoner in men
  • HP found in over 90%
  • NSAIDs also implicated
  • Zollinger-Ellison syndrome rarely

Clinical

  • Patients present with epigastric discomfort an hour after food
  • Vomiting may relieve symptoms.
  • May have radiation of pain into back.
  • Duodenal ulcer pain worse when hungry and at night - the night time glass of milk remedy
  • Weight gain

Investigations

  • FBC - anaemia
  • Endoscopy - shows ulcer crater in 1st part of duodenum
  • HP testing
  • Amylase to exclude acute pancreatitis but amylase may be elevated if perforates posteriorly

Complications

  • Anaemia
  • Localised scarring
  • Bleeding - Gastroduodenal artery lies posteriorly
  • Perforation posteriorly with peritonitis and acute abdomen requires urgent laparotomy

Management

  • HP eradication
  • Surgery for complications

Gastric Ulcer

Introduction

  • A gastric ulcer is defined as a break in the mucous membrane lining the stomach
  • Exclude malignancy by rescoping and biopsy

Aetiology

  • HP in > 80%
  • Gastric ulcers are commonest along the lesser curvature of the stomach
  • Hyperparathyroidism
  • Zollinger Ellison syndrome
  • Stress ulcer "Cushing's ulcer" seen in ITU patients

Clinical

  • Epigastric pain may be worsened by food
  • Weight loss typically, Vomiting

Investigations

  • FBC - anaemia
  • Amylase to exclude acute pancreatitis
  • Endoscopy - ulcer crater commonest on lesser curve
  • Biopsies needed to exclude malignancy and test for HP

Differential

  • Gastric cancer
    • Atypical ulcer history
    • Large ulcer
    • No use of NSAID
  • Gastric lymphoma

Complications

  • Haemorrhage - manage as Upper GI bleed
  • Perforation - urgent laparotomy
  • Gastric outlet obstruction - results in severe vomiting and a succussion splash and a hypochloraemic hypokalaemic metabolic alkalosis. Patients need fluid and electrolyte replacement, acid suppression and stabilisation and then consider for Stenting or surgery.

Management

  • Eradicate HP
  • Rescope after 6 weeks to ensure healing and not malignancy
  • H2 blockers or PPI inhibitors
  • Prophylactic use of sucralfate or PPI/H2 blockers in ITU

Zollinger Ellison syndrome (Gastrinoma)

Introduction

  • Zollinger Ellison syndrome is gastrinoma related peptic ulcer disease (DU+GU)
  • 20% are associated with MEN

Aetiology

  • A gastrinoma is a tumour often within the pancreas secreting gastrin causing peptic ulcer disease.
  • Patients present with multiple peptic ulcers as excess Gastrin stimulates acid production
  • Gastrinoma location
    • pancreas
    • duodenal wall

Histology

  • Five fold increase in gastric parietal cells
  • 75% of gastrinomas malignant
  • 25% are related to MEN 1

Clinical

  • As for peptic ulcer disease above but more severe symptomatology
  • Diarrhoea (acid deactivates pancreatic enzymes)

Investigations

  • Raised gastrin level > 150 pg/mL
  • Elevated calcium - Screen for MEN 1
  • IV secretin causes a further rise in gastrin (it lowers gastrin in the other differentials)
  • CT abdomen and pancreatic imaging may identify a tumour. There may be hepatic metastases.
  • Localisation with somatostatin scintigraphy and endoscopic ultrasound

Differential of raised gastrin

  • Gastrinoma
  • On PPI/H2 blockers
  • G cell hyperplasia
  • H Pylori infection
  • Gastric outlet obstruction

Management

  • Acid suppression with High dose PPI or H2 blockers.
  • Exploratory laparotomy may be needed to locate tumour
  • Surgical cure may be possible - pancreaticoduodenectomy
  • Embolisation of hepatic metastases
  • Interferon, Octreotide
  • If hypercalcaemia identified then treat
  • Genetic counselling if MEN 1 identified

Gastritis

Introduction

  • Gastritis is a inflammation of gastric mucosa and is due to a variety of causes
  • Look for Helicobacter pylori
  • Pernicious anaemia leads to an atrophic gastritis

Aetiology

  • Atrophic gastritis - pernicious anaemia
  • Erosive gastritis - NSAIDs which inhibit COX1 and reduces basal protective prostaglandin levels, Infection such as Cytomegalovirus, Herpes simplex, Alcohol - especially in large amounts damage gastric mucosal protection, Stress Ulcers seen in the critically ill ITU patients and Curling's ulcer seen in those with severe burns.

Clinical

  • It may present with anaemia or dyspepsia or haematemesis/melaena.

Investigations

  • FBC - anaemia (Iron deficient or B12 or both)
  • Endoscopy and biopsy

Management

  • Remove cause if possible e.g. alcohol, caffeine, smoking, NSAIDS
  • Eradicate Helicobacter if present
  • Gastro-protection which can be aided by exogenous PGE1 - misoprostol
  • Proton pump inhibitors or H2 blockers

Menetrier's disease

Introduction

  • Rare disease due to excessive release of transforming growth factor alpha (TGF-alpha)
  • Increased risk of gastric adenocarcinoma

Pathology

  • Hypertrophy of the gastric epithelium

Clinical

  • Seen in children and adults
  • Weight loss, diarrhoea
  • Oedema due to hypoalbuminaemia

Investigations

  • Low protein
  • Endoscopy shows typical gastric appearance with enlarged gastric rugae in body and fundus
  • Gastric biopsies

Management

  • IV albumin and parenteral supplementation
  • Gastrectomy in severe cases
  • Blockers of TGF-alpha may have a future role

Upper Gastrointestinal Bleeding

Introduction

  • Gastrointestinal bleeding from a lesion above the ligament of treitz

Causes

  • Peptic ulcer disease - usually lesser curve of stomach or duodenal bulb where ulcer can erode into large vessels
  • Acute Gastritis/erosions - NSAID's make this more likely
  • Oesophagitis
  • Variceal bleed - Check for alcohol history and look for signs of chronic liver failure and Caput medusa. Splenomegaly suggests portal hypertension. Consider other causes of chronic liver disease that can result in cirrhosis and portal hypertension
  • Mallory-Weiss tear - a history of retching and often alcohol
  • Malignancy - chronic blood loss more usual
  • Dieulafoy's lesion - ectatic artery which bleeds. Cautery or embolisation

Clinical

History

  • Black "coffee ground" vomitus may be blood or it may simply be bile.
  • Bright red blood is however a fairly clear cut sign of GI bleeding as is melaena.
  • Melaena represents bleeding that occurred at an earlier point in time depending on gut transit time and amount.
  • A history of liver disease and Alcohol intake
  • Use of drugs - Aspirin, NSAID's, Warfarin, Steroids
  • A history of bleeding problems - dental extractions etc

Examination

  • Signs of chronic liver disease and portal hypertension
  • Signs of liver decompensation - Asterixis, Liver flap
  • Aneurysm or repair - fistula formation
  • Rectal examination to look for or confirm melaena
  • Signs of shock - low Blood pressure, thready pulse, thirst, poor skin turgor, increased capillary refill time, postural BP drop - even sitting/lying will show a difference. Oliguria - catheterise if poor urinary output
  • Abdominal exam - tenderness, pain, perforation with acute abdomen

Rockall score is increasingly used to assess rebleed and mortality risks

Age

  • 0: <60 years
  • 1: 60-79 years
  • 2: >80 years

Shock

  • 0: None
  • 1: Pulse > 100 + systolic > 100 mmHg
  • 2: SBP < 100 mmHg

Comorbidity

  • 0: None
  • 2: Cardiac failure, IHD
  • 3: Renal/Liver failure/Disseminated malignancy

Pre endoscopy score out of 7

Endoscopic diagnosis

  • 0: Mallory -Weiss tear or no lesion and no stigmata of recent haemorrhage
  • 1: All other diagnosis
  • 2: Malignancy of upper GI tract

Major Stigmata of recent haemorrhage

  • 0: None or dark spot only
  • 2: Blood in upper GI tract, adherent clot, visible spurting vessel

Final Rockall score out of 11

Risks

  • Low risk is <= 2 with rebleed rate of <5% and 0% mortality
  • High risk 5-11 with 11-41% risk of death

Management

  • Get good venous access early before the patient goes into shock and it is then near impossible to find a vein. A large bore venflon is a much faster route to transfuse than a central line. If bleeding give blood rather than fluids if possible. N-saline has poor oxygen carrying capacity. Ideally 2 large bore venflons in each antecubital fossa. Get help if not quickly successful.
  • A central line is not good for giving large volumes quickly and there are likely better things to be doing. It may be used later for monitoring once patient stable.
  • Take Blood at same time and group and cross match 4-6 units if actively bleeding.
  • Check FBC, U&E, LFT, Coagulation - FBC unreliable acutely. Raised Urea may suggest GI blood.
  • Give O negative if patient too ill to wait for cross match.
  • Urinary catheter to measure output as a surrogate marker of renal and general perfusion
  • Sengstaken tube for oesophageal varices
  • Assess Rockall score and Inform Gastroenterologists who may proceed to upper GI endoscopy
  • Gastroenterologists may suggest IV omeprazole if endoscopic evidence of bleeding
  • If bleeding continues despite endoscopic therapy then surgeons and anaesthetists will be involved as surgery may be the only way to stop the bleeding and the patient becomes a surgical rather than a medical emergency

Gastric Adenocarcinoma

Introduction

  • Gastric cancer is seen increasingly with age - most are adenocarcinoma.

Incidence

  • It is the 6th commonest cause of cancer in UK with a 10% 5 year survival
  • Commonest in Japan and Chile. Cancer of cardia and GOJ increasing and antrum falling

Risks

  • Atrophic gastritis, Blood group A, Pernicious anaemia, Adenomatous polyps
  • Smoked processed spicy and salty foods, Smoking, Alcohol, Helicobacter pylori

Pathology

  • Can be infiltrating, a malignant ulcer or malignant polypoid tumour or colloid
  • Linitis plastica - leather bottle stomach with infiltrating tumour
  • Local spread to stomach wall, peritoneal deposits, porta hepatis
  • Can be classified as
    • Intestinal - arises in atrophic gastritis to form a well circumscribed adenocarcinoma
    • Diffuse - infiltrates rapidly into submucosa and spreads locally to liver, pancreas and transverse colon
  • Lymph spread is to nodes along lesser and greater curves of stomach and then to supraclavicular nodes
  • Spread via bloodstream to liver and lungs
  • Transcoelomic spread to ovaries - Krukenberg tumour

Clinical

  • Dyspepsia, Early satiety, epigastric discomfort, Anorexia, Weight loss, nausea, vomiting, dysphagia
  • Severe vomiting due to gastric outlet obstruction, GI bleed with Haematemesis, Melaena
  • Liver spread causes jaundice and pain and ascites. Epigastric mass
  • Lymph nodes left supraclavicular fossa (Virchow's node/ Troisier's sign)
  • Metastatic nodule at Umbilicus - Sister Mary Joseph nodule

Investigations

  • Screening is done in Japan where there is a high incidence
  • Upper GI endoscopy - biopsy lesions
  • FBC - iron deficient anaemia
  • CXR
  • LFT/USS - metastatic disease
  • CT/MRI staging
  • Laparoscopy to assess operability - peritoneal spread cannot be seen on imaging

Management - Surgical

  • Total gastrectomy and removal or drainage lymph nodes for proximal lesions with a Roux-en-Y loop reconstruction anastomosing small bowel to distal oesophagus
  • Subtotal gastrectomy if distal pylorus or antral lesions
  • Adjacent involved tissues may also be resected e.g. tail of pancreas, spleen, colon, omentum, duodenum etc
  • Advanced cases then case by case assessment of benefits of surgery, radiotherapy and chemotherapy
  • Advanced cancer with Pyloric obstruction - palliative gastroenterostomy
  • Overall prognosis is poor with 20% 5 year survival

Gastric lymphoma

Introduction

  • Seen in those on cyclosporin
  • MALT in those with HP infection

Types

  • Immunosuppressed EBV positive B cell lymphomas most common at site of drug (cyclosporin) absorption
  • Mucosa associated lymphoid tissue (MALTomas) - responds to HP eradication

Clinical

  • Anaemia, dyspepsia, Gastric ulcer type symptoms, mass
  • Lymphadenopathy

Investigations

  • FBC - anaemia
  • Endoscopy and biopsy
  • CT staging
  • MALTomas express B cell markers CD19 and CD20

Management

  • HP eradication for MALTomas
  • Chemotherapy/Radiotherapy for lymphomas

Pyloric Stenosis (Adult)

Introduction

  • Gastric outlet obstruction
  • Malignancy or peptic ulcer disease or other

Clinical

  • Vomiting immediately postprandial
  • Vomiting is non-bilious
  • Weight loss
  • Succussion splash

Investigations

  • Hypokalaemia is not seen until late e.g. after 2-3 weeks
  • Hypochloraemic, (eventually hypokalaemic) metabolic alkalosis
  • Endoscopy and biopsy

Management

  • Rehydration and fluid and electrolyte replacement
  • Depends on cause
  • Stenting and palliation in some advanced malignancies