Gastroenterology

Oesophagus

Swallowing

Gastro-oesophageal reflux(GORD)

About

Aetiology

Clinical Findings

Complications

Investigations 

Management

Barrett's oesophagus

Hiatus Hernia

About

  • These are common and become increasingly more so with age.
  • It is defined as herniation of stomach into the thorax

There are two types

  • Sliding 90% : OGJ moves above diaphragm
  • Rolling 10%: Part of stomach herniates through

Risk factors

  • Increased abdominal pressure e.g. lifting or bending
  • Pregnancy
  • Vomiting
  • Straining
  • Obesity
  • Smoking

Clinical Findings

  • Mostly asymptomatic
  • can be associated with GORD symptoms. 

Investigations

  • The HH can be seen on a simple CXR often as a retrocardiac shadow
  • Can be diagnosed at endoscopy.

Management

  • Treat GORD symptoms. If asymptomatic there is nothing to be done
  • Treat as for reflux. In severe cases consider Nissen fundoplication

Mallory-Weiss Syndrome

About

  • Tear in gastric mucosa may lead to Upper GI bleeding

Aetiology

  • Vertical tear found at cardio-oesophageal junction
  • Usually follows severe vomiting

Precipitant

  • Alcohol excess (bleeding more noted if coagulopathy or varices)
  • Hyperemesis gravidarium
  • Other causes of retching/vomiting e.g. Bulimia 

Clinical Findings

  • Haematemesis/Melaena
  • Shock

Investigations

  • FBC
  • Endoscopy shows mucosal tear and bleeding

Management

  • As for Upper GI bleed - Localised adrenaline, even balloon tamponade
  • Usually conservative, Surgery rarely indicated

Achalasia

About

  • The term achalasia comes from the greek "fails to relax"
  • There is a defect in the lower oesophageal sphincter (LOS) which fails to relax accompanied by decreased peristalsis

Aetiology

  • Histologically there is a loss of ganglionic cells in myenteric complex in the oesophagus and degeneration of vagal supply
  • There are some similarities with the infectious disease Chagas disease seen in South America.
  • All age groups can be affected and so it should be considered in the young.

Clinical Findings

  • Dysphagia to solids and liquids (strictures block solids but allow liquids) and an inability to belch
  • Patient drinks fluids after eating to force food across LOS.
  • Patient may regurgitate undigested food trapped in the lower oesophagus.
  • May complain of hiccoughs and chest pain may be seen. Weight loss uncommon.

Investigations 

  • CXR which may show a dilated oesophagus possibly with a fluid level with absent fundal gas shadow.
  • Barium meal shows a dilated oesophagus above LOS with a rat's tail or "beaked" appearance as barium trickles through.
  • Manometry shows raised pressure at LOS and its failure to relax and asynchronous contractions.
  • Endoscopy shows a dilated oesophagus and usefully excludes a benign or malignant stricture.
  • Endoscope usually passes the LOS without difficulty.

Differential

  • Oesophageal stricture which may be benign or malignant
  • Extrinsic oesophageal compression
  • Oesophageal scleroderma
  • Chagas disease if the patient is from an endemic area. If so then appropriate serology should be checked.

Complications

  • Food collection in lower oesophagus may lead to aspiration and pneumonia especially overnight.
  • Long term there is increased risk of oesophageal squamous carcinoma.
  • Severe cases are associated with malnutrition and weight loss.

Management

  • Calcium antagonists (verapamil or nifedipine) and nitrates may reduce LOS tone and these can be taken before meals.
  • Endoscopic hydrostatic balloon dilation of the LOS is more commonly used. There is a risk of perforation.
  • Botulinum toxin often used for those not fit for operative treatment.
  • Surgical treatment is Heller's cardiomyotomy which may include a fundoplication to reduce subsequent reflux
  • Surveillance may be needed for risk of oesophageal cancer

Diffuse oesophageal spasm

About

  • Severe chest pain usually following swallowing

Clinical Findings

  • Retrosternal pain - can be severe usually transient
  • May follow swallowing. Often recurrent 
  • Precipitated by hot or cold foods (I get it with cold cans of diet coke)

Investigations

  • Endoscopy normal
  • Barium swallow during spasm may show changes - hyperperistalsis
  • Manometry can show huge pressures > 170 mmHg
  • ECG to exclude Acute coronary syndrome

Differential

  • Cardiac pain - the history should help

Management

  • Avoid precipitants
  • Nitrates may help
  • Oesophageal myomectomy if severe and recurrent

Oesophageal Web

About

  • Seen with Plummer-Vinson/Patterson-Brown Kelly syndrome

Aetiology

  • Thin membranes seen high in the oesophagus at cricoid level
  • Iron deficiency precedes web formation

Clinical Findings

  • Dysphagia
  • Anaemia symptoms and signs
  • Koilonychia (spoon shaped nails)

Investigations

  • Lateral view of Barium swallow shows web
  • Microcytic anaemia and low ferritin
  • Endoscopy may miss web and disrupt web

Management

  • Treat Iron deficiency
  • OGD can disrupt web
  • Dilatation if it persists

Benign Oesophageal Stricture

About

  • Exclude malignancy

Causes

  • GORD related scarring of oesophagus "peptic" stricture 
  • Oesophageal trauma in past e.g. burn, chemical burn, previous surgery, infection

Clinical Findings

  • Progressive dysphagia to solids
  • Weight loss
  • Reflux symptoms

Differential

  • Oesophageal cancer
  • Achalasia
  • Oesophageal web
  • Left atrial enlargement pressing on oesophagus (Mitral stenosis)

Investigations

  • FBC
  • Barium swallow
  • Endoscopy shows stricture and allows biopsies to be taken

Management

  • Optimise nutrition
  • Oesophageal dilatation
  • Surgical treatment may be needed

Oesophageal cancer

About

  • Oesophageal cancer is increasing in incidence in the UK.
  • It really is composed of two different types of tumours with different aetiologies.
  • Prognosis is poor with only 10% 5 year survival.
  • Most in fact 99% are squamous cell carcinoma affecting the upper 2/3rds and the rest are adenocarcinoma which is increasing in incidence and is associated with Barrett's oesophagus.

Risks

  • Squamous cell cancer: Heavy alcohol intake, heavy smoking, Tylosis - Autosomal dominant condition with hyperkeratosis of palms and soles, Dietary - high salted fish and pickled vegetables, Achalasia, Coeliac disease, Geographical risk - high incidence Iran, also South Africa and China and Strictures. Possibly low levels of serum selenium.
  • Adenocarcinoma: Smoking, Obesity and Barrett's Oesophagus (x 40 fold).

Clinical Findings

  • Progressive dysphagia to solids and lastly liquids as well as anaemia 
  • Weight loss 

Investigations

  • OGD is the procedure of choice as this allows both visualisation of the tumour and tissue biopsy and cytology.
  • Barium swallow may be used if OGD not possible and delineates tumour but does not provide a tissue diagnosis.
  • Further imaging including CT/MRI/PET of chest and upper abdomen are used for staging.
  • CXR should always be performed and may show secondary pneumonia due to aspiration.

Management 

  • Surgery in the minority with localised disease resectable disease fit enough for thoracotomy.
  • The procedure is an "Ivor-Lewis" where the tumour in the lower oesophagus or cardia is resected by mobilising the stomach and performing a high anastomosis in the right chest. In tumours of the upper two-thirds of the oesophagus, a total oesophagectomy is preferable.
  • Chemotherapy (cisplatin + 5 FU) can be used preoperatively to improve 5 year mortality at the expense of toxicity. Where surgery is not feasible consider radiotherapy to reduce tumour bulk and it may help dysphagia.
  • Inoperable Dysphagia may be treated by stenting with the risk of perforation or by palliative Laser ablation to cut through bulky luminal tumour. Aim to maximise nutrition and involvement of palliative services where appropriate.

Oesophageal perforation

About

  • Oesophageal perforation leads to possible mediastinitis from oesophageal contents and air entering the mediastinum.
  • It is life threatening and must be quickly diagnosed and managed. Delayed surgery increases mortality.

Aetiology

  • The causes are usually following an endoscopic procedure involving dilatation or stent placement when there is an oesophageal tumour.
  • A rarer cause is a mucosal tear from forceful vomiting Boerhaave's syndrome usually in the left posterolateral wall of the lower third of oesophagus.
  • A tumour may perforate due to endoscopy or other.
  • Ingested sharp or corrosive objects can also perforate. 

Clinical Findings

  • Patient is quickly toxic with fever and malaise and vomiting.
  • There may be chest or back discomfort and pain.
  • Subcutaneous surgical emphysema may be present if air has tracked into the mediastinum and into subcutaneous tissues. 
  • There may be crackling sounds audible on cardiac auscultation suggesting a pneumomediastium
  • Rigid abdomen, tachypnoea 

Investigations

  • CXR may show pneumomediastinum and subcutaneous emphysema as well as a left pleural effusion.
  • Pleural aspirate - low pH and high amylase and purulent with food matter and empyema may be found.
  • Gastrograffin (water soluble) oesophagram shows a leak but may be falsely negative
  • Elevated amylase
  • Endoscopy should be avoided or done with expert advice as air insufflation can worsen any tear and leak if perforation is suspected.
  • Contrast enhanced CT may be useful.

Management

  • Transfer of the patient to ITU with access to cardiothoracic input for a surgical assessment.
  • IV access, Fluid replacement, Oxygen and Broad-spectrum intravenous antibiotics - cover anaerobes and aerobic gram negative and positives should be commenced immediately.
  • Patient should be kept nil by mouth and consider NG tube according to senior advice if vomiting gastric contents.
  • Close Liaison with cardiothoracic surgeons - a more conservative non operative approach is more in favour nowadays at least initially
  • Consider Oesophageal stenting which may occlude perforation in malignant disease

Complications

  • Patients are at risk of mulitorgan failure, overwhelming sepsis and ARDS

Oesophageal Varices

About

  • Any cause of liver cirrhosis and portal hypertension

Aetiology

  • Varices occur due dilation in the veins at the interface between the portal and systemic systems.
  • This is due to an increase in portal hypertension and a third of varices bleed.
  • Bleeding can be massive and mortality is then 50%.
  • The most common cause is chronic liver disease (differential of gastritis, peptic ulcer disease, Mallory-Weiss tear).
  • Portal system carries 1500 ml of blood from gut to liver each minute

Clinical Findings

  • Presentation is the same us Upper GI bleed but there may be evidence of chronic liver disease.
  • Pallor, Haematemesis, Melaena. Patient is Shocked - hypotensive, tachycardiac and there is postural hypotension (sitting/lying).
  • The blood protein load can tip the CLD patient into hepatic encephalopathy.
  • Splenomegaly may be seen in established portal hypertension.
  • Blood/Melaena on rectal exam

Investigations 

  • Group and cross match 4-6 units
  • FBC U&E LFT'S Coagulation screen
  • Check Hepatitis serology and a liver screen if aetiology unclear and evidence of CLD.

Management

  • ABC's and basic resuscitation. At least 2 Large bore venflons. Reverse any coagulopathy with Vitamin K and Endoscopic and other therapies (see below) should be considered. Discuss with gastroenterologist. ITU bed may be needed.
  • Ciprofloxacin 500 mg bd for 1 week to reduce risk of bacterial infection. Lactulose reduces protein load and helps prevent portosystemic encephalopathy. Sucralfate reduces oesophageal ulceration

Specific therapies

  • Endoscopic therapy can stop and control bleeding in 80% of cases. This can be by banding of varices or injection with sclerosant. High risk markings appearance are those with cherry red spots, red whale markings and blue varices
  • Reduce portal pressures with IV Terlipressin (an analogue of vasopressin) which causes vasoconstriction of the splanchnic arteries and in this way reduces portal blood flow. Avoid in those with ischaemic heart disease. Octreotide is a less effective alternative.
  • Balloon tamponade with a Sengstaken tube can be life saving. The tube has several balloons. It is places as one with the distal end in the stomach and distal balloon then inflated and the tube is pulled back putting pressure on the Oesophagogastric junction tamponading the bleeding varices. In some cases the oesophageal balloon is inflated. Great care is taken. Complication include aspiration and oesophageal trauma and perforation.
  • Transjugular portosystemic shunting (TIPS) - if bleeding continues despite above consider. A stent is placed radiologically and an artificial shunt made between portal and hepatic veins.

Long term Prophylaxis

  • Recurrence is common so a repeated regimen of variceal banding should be followed till all are obliterated. Oral propranolol is useful and reduces portal pressures. Compliance and side effects are issues.
  • TIPS may be considered.
  • Liver Transplantation