Oesophagus, Stomach and Duodenum 2

Question 1

GORD - Definitions

Answer 1

A condition which develops when the reflux of stomach contents causes troublesome symptoms – >2 episodes of heartburn per week and/or complications.

Dysfunction of the lower oesophageal sphincter predisposes to the gastro-oesophageal reflux of acid.

If reflux is prolonged or excessive it may cause oesophagitis, benign oesophageal stricture or Barrett’s oesophagus.

Question 2

GORD - Predisposing Factors

Answer 2

Hiatus hernia, lower oesophageal sphincter hypotension, loss of oesophageal peristaltic function, abdominal obesity, gastric acid hypersecretion, delayed gastric emptying, overeating, smoking, alcohol, pregnancy, surgery in achalasia, drugs (TCAs, anticholinergics or nitrates), systemic sclerosis or Helicobacter pylori.

Question 3

GORD - Los Angeles Classification

Answer 3

• Grade 1 – more than 1 mucosal break <5mm long not extending beyond 2 mucosal fold tops.
• Grade 2 – a mucosal break >5mm long but limited to the space between 2 mucosal fold tops.
• Grade 3 – a long mucosal break which involves <75% of the oesophageal circumference.
• Grade 4 – a long mucosal break that involves >75% of the oesophageal circumference.

Question 4

GORD - Symptoms

Answer 4

• Oesophageal – heartburn (burning, retrosternal discomfort related to meals, lying down, stooping or straining and relived by antiacids), belching, acid brash (acid or bile regurgitation), waterbrash (excessive salivation) and odynophagia (painful swallowing from oesophagitis).
• Extra-oesophageal – nocturnal asthma, chronic cough, laryngitis (throat clearing) and sinusitis.

Question 5

GORD - Complications

Answer 5

Oesophagitis, ulcers, benign strictures, Barrett’s oesophagus (transformation of the distal oesophagus from squamous to columnar epithelium) and oesophageal adenocarcinoma.

Question 6

GORD - Investigations

Answer 6

Isolated symptoms do not require investigation but perform upper GI endoscopy if patient >55 years, symptoms >4 weeks, dysphagia, persistent symptoms despite treatment, relapsing symptoms or weight loss.

A barium swallow may show a hiatus hernia and 24 hour oesophageal pH monitoring ± manometry can help to diagnose GORD when endoscopy is normal.

Question 7

GORD - Conservative Management

Answer 7

Lifestyle – encourage weight loss, smoking cessation, raise the bed head and have small, regular meals. Avoid hot drinks, alcohol, citrus fruits, tomatoes, onions, carbonated drinks, spicy food, coffee, tea, chocolate and eating <3 hours before going to bed.

Avoid drugs affecting oesophageal motility (nitrates, anticholinergics, tricyclic antidepressants or calcium channel blockers) or that damage the mucosa (NSAIDs, K+ salts or bisphosphonates).

Question 8

GORD - Medical Management

Answer 8

Give antacids e.g. 10mL Magnesium trisilicate mixture TDS or alginates e.g. 10-20mL Gaviscon advance TDS to relieve symptoms.

For oesophagitis give 30mg Lansoprazole OD/BD.

Question 9

GORD - Surgical Management

Answer 9

A Nissen’s fundoplication is indicated if symptoms are severe, refractory to medical therapy and there is severe reflux confirmed by pH monitoring.

Atypical symptoms e.g. cough or laryngitis are less likely to improve following surgery than typical symptoms.

Question 10

Hiatus Hernia - Definition

Answer 10

Common affecting 30% of patients over 30 years and 50% have symptomatic GORD.

80% are sliding where the gastro-oesophageal junction slides into the chest (through diaphragm) causing lower oesophageal sphincter to become less competent.

20% are rolling where the junction remains in the abdomen but a section of the stomach herniates into the chest next to the oesophagus.

Question 11

Hiatus Hernia - Investigations

Answer 11

Barium swallow is the best diagnostic test (upper GI endoscopy can visualise the mucosa and diagnose oesophagitis but cannot reliably exclude a hiatus hernia).

Question 12

Hiatus Hernia - Management

Answer 12

Lose weight, stop smoking, eat smaller meals earlier in the evening, raise the head of the bed and treat the symptoms of reflux – with antacids, H2 receptor antagonists, proton pump inhibitors or alginate preparations (form a raft on top of the stomach).

Indications for surgery are intractable symptoms despite aggressive medical therapy or complications e.g. ulceration, bleeding or stricture formation. However it is also advised to electively repair a rolling hiatus hernia prophylactically as it may strangulate which would be an emergency.

Question 13

Laparoscopic Nissens Fundiplication

Answer 13

Fundus of the stomach is mobilised and wrapped around the lower end of the oesophagus providing a high pressure area designed to prevent reflux.

Question 14

Ulcers - Definition and Epidemiology

Answer 14

• Definition – ulcer formation associated with acid and can occur at several sites e.g. the duodenum (most common), stomach, oesophagus, jejunum (in Zollinger-Ellison syndrome), Meckel’s diverticulum (if it contains ectopic gastric mucosa) or occasionally at the site of previous gastroenterostomy.
• Epidemiology – duodenal ulceration commonly occurs in men aged 45-55 years. Gastric ulceration tends to present later between 55-65 years. 95% of duodenal ulcers occur within 2cm of the pylorus.

Question 15

Ulcers - Presentation

Answer 15

Peptic ulcers present with epigastric pain (worse at night and may radiate to the back), dyspepsia or bleeding.

There is no reliable method of distinguishing clinically between gastric and duodenal ulcers although pain may be eased by food in duodenal or worsened by food in gastric ulcers.

Question 16

Ulcers - Risk Factors

Answer 16

Helicobacter pylori infection, prolonged use of NSAIDs, smoking, increased acid secretion, coffee consumption and co-morbidities such as liver or renal failure or hyper-parathyroidism.

Helicobacter pylori – the mechanism of injury is 2 fold – firstly the effects of toxins released from the bacteria and the body’s inflammatory response leads to direct injury of the protective gastric mucosal barrier. Secondly the associated gastritis is associated with increased gastrin induced acid secretion.

Question 17

Ulcers - Investigations

Answer 17

Upper GI endoscopy to confirm the presence of an ulcer and to test for the presence of H pylori.

Biopsy of all gastric ulcers is essential to avoid missing early gastric malignancy.

Question 18

Ulcers - Medical Management

Answer 18

Those colonised with H pylori should undergo eradication therapy (PPI and antibiotic regime).

Smoking cessation should be advised and NSAIDs and aspirin should be stopped and alternatives prescribed. With this regime the majority of ulcers can be managed medically.

Question 19

Ulcers - Surgical Management

Answer 19

Usually only required for complications such as haemorrhage, perforation or pyloric stenosis though may be considered for the few patients who are not responsive or tolerant to medical therapy.

Question 20

Ulcers - Elective Surgery

Answer 20

• Truncal or selective vagotomy – the vagus nerve stimulates acid secretion so division of these branches can reduce the amount of acid produced. Unfortunately other branches of the vagus nerve (called the nerves of Latarjet) normally relax the pyloric muscles enabling emptying of the stomach so a drainage procedure e.g. a pyloroplasty (a longitudinal incision is closed transversely to widen the pylorus) or gastroenterostomy (pylorus is bypassed) is also required.
• Antrectomy with vagotomy – the distal half of the stomach is removed (partial gastrectomy) in combination with a vagotomy. The stomach is then anastomosed directly with the duodenum (Bilroth I procedure) or with a loop of the jejunum (Bilroth II procedure or Polya gastrectomy).
• Gastrectomy with Roux en Y – is rarely required but may be in Zollinger-Ellison syndrome.

Question 21

Ulcers - Emergency Surgery

Answer 21

• Haemorrhage – may be controlled endoscopically with adrenaline injection, diathermy, laser coagulation or heat probe. An operation should be considered for severe haemorrhage or re-bleeding especially in elderly. During surgery the bleeding ulcer base is underrun or oversewn.
• Perforation – most patients undergo surgery though some advocate an initial conservative approach in patients without generalised peritonitis – nil by mouth, NG tube and IV antibiotics can prevent surgery in up to 50%. If emergency surgery is required a laparoscopic repair of the hole will usually suffice (although it has a worse reoccurrence rate than open repairs).
• Pyloric stenosis – a late complication presenting with vomiting of large amounts of food some hours after meals. First line management is with endoscopic balloon dilatation followed by maximal acid suppression (risk of perforation is 5%). If this is unsuccessful a drainage procedure e.g. gastro-enterostomy or pyloroplasty ± a highly selective vagotomy may be performed.

Question 22

Types of Gastric Surgery

Answer 22

• For early gastric malignancy – may be treated with endoscopic resection.
• For localised disease – treated by curative gastrectomy – D1 resection – excision of tumour and perigastric nodes or D2 resection – a D1 procedure plus excision of coeliac axis lymph nodes.
• Roux en Y anastomosis – the proximal duodenum is oversewn, the proximal jejunum is divided from the distal duodenum and connects with the oesophagus (or proximal stomach after subtotal gastrectomy) whilst the distal duodenum is connected to the distal jejunum.

Question 23

Gastric Surgery - Early Complications

Answer 23

Haemorrhage, duodenal stump leakage or failure of the stomach to empty and bilious vomiting – this is difficult to treat but again usually improves over time.

Question 24

Gastric Surgery - Late Complications

Answer 24

Postvagotomy diarrhoea (give codeine phosphate), blind loop syndrome (e.g. in Bilroth II procedure leads to bacterial overgrowth, anaemia, malnutrition, weight loss), biliary vomiting, alkaline gastritis, anaemia (due to lack of intrinsic factor, vitamin B12 and iron), osteomalacia (due to lack of vitamin D and calcium) and recurrent ulceration or malignancy.

Dumping syndrome – abdominal distension, flushing, sweating, nausea and fainting after eating due to food of high osmotic potential being dumped in the jejunum causing oligaemia from rapid fluid shifts. Late dumping is due to rebound hypoglycaemia and occurs 1-3 hours after meals. Both tend to improve over time but may be helped by eating less carbohydrate and more guar and pectin (slows glucose absorption).

Question 25

Upper GI bleeding - Definition and Causes

Answer 25

• Haematemesis – vomiting of blood which may be bright red or coffee grounds. Malaena – means black motions, often tar like and has a characteristic smell of altered blood. Both indicate upper GI bleeding.
• Causes – duodenal ulcer (30%), gastric ulcer (20%), acute erosions or gastritis (20%), Mallory-Weiss tear (10% - due to vomiting), oesophageal varices (5%), oesophagitis (5%) or malignancy (<3%).

Question 26

Upper GI Bleeding - History and Examination

Answer 26

• History – ask about previous GI bleeds, dyspepsia, known peptic ulcers, liver disease or varices, dysphagia, vomiting or weight loss. Check current medication and alcohol use. Are there any serious co-morbidities e.g. cardiovascular or respiratory disease, hepatic or renal impairment or metastases.
• Examination – look for signs of chronic liver disease and perform a PR to check for melaena. Is the patient shocked - cool and clammy to touch, delayed capillary refill, altered GCS, pulse >100 bpm, systolic BP <100mmHg, postural BP drop of >20mmHg on standing and urine output <30mL/h.

Question 27

Upper GI Bleeding - Rockall Score

Answer 27

The pre-endoscopy criteria make up the initial Rockall score and the post-endoscopy criteria make up the final Rockall score – together = the final Rockall score. An initial score >6 is said to be an indication for surgery but the decision is usually more complex.

Pre-endoscopy - 0,1, 2 or 3 points:

• Age - <60 years, 60-79 years, >80 years
• Shock - pulse <100 bpm, pulse >100 bpm or SBP <100 mmHg.
• Comorbidity - nil major, HF or IHD, RF or LF and metastases
• ** Post-endoscopy -*** 0, 1, 2 or 3 points:
• Diagnosis - mallory Weiss, all other dx or a GI malignancy
• Haemorrhage - dark red spot (0 points) or blood or vessel (2 points).

Question 28

Upper GI Bleeding - Management if not Shocked

Answer 28

Insert 2 large bore cannulae and start a slow saline IVI to keep lines patent. Check bloods and monitor vital signs and urine output. Aim to keep Hb >8 g/dL at all times.

Question 29

Upper GI Bleeding - Management if Shocked

Answer 29

• Protect the airway, give high flow oxygen and keep the patient nil by mouth.
• Insert 2 14G cannulae and take bloods – FBC, Us+Es, LFTs, glucose, clotting, cross match (4 units).
• Start a rapid crystalloid infusion up to a maximum of 1L.
• If the patient remains shocked start blood transfusion otherwise start slow saline infusion.
• Correct clotting abnormalities with vitamin K, FFP or platelet concentrate and give IV PPI.
• Set up a CVP line to guide fluid replacement and catheterise to monitor urine output.
• Monitor vital signs every 15 minutes and perform emergency endoscopy for diagnosis.

Question 30

Upper GI Bleeding - Endoscopy

Answer 30

Should be arranged after resuscitation, within 4 hours of a suspected variceal haemorrhage or when bleeding is ongoing within 24 hours of admission.

It can be used to identify the site of bleeding, to estimate the risk of rebleeding and to administer treatment – preferably 2 of adrenaline, sclerotherapy, variceal banding or argon plasma coagulation (for superficial lesions).

Question 31

Upper GI Bleeding - Rebleeding

Answer 31

Risk can be assessed during endoscopy – 80% if there’s active arterial bleeding, 50% if there’s a visible vessel and 30% if there’s visible clots or black dots.

40% of those who rebleed will die of complications so high risk patients need to be identified and closely monitored.

Give an IV infusion of Omeprazole and get a surgeon if haematemesis with melaena or any signs of shock are present.

Question 32

Portal Hypertension - Causes

Answer 32

• Pre-hepatic – portal or splenic vein thrombosis.
• Intra-hepatic – cirrhosis (causes 80% of cases - most common in the UK), schistosomiasis (most common worldwide), sarcoidosis, myeloproliferative disorders or congenital hepatic fibrosis.
• Post-hepatic – Budd-Chiari syndrome, RHF, constrictive pericarditis or veno-occlusive disease.

Question 33

Oesophageal Varices - Prophylaxis

Answer 33

Treatment reduces the risk of varices in a cirrhotic patient bleeding from 30% to 15%.

Should give 40-80mg Propanolol BD and/or endoscopic banding ligation but 80% will re-bleed within 2 years.

Resistant cases can be given a TIPSS – transjugular intrahepatic portosystemic shunt.

Question 34

Oesophageal Varices - Acute Management

Answer 34

Resuscitate until haemodynamically stable (but do not give 0.9% saline), correct clotting abnormalities with vitamin K and FFP, start an IVI of Terlipressin – 2mg bolus followed by 1-2mg/4 hours for <3 days.

Endoscopic banding or sclerotherapy should then be attempted.