About Gastroenterology

Nausea and vomiting

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The timing, amount and content of the vomitus are important. Associated symptoms often indicate the cause, since isolated nausea and vomiting are rarely organic.

Causes

The list of causes is long and the likelihood depends on the clinical circumstances. Gastrointestinal disease

Mechanical obstruction

• Pyloric stenosis
• Achalasia
• Small bowel obstruction

Functional gastrointestinal disorders

• Gastroparesis
• Intestinal pseudo-obstruction
• Non-ulcer dyspepsia
• Irritable bowel syndrome

Organic gastrointestinal disease

• Peptic ulcer (especially pyloric canal ulcers)
• Pancreatitis
• Hepatitis
• Cholecystitis
• Mesenteric ischaemia

Drugs

Chemotherapy

• Cisplatinum
• Methotrexate
• Tamoxifen

Analgesics

• NSAIDs
• Opiates

Cardiovascular drugs

• Digoxin
• Antiarrthymics
• P-blockers
• Diuretics

Hormonal drugs

• Oral contraceptive
• Oral hypoglycaemics

Antibiotics/Antivirals

• Erythromycin
• Sulphonamides
• Acyclovir

Gastrointestinal drugs

• Azathioprine
• Sulfasalazine

CNS active drugs

• Antiparkinsonian drugs
• Anticonvulsants

Alcohol

Nicotine (including patches)

Infectious

• Gastroenteritis
• Non-gastrointestinal

Endocrine

• Pregnancy (easy to forget!)
• Diabetic ketoacidosis
• Hyperthyroidism
• Addison's disease
• Hyper- and hypoparathyroidism

Metabolic

• Uraemia
• Hypercalcaemia
• Hyponatraemia
• Acute intermittent porphyria

Neurological

• Migraine
• Raised intracranial pressure
• Seizures
• Demyelination
• Labyrinthine disorders
• Motion sickness
• Labyrinthitis
• Meniere's disease
• Tumours (especially near the fourth ventricle)
• Fluorescein angiography

Psychiatric

• Anorexia nervosa
• Bulimia nervosa
• Pyschogenic vomiting
• Pain
• Depression
• Cyclic vomiting syndrome Post-operative miscellaneous Cardiac
• Myocardial infarction
• Congestive heart failure

Starvation

Investigations and management

Assessment

• Look for signs of dehydration
• Look for visible peristalsis and abdominal herniae. Feel for a mass and listen for a gastric succussion splash and bowel sounds
• Inspect the teeth for loss of dental enamel, which may indicate recurrent vomiting due to bulimia or severe reflux disease
• Carry out a neurological examination
• Examine the vomitus for volume, blood and bile (the latter indicates patent pylorus)
• Check the urine—osmolality, glucose and a pregnancy test
• Request serum electrolytes, urea, random glucose and calcium
• Metabolic alkalosis (pH > 7.44, PaCO2 > 45 mmHg or 6.0 kPa) only occurs in severe vomiting
• Arrange an endoscopy if vomiting is persistent

Drug therapies

There are two broad drug groups—centrally acting antiemetics and peripherally acting prokinetics:

• Phenothiazines (e.g. prochlorperazine 25 mg suppository or 12.5 mg intramuscularly) act centrally through an antidopaminergic mechanism. Useful for vomiting due to metabolic, drug-induced, postoperative, or vestibular causes. Side-effects include sedation, orthostatic hypotension, or extrapyramidal symptoms.
• Domperidone (10-20 mg orally or 60 mg suppository, where available) or metoclo-pramide (10 mg three times daily) exert both antiemetic and prokinetic effects. Domperidone does not cross the blood brain barrier and is free of extrapyramidal effects, so is preferable to metoclopramide in the elderly or patients aged <21 years.
• 5-HT3 antagonists (e.g. ondansetron 8 mg three times daily) act centrally on the chemoreceptor trigger zone and are particular useful in drug-induced nausea.
• Antihistamines with H1 receptor antagonistic properties (e.g. diphenhydramine 25-50 mg three times daily) are useful in vomiting of labyrinthine origin including motion sickness, vertigo and migraine.
• Dexamethasone, lorazepam, methotrimeprazine, and combination therapy are effective in special circumstances (below)
Specific clinical situations

Pregnancy

• Avoid all drugs if at all possible. Ginger may be helpful but is unproven
• Phenothiazines (promethazine 25 mg oral/injection) and antihistamines (cyclizine) may be given in the first trimester
• Thiamine 100 mg daily may also help
• Recurrent vomiting is likely to provoke oesophagitis and further vomiting. A PPI (although unlicensed in pregnancy) can break the cycle and appears to be safe
• Corticosteroids (dexamethasone), enteral or very rarely parenteral nutrition may be necessary for intractable hyperemesis gravidarum

Gastroparesis

• Meticulous glycaemic control may reverse gastroparesis in diabetics
• Erythromycin (motilin agonist) 4 g daily and other prokinetics are tried more in hope than expectation
• Percutaneous endoscopic gastrostomy with a jejunal extension (PEG-J, p. 401) secures nutrition and assists glycaemic control in insulin-dependent diabetics
• Gastric pacing remains experimental
• Subtotal gastrectomy is a last resort, but results are disappointing.

Chemotherapy and radiation-related nausea and vomiting

• A combination of a 5-HT3 antagonist (e.g. oral ondansetron 8 mg three times daily, for 48 h) and dexamethasone (intravenous 8 mg immediately prior) is usually effective for prevention
• Prevention and treatment of delayed vomiting is less effective. Combining dexam-ethasone and domperidone (or ondansetron) is recommended
• Benzodiazepines (lorazepam 2 mg) and relaxation therapy may be helpful by reducing anticipatory symptoms

Persistent vomiting

• Review the diagnosis, especially considering cerebral, brain stem (fourth ventricle), metabolic and mechanical causes
• Arrange an endoscopy if not already performed
• Combination therapy occasionally helps when single drugs fail
• Methotrimeprazine 100 mg by continuous subcutaneous infusion daily is useful in terminal care

In patients with chronic unexplained nausea and vomiting, lorazepam or psychological

Dyspepsia

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• Dyspepsia (indigestion) is defined as chronic or recurrent pain or discomfort centred in the upper abdomen (epigastrium)
• The annual prevalence in Western Europe and the USA is 25%, accounting for 5% of all primary care consultations
• Although frequently grouped together, dyspepsia should be distinguished, where possible, from gastro-oesophageal reflux disease. The management of patients with the two symptom complexes differs substantially
• Dyspepsia due to organic disease must be detected and distinguished from 'non-ulcer dyspepsia' or 'functional dyspepsia', so that specific treatment can be given. Table 3.1 shows the differential diagnosis of epigastric pain

Clinical features

Common symptoms

• Epigastric, usually central upper abdominal, or retrosternal discomfort related to eating, specific foods, hunger or time of day
• Heaviness, unease, postprandial fullness or early satiety are common descriptive terms, often associated with flatulence or borborygmi
• Heartburn and acid brash are more likely to indicate underlying GORD than dyspepsia

Indicators of organic disease

Examination

• Epigastric tenderness is non-specific
• Palpate carefully for an upper abdominal mass
• Feel for supraclavicular nodes and hepatomegaly
• Check for ascites

Investigations

• Not all patients need investigation

• Patients with predominant symptoms of GORD should first be identified and excluded

• Most low-risk patients who are H. pylori-negative will have non-ulcer dyspepsia, and treatment should be directed at the most troublesome symptom (see Non-ulcer dyspepsia below). The main caveat is an increasing incidence of H. pylori-negative ulcers. This should be carefully considered when treating patients with non-ulcer dyspepsia

Helicobacter testing

• Testing for H. pylori without endoscopy has been shown to be more cost-effective for new onset dyspepsia, cause less patient distress and achieve equivalent satisfaction levels as endoscopy

• The argument is that gastric carcinoma exceptionally rarely presents without alarm symptoms at any age and that outcome is no different between those with and without alarm symptoms. Peptic ulcers are almost all H. pylori-positive and treated effectively with eradication therapy

• This is a radical change to previous practice, but has been instituted in some areas and is likely to gain wider acceptance

• Low-risk patients with residual symptoms following H. pylori eradication should be managed in the same way as patients who originally test H. pylori-negative (see Non-ulcer dyspepsia below)

Endoscopy

Early endoscopy should be considered for

• Patients > 55 years (the age threshold should be defined by the local epidemiology of gastric cancer)

• All patients with alarm symptoms, regardless of age

• All patients with history of NSAID usage regardless of age

Specific investigations

• Blood tests—anaemia, a high platelet count or ESR and abnormal liver function tests indicate an organic cause

• Barium meal—only indicated in preference to endoscopy if endoscopy is difficult or impossible or oesophagogastric anatomy needs defining. Anastomoses can confuse endoscopists and it is easier to evaluate pyloric stenosis by barium meal

• Ultrasound of the gall bladder and pancreas, if the endoscopy is normal

Organic dyspepsia

Dyspepsia due to lesions readily identified on routine investigation:

• Duodenal or gastric ulcer

• Duodenitis—usually part of the duodenal ulcer diathesis

• Gastric cancer

• Reflux oesophagitis

• Gastritis—this is controversial. It is best considered a histological diagnosis

• Cholelithiasis—pain is usually severe

• Management of organic disease is discussed in the appropriate sections

Non-ulcer (functional) dyspepsia

Defined as upper abdominal discomfort related to meals, lasting for more than 4 weeks and for which no cause can be found after investigation. Attempts have been made to classify non-ulcer dyspepsia (NUD) into discrete symptom groups. Although this does not predict underlying disease, it may help predict the response to particular therapy.

Ulcer-type non-ulcer dyspepsia

• Epigastric pain:

• may be described as epigastric burning

• may be episodic, occasionally at night

• Relieved by antacids or food, or worse after meals

• No ulcer, past or present

Dysmotility-type non-ulcer dyspepsia

• Upper abdominal pain:

• poorly localised

• variable character

• not at night

• continuous, rather than episodic

• Abdominal distension

• Premature satiety

• Nausea—but vomiting is unusual

• Food intolerance—variable, but often several types of food

Reflux-type non-ulcer dyspepsia

• Retrosternal discomfort:

• on stooping

• after large meals

• on lying flat

• temporary relief from antacids

• Recent weight gain

• Smoker

• Cyclical severity

• No endoscopic or histological evidence of oesophagitis

It should be noted that there is often considerable symptom overlap and that many also have symptoms of IBS. There remain some patients who have upper abdominal pain after meals, who do not fit into one of these patterns. Features common to all patients with NUD are:

• The patient remains well

• Weight is steady or fluctuating

• Normal investigations

Treatment of non-ulcer dyspepsia

• Explanation and reassurance are essential

• Lifestyle changes (regular meals, weight loss, less alcohol, stopping smoking) often help

• Drugs should only be used when symptoms are intolerable. The following recommendations are made, but controlled trials have either not shown clear benefits from drug treatments, or have not been performed

• If not already tried, antacids should be given for NUD. Patients with reflux-type NUD are more likely to benefit. Subsequent empirical management may be influenced by the symptom pattern:

• Dysmotility-type—prokinetic agents (e.g. domperidone 10 mg three times daily, or metoclopramide 10 mg three times daily) have been shown to be superior to placebo. Antispasmodics, e.g. hyoscine 10-20 mg, three times daily may occasionally be helpful

• Ulcer-type—PPIs (e.g. omeprazole 20 mg, lansoprazole 30 mg or rabeprazole 20 mg daily) are more effective than H2 antagonists and will heal H. pylori-negative ulcers

• Reflux type—heartburn may become the predominant symptom after H. pylori eradication. A therapeutic trial of a PPI is reasonable (and difficult to avoid), but if symptoms persist, this effectively excludes an acid-related disorder and treatment should be stopped. If symptoms are controlled by empirical therapy, a trial of treatment withdrawal is appropriate, with therapy repeated if symptoms recur. Eradication therapy is appropriate for H. pylori-positive patients who have not previously had eradication therapy. This remains controversial, because 15 infected patients need to be treated to cure one patient with NUD, but may be equivalent to other empirical treatment. If symptoms persist, try switching treatment (e.g. from a prokinetic to a PPI). As needed therapy with a PPI is safe and may be effective

• Only if symptoms persist is referral for endoscopy appropriate

• Patients with resistant NUD may respond to an exclusion diet, or other measures to treat an irritable bowel

Clinical dilemmas

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General advice for diagnostic dilemmas is given in Appendix 4.

Causes of chest pain 20-40% of patients with chest pain, normal exercise ECG and normal angiography have an oesophageal disorder. The pain may be severe, wake patients from sleep, or occur during emotional stress.

• Confirm the history—especially the duration and type of pain, provoking and relieving factors
• Oesophageal reflux and diffuse oesophageal spasm most commonly mimic angina
• An endoscopy to identify oesophagitis is indicated. Although a therapeutic trial of a PPI may be appropriate, patients must avoid acid-suppressing medication for 3 weeks prior to endoscopy
• Oesophageal manometry and 24 h pH monitoring with symptom recording should be performed after referral to a specialist centre. Provocation tests (edrophonium for spasm or acid perfusion (Bernstein test) for reflux) occasionally help
• A video barium swallow in the recumbent position is an alternative method of diagnosing dysmotility

Dysphagia with a 'normal' barium swallow

Globus hystericus is not the only cause. Diffuse spasm, achalasia and strictures may be overlooked.

• Confirm the history—especially whether dysphagia is for solids or liquids and the duration of symptoms
• Document the present weight and any loss
• Arrange a bread/marshmallow barium swallow recorded on video, after discussion with the radiologist
• Referral for manometry is indicated for persistent symptoms. Obscure cases of diffuse spasm or achalasia may be detected

Oesophageal dysmotility

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Accounts for many patients referred with oesophageal symptoms. Chest pain or dysphagia for liquids and solids are the presenting features. Diffuse oesophageal spasm is the best-characterised motility disorder other than achalasia, but is rare in its classical form. Symptoms are caused by high-amplitude, aperistaltic oesophageal contractions without a demonstrable organic lesion. When symptoms occur without typical manometric or radiological features, the term 'oesophageal dysmotility' is appropriate.

Symptoms

• Dysphagia—intermittent, variable intensity, for both liquids and solids
• Chest pain—may mimic cardiac pain or reflux and be provoked by stress. A persistent ache between severe episodes usually distinguishes it from angina ('oesophagodynia'), but an identifiable oesophageal cause only accounts for 20% of non-cardiac chest pain
• Coexistent symptoms of IBS, anxiety or depression are also common
• Weight loss is notably absent

Investigations

• Barium swallow—a corkscrew appearance is classic but unusual. Aperistaltic 'tertiary' contractions are common when recumbent, but stasis does not occur, unlike achala-sia. Similar asymptomatic changes can occur in the elderly
• Manometry—diagnostic if positive. Repetitive contractions, high-amplitude waves and periods of normal peristalsis are typical, but occur together in a minority (< 10%). Negative results on static testing do not exclude the diagnosis; ambulatory monitoring increases the yield, but the gain is small because abnormal motility may not relate to symptom events
• Endoscopy—should be normal, but helps exclude oesophagitis or a stricture

Treatment

• Symptoms are difficult to relieve totally. Reassurance that the pain is not cardiac is essential, also explaining that the drugs prescribed are often used for angina
• A PPI (lansoprazole 30 mg or omeprazole 20-40 mg daily) should be tried first since dysmotility may be provoked by acid reflux
• Isosorbide dinitrate 5-10 mg sublingually four times daily or nifedipine 5-10 mg three times daily are adjunctive treatments, but response is unpredictable and side-effects (e.g. headache) are common and often not well tolerated
• Prokinetic agents may make symptoms worse
• Empirical treatment with amitriptyline in low dose (10-30 mg daily) can help
• Pneumatic dilatation or botulinum toxin injection should be reserved for the most severe cases with focal high pressure on oesophageal manometry, because the outcome is unpredictable

Oesophageal webs

• Not circumferential, unlike rings
• Demonstrated radiologically, but difficult to see at endoscopy
• May be associated with mucocutaneous disorders such as epidermolysis bullosa
• Check for iron-deficiency anaemia, associated with a postcricoid web and high oesophageal carcinoma (Plummer-Vinson syndrome)
• Exclude carcinoma of the upper third of the oesophagus by careful radiology and endoscopy. ENT advice may be necessary

Schatzki's ring

• Circumferential contraction in the middle or lower third, usually diagnosed radio-logically rather than by endoscopy
• Typically causes intermittent dysphagia for solids over a long period, but often asymptomatic and of no significance
• If dysphagia is present, dilatation is justified after biopsy. Occasionally pneumatic dilatation is necessary

Diverticula

• Pharyngeal pouches (Zenker's diverticulum) present with intermittent dysphagia and regurgitation in the elderly. Regurgitation of fluid when recumbent may lead to aspiration
• An ENT opinion is advisable after diagnosis by barium swallow taking care to show the upper oesophagus
• Routine endoscopy is not indicated and may be dangerous if oesophageal intubation is not carefully performed under direct vision
• Surgical excision with cricopharyngeal myotomy is the treatment of choice for symptoms. Endoscopic excision by an experienced ENT surgeon is effective
• Mid-oesophageal and epiphrenic diverticula are an endoscopic hazard, but of no other consequence

Systemic sclerosis

• Dysphagia and heartburn with Raynaud's phenomenon are characteristic
• Recurrent strictures caused by reflux and stasis are the principal problem• CREST syndrome (digital calcinosis, Raynaud's phenomenon, dysphagia, sclero-dactyly and telangiectasia) should be distinguished clinically from systemic sclerosis, because it has a better prognosis
• PPIs at doses higher than standard recommended dosage (e.g. omeprazole 80 mg/ day or more) are the best treatment, because standard antireflux treatment is ineffective
• Endoscopic dilatation is necessary for strictures
• Antireflux surgery may make the situation worse. Refractory cases should be referred to a specialist unit
• Other gastrointestinal complications (nutritional deficiency, malabsorption due to small bowel bacterial overgrowth or constipation) should be looked for and treated

Oesophageal infections

Oesophageal infections occur in the debilitated and immunocompromised. Underlying disease should be sought and treated.

Candidiasis

• Painful dysphagia (odynophagia) with oral candidiasis is typical
• Barium swallow, blind oesophageal brushings, or endoscopy with biopsy are diagnostic
• Nystatin suspension 1-2 mL four times daily for 10 days is as effective
• Oral fluconazole 100-200 mg once daily is indicated for patients with AIDS (maintenance therapy may be needed) or if nystatin is ineffective
• Fever or neutropenia make systemic invasion likely and intravenous fluconazole is indicated

Cytomegalovirus

• Serpiginous or large ulcers in the mid-oesophagus cause painful dysphagia in the immunocompromised
• Oesophageal biopsy is diagnostic (epithelial inclusion bodies)
• Ganciclovir (intravenous 5 mg/kg over 1 h, twice daily) for 14 days is only appropriate for severe infection. Recurrence is common

Herpes simplex

• Small, circumscribed ulcers in the mid-oesophagus are seen endoscopically. Ulcers may coalesce or bleed
• Electron microscopy of brushings transported in 4% glutaraldehyde is diagnostic
• Intravenous acyclovir 5 mg/kg three times daily, until tablets can be swallowed (200 mg five times daily for 5 days)

Rumination and regurgitation

Rumination is the chewing of regurgitated food that is then swallowed or spat out. Regurgitation is effortless and involuntary, although it may be a learned habit or indicate psychiatric disease such as bulimia or an anxiety state. It should be distinguished from recurrent vomiting by the lack of nausea and from gastro-oesophageal reflux in which bitter liquid reaches the mouth. Recognition of the disorder and 'unlearning' the habit through biofeedback techniques may help.

Achalasia

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Achalasia is a motility disorder characterised by absent peristalsis in the body of the oesophagus, increased lower oesophageal sphincter pressure (> 40 mmHg) and failure of sphincter relaxation during swallowing. It is due to degeneration of the myenteric plexus of unknown cause. Carcinoma of the cardia must be excluded.

Clinical features

• Occurs at any age
• Dysphagia—all patients. Unlike a stricture, dysphagia for liquids as well as solids occurs early. Slowly progressive; swallowing may be helped by a trick movement of the head, or Valsalva's manoeuvre
• Regurgitation—70%; undigested food, with aspiration
• Weight loss—quite common
• Pain—substernal cramps may be severe and precede dysphagia
• Symptoms for < 1 year and age > 50 years, with weight loss, suggest carcinoma
• Achalasia may present at an advanced stage. Megaoesophagus is a late manifestation that has been reported to cause respiratory obstruction (stridor). The risk of oesophageal carcinoma is increased in megaoesophagus
• Carcinoma of the cardia, gastric lymphoma, diffuse spasm, systemic sclerosis, Chagas' disease (South American trypanosomiasis), neurofibromas and amyloidosis can simulate achalasia

Investigations

• Chest X-ray—an oesophageal fluid level at the aortic knuckle and right lower lobe consolidation, or fibrosis, may be present. The gastric air bubble is characteristically absent
• Barium swallow—food debris in the oesophagus with a smooth, tapered distal narrowing and aperistaltic contractions when recumbent are characteristic. Oesophageal dilatation develops later. A video or bread/marshmallow barium swallow may elucidate difficult cases

Endoscopy must always be performed to exclude a stricture and to examine the cardia for carcinoma. Once food debris is negotiated the endoscope easily passes the lower oesophageal sphincter
Manometry may be the only way to distinguish oesophageal spasm from achalasia and should be performed if dysphagia persists despite a normal barium swallow

Management

The choice is between endoscopic dilatation and surgery (Heller's cardiomyotomy). Dilatation is often preferred by the patient, with surgery reserved for recurrent symptoms. Drugs have no role.

Botulinum toxin

• Intrasphincteric injections of botulinum toxin (25 MU into each of four quadrants of the lower oesophageal sphincter using an endoscope and sclerotherapy needle) paralyse the hypertensive sphincter and abolish dysphagia in 60% of patients for 6-9 months
• The toxin is expensive and sphincter tone returns with time, with recurrence of dysphagia, but the risk of perforation with pneumatic dilatation is avoided
• This treatment is best performed in specialist units, but should only be considered for frail elderly patients because of the high risk of recurrence

Dilatation

• Pneumatic balloon dilatation with X-ray screening is effective in 90% at 1 year, but repeat dilatations are often required
• Dilatation should only be performed by experienced endoscopists and the patient should normally be admitted overnight
• A chest X-ray in expiration is necessary 1 h after dilatation, before the patient eats, to look for mediastinal gas or pneumothorax. Perforation occurs in 2%

Surgery

• Indicated for young patients with high sphincter pressures, when symptoms recur after three attempts at dilatation, or if the patient prefers a definitive procedure at the outset
• Cardiomyotomy is effective in 90% and gives long-term relief. Laparoscopic car-diomyotomy is safe and as effective in experienced hands and is evolving as the procedure of choice

Complications

• Megaoesophagus is now rare
• Aspiration pneumonia can be chronic, or the presenting feature
• Carcinoma may occur in untreated achalasia, but probably not after treatment. It is less common (< 5%) than previously thought
• Treatment (dilatation or surgical) may lead to reflux, stricture, failure to relieve symptoms (reassess the diagnosis), or persistent pain, even after apparent relief of obstruction

Oesophageal carcinoma

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Oesophageal carcinoma accounts for 2% of all cancers. The incidence is increasing rapidly for unknown reasons, but may be due to the increasing prevalence of reflux. Whilst only 30% are resectable and 5-year survival is 10% in European studies, palliation is vital because inability to swallow saliva after oesophageal obstruction is a miserable wayto die. Carcinoma of the cardia may mimic carcinoma of the lower third oesophagus, or achalasia.

Causes

The cause is usually unknown. The importance of different factors varies in different parts of the world. Associations are:

• Gastro-oesophageal reflux (eightfold increase for adenocarcinoma, not for squamous carcinoma)
• Alcohol
• Tobacco
• Barrett's oesophagus—the degree of risk is debated. Carcinoma in Barrett's oesophagus occurs before the diagnosis of Barrett's is known in 98%
• Following corrosive injury
• Achalasia —the risk (< 1%) is less than previously considered
• Iron-deficiency anaemia and postcricoid web, with high oesophageal carcinoma (Patterson-Brown-Kelly or Plummer-Vinson syndrome)—10 times commoner in women, often aged 40-50 years
• Geographical: Caspian littoral (northern Iran: commonest malignancy, although alcohol not consumed); northern China (20 times more common than in Britain); Transkei (South Africa). Selenium or molybdenum deficiency, aflatoxin contamination of cereals and nitrosamines are postulated reasons for this variation
• Familial tylosis (palmar hyperkeratosis) is exceedingly rare

Clinical features

Progressive dysphagia and weight loss are typical, but pain and hoarseness of the voice may occur due to local spread. Patients are usually aged 60-80 years. Rapidly recurrent dysphagia after dilatation should be considered malignant until proven otherwise.

Pathology

• Cervical or midthoracic carcinomas are usually squamous
• Dysplasia may precede carcinoma
• Distal oesophageal tumours are often adenocarcinomas due to spread from the gastric fundus, or malignant change in Barrett's oesophagus. The incidence is increasing by 3-7% per year
• Pathology influences adjuvant therapy (see below)

Spread

• Local invasion along submucosal lymphatics, or directly into mediastinal nodes is the rule
• Hiccups or a persistent midthoracic ache are ominous, indicating diaphragmatic or mediastinal invasion
• Oesophagobronchial fistula, recurrent laryngeal nerve palsy and atrial fibrillation may occur
• Death usually precedes distant metastases
Investigations

Diagnostic

• Barium swallow remains the most useful initial investigation
• Endoscopy, biopsy and brushings (98% detection rate), for a tissue diagnosis
• Endoscopists should define the upper and lower limits of macroscopic tumour

Look for complications

• Chest X-ray—mediastinal lymphadenopathy, evidence of aspiration
• EUS—better than CT scan or MRI for staging mural invasion, nodal involvement and assessing operability
• Other head and neck tumours are common (about 10%) in squamous oesophageal carcinoma

Surgical assessment

• Thoracoabdominal CT scan, with a specific request to look for nodal involvement. It may underestimate mural and lymph node invasion and should be compared with EUS
• Take into account age, cardiorespiratory disease and nutrition
• 'Operability' (patients considered able to survive an operation and live for more than 4 weeks) does not imply resectability
• Pulmonary function tests (including arterial gases), to estimate respiratory reserve
• The presence of lymph nodes is an indication for adjuvant therapy prior to surgery

Management

The objectives are to relieve dysphagia, prolong survival and to cure a minority. There is no ideal treatment; the site and type of the carcinoma and the general health of the patient determine the approach. Operability is the first decision.

Surgery

• Indicated for fit patients under 70 years without evidence of local invasion, when satisfactory resection can be achieved. This is less than one-third of patients with oesophageal cancer
• An experienced oesophageal surgeon, perioperative nutritional support and good physiotherapy are important
• Subtotal oesophagectomy and formation of a gastric tube is usually appropriate, usually requiring separate thoracic and abdominal incisions
• Operative mortality is < 10% in experienced hands
• Surgery alone can only be expected to cure disease confined to the oesophageal wall
• The advent of endoscopically placed self-expanding metal stents has made it difficult to justify surgery for palliation alone

Radical radiotherapy

• Squamous carcinomas that are postcricoid or in the upper third may be radiosensitive
• Commonly converted into palliative therapy because of side-effects. Radiotherapy alone relieves dysphagia in < 50%, so continued endoscopic dilatation is necessary

Palliation

• For most (70%) patients
• Endoscopic dilatation should be performed initially for unresectable tumours, to allow patients to swallow food and saliva
• Endoscopic placement of a self-expanding metal stent is usually optimal. These are safer and provide better palliation of dysphagia than traditional plastic stents. A variety (covered, uncovered, flanged) are available; covered stents are the tube of choice for perforated tumours. Complications include exacerbation of dyspha-gia in high (< 27 cm from incisors) tumours, perforation, tube migration and occlusion
• Obstructing tumours are most effectively relieved by endoscopic laser therapy, although this is not always available. Alcohol injection into the tumour through a scle-rotherapy needle is cheaper and safe, but less effective
• Surgical palliation is effective in experienced hands, but morbidity is much higher than stenting
• Palliative radiotherapy may relieve pain, but is ineffective for long tumours or adeno-carcinomas
• Neoadjuvant chemotherapy is showing encouraging results, especially with epiru-bicin and 5-fluorouracil. Specialist advice should be sought

Terminal care

Treatment should be carefully considered after assessing the patient, seeing the family and discussion with senior colleagues. Hydration, but not alimentation or antibiotics, is usually appropriate. Good mouth care, pharyngeal suction and liaison with the nursing staff are vital. Aspiration pneumonia is the usual cause of death.

Prognosis

• Mean survival is 10 months after diagnosis
• Overall 5-year survival is about 5%, which has changed little in the last 40 years
• In the minority (30%) who are selected for 'curative' surgery, 5-year survival is up to 25%. This is similar to the results of radical radiotherapy, but there are no direct comparative trials for equivalent stages of disease

Benign strictures

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Causes

• Peptic—95%
• Anastomotic—following a surgical procedure
• Radiotherapy—for carcinoma of the breast or bronchus. Stenosis after radiotherapy for oesophageal carcinoma is almost always malignant
• Corrosives—bleach or drugs such as slow-release potassium tablets. Patients taking NSAIDs have a higher incidence of strictures. Pills (tetracycline tablets, slow-release potassium) may cause strictures. Advise elderly patients with poor oesophageal motility to take such drugs when standing, with plenty of fluid
• Mucocutaneous disorders—epidermolysis bullosa and oesophageal lichen planus are very rare

Clinical features

Dysphagia is the main symptom and reflux is usually present. The main differential diagnosis is carcinoma. Dysphagia for < 3 months or rapid weight loss favour carcinoma.

Investigations and management

Initial investigations

• As for dysphagia
• Check the results of biopsies and brushings

Dilatation

• Endoscopic dilatation as an outpatient procedure is safe in experienced hands. The technique is beyond the scope of this book
• A subsequent chest X-ray is not necessary unless pain occurs or perforation is suspected
• Repeat dilatations may be needed. Encourage the patient to make appointments directly with the endoscopy unit if dysphagia recurs, to save time
• Recurrent symptoms < 4 weeks after dilatation suggests carcinoma

Other advice

• Ensure that the patient remains on full dose PPI (e.g. lansoprazole 30 mg, omepra-zole 40 mg, rabeprazole 20 mg daily) long term, because this substantially reduces the risk of recurrent strictures
• Prevention of oesophageal obstruction

Gastro-oesophageal reflux disease

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Gastro-oesophageal reflux symptoms occur monthly in almost 50% and weekly in 20% of US males, but may be asymptomatic. Abnormal reflux is predominantly caused by dysfunction of the lower oesphageal sphincter (frequent transient relaxations) and not necessarily by a hiatus hernia. Delayed clearance of refluxate prolongs mucosal exposure to a low pH (< 4), which damages the oesophageal mucosal barrier and initiates oesophagitis. In addition to acid, bile acids and pepsin also disrupt mucosal integrity or provoke oesophageal dysmotility. Peptic stricture of the oesophagus is an unusual complication, in view of the high prevalence of gastro-oesophageal reflux. Prolonged, symptomatic gastro-oesophageal reflux increases the risk of oesophageal adenocarci-noma by about eightfold. It is not yet clear whether potent acid suppression reduces this risk.

Clinical features

• Heartburn—retrosternal pain related to meals, lying down, stooping, straining and occasionally to exercise
• Regurgitation of acid or bile. Patients often have difficulty in describing the taste, usually bitter or sour
• Dysphagia may be due to peristaltic dysfunction. Pain during swallowing (odynopha-gia) is unusual unless there is severe oesophagitis or a stricture (when dysphagia for solids is also present)
• Excess salivation (water brash), usually during pain
• Relief by antacids
• Chest pain, related to posture or exercise (both of which increase intra-abdominal pressure), can be difficult to distinguish from angina
• Nocturnal asthma (cough or wheeze) may be the only symptom, and can be relieved by treatment of reflux
• Oesophagitis can be asymptomatic. There is no clear relation between symptom severity and endoscopic severity of oesophagitis, although the severity of symptoms correlates with increasing risk of adenocarcinoma

Hiatus hernia

The common sliding hiatus hernia is compatible with normal lower oesophageal sphincter function. It is not necessarily pathological and no symptoms can be attributed to the hernia itself. Symptoms are due to oesophagitis or oesophageal dysmotility provoked by reflux.

• More than 30% of patients over 50 years have a hiatus hernia and less than half have symptomatic gastro-oesophageal reflux
• A report of a sliding hiatus hernia on barium radiology is not a diagnosis. If a patient's symptoms warrant investigation, endoscopy to identify oesophagitis is appropriate, with further investigation if this is normal
• Never accept a hiatus hernia as a cause of iron-deficiency anaemia—there is usually another cause, such as a silent caecal carcinoma
• Rolling (paraoesophageal) or incarcerated hiatal herniae are diagnosed radiologically. A chest X-ray may show a fluid level behind the heart. Episodic pain and vomiting are indications for a barium meal, as partial or complete gastric volvulus may occur, for which surgery is needed

Investigations

• Typical symptoms of gastro-oesophageal reflux do not require investigation unless they are frequent, severe or progressive
• Endoscopy should be considered if symptoms are atypical (partial relief by PPI, associated epigastric pain or associated symptoms) to evaluate the severity of oesophagi-tis or to identify Barrett's oesophagus
• It is common to get symptomatic reflux with no signs of oesophagitis at endoscopy
• Macroscopic oesophagitis indicates reflux, but the severity does not correlate with symptoms.
• If Barrett's oesophagus (see below) is found, multiple biopsies should be taken
• Iron-deficiency anaemia should not be attributed to oesophagitis but can rarely occur in patients with severe ulcerative oesophagitis
• H. pylori is unrelated to (or negatively associated with) reflux oesophagitis
• A therapeutic trial of a PPI is a reliable method of confirming the diagnosis. Debate continues about whether an endoscopy is necessary if symptoms are relieved
• 24 h oesophageal pH monitoring is indicated when it is difficult to distinguish symptomatic reflux from other causes of chest pain, but is not part of routine management

General measures

General measures to reduce reflux are more important than drugs in most patients.

• Reduce fat intake (fat promotes reflux by delaying gastric emptying)
• Weight reduction
• Stop smoking
• Raise the head of the bed by about 10 cm, using blocks or bricks (especially if symptoms are nocturnal)
• Small, regular meals
• Allow 3 h between last meal and retiring at night
• Avoid hot drinks or alcohol before bed
• Avoid drugs that adversely affect oesophageal motility (nitrates, anticholinergic agents, antidepressants, theophylline compounds), or that damage the oesophageal mucosa (NSAIDs, slow-release potassium)
• Use antacids or alginates (e.g. Gaviscon, Maalox, Mylanta) for initial symptomatic relief. There is no evidence that one is better than another, but none will heal oesophagitis

Management

If general measures alone are insufficient, drug treatment is indicated. Controversy persists about the best approach, but PPIs are unequivocally the most effective treatment and are best given in the morning. At first presentation, liquid antacids or algi-nates are more cost-effective than H2-receptor antagonists, since 50% respond equally well to either. After antacids or alginates, an incremental approach is recommended, using the minimum effective treatment to relieve symptoms. Only a minority of patients with reflux have severe oesophagitis.
• There is probably little difference between the PPIs (esomeprazole, lansoprazole, omeprazole, pantoprazole, rabeprazole) in terms of efficacy or side-effect profile in most patients, although costs may vary. Many hospitals and practices have their own prescribing policy. For rare patients, incremental doses above 40 mg of omeprazole, esomeprazole, or rabeprazole may enhance acid suppression, in contrast to a dose ceiling with lansoprazole 30 mg or pantoprazole 40 mg
• Intermittent treatment of recurrent symptoms is often necessary. This is safe and effective in the long term (see national guidelines, such as www.nice.org.uk/CG017)
• Symptomatic erosive oesophagitis relapses within 6 months in 80% on no maintenance treatment, 40% on ranitidine 300 mg or omeprazole 10 mg daily and 15% on omepra-zole 20 mg daily, but these represent a small proportion of all patients with reflux
• Maintenance treatment with lansoprazole 15-30 mg daily, omeprazole 20-40 mg or rabeprazole 10-20 mg daily is indicated for patients with refractory symptoms or confluent oesophagitis, Barrett's oesophagus or a peptic stricture
• Concerns about long-term sequelae of PPIs appear unfounded, but postmarketing surveillance continues. Interference with vitamin B12 absorption, intestinal bacterial overgrowth, pronounced hypergastrinaemia with G-cell hyperplasia and accelerated atrophic gastritis in those with H. pylori are areas of interest in long-term treatment
• The current consensus is to eradicate H. pylori in patients who need PPIs long term
• Overweight, smoking boozers characteristically continue to have symptoms

Refractory symptoms

Symptoms that persist despite treatment with a PPI (such as omeprazole up to 40 mg, lansoprazole 30 mg, rabeprazole 20 mg daily) are usually due to coexistent oesophageal dysmotility, or a non-oesophageal cause.

• Retake the history. Abdominal bloating is common in oesophageal dysmotility. Exercise-related pain may be angina. Confirm compliance with therapy
• Consider endoscopy. Stop PPIs prior to endoscopy if oesophagitis has not previously been identified. Otherwise continue treatment, since up to 15% fail to respond
• If the endoscopy is normal, arrange oesophageal manometry or a bread/marshmal-low barium swallow to exclude achalasia or oesophageal dysmotility. 24 h manometry may be needed to identify oesphageal spasm
• Arrange 24 h pH monitoring if radiology or manometry is normal, or investigate for non-oesophageal causes by abdominal ultrasound or exercise test as appropriate

Indications for antireflux surgery

Surgery is rarely indicated. Laparoscopic antireflux surgery currently has similar risks (lack of efficacy, postoperative stricture, vagal denervation, inability to belch, splenic or oesophageal damage) to open procedures. Mortality is 1%, but results can be good in well-selected patients in experienced hands.

Consider surgery by an experienced surgeon if all the following criteria are met:

• Severe symptoms persist despite all medical treatments vigorously applied. Symptoms of volume reflux (water brash or fluid regurgitation into the mouth) have traditionally favoured surgery, but the concept of volume reflux is now questioned
• pH monitoring confirms objective evidence of gross reflux
• Oesophageal manometry has excluded a specific dysmotility syndrome (e.g. achalasia, scleroderma, diffuse oesophageal spasm)
• Age < 65 years (surgery may still be considered in older, medically fit individuals)
• Some individuals (particularly younger patients) may opt for fundoplication because of concerns regarding the safety and/or cost of long-term PPI therapy even when symptoms are well controlled on PPIs. They should know that the mortality of laparoscopic or open fundoplication is about 1%, serious morbidity is around 10% and that no patient is known directly to have died from PPIs

Endoscopic antireflux procedures

• Endoscopic stapling or suturing devices to reduce reflux are being developed, but at present the same selection procedures as for antireflux procedures should apply
• Complications from mechanical antireflux procedures can be intractable and this hazard should be compared with the tolerability and safety of medication

Barrett's oesophagus

Fifty years after the description associating Barrett's oesophagus with oesophageal carcinoma, diagnostic criteria remain debated. Division into long segment (> 5 cm), short segment (< 5 cm) and ultrashort segment (biopsy evidence only) are of potential clinical importance, since the risk of carcinoma relates to the length of metaplasia. However, > 15% of the population have intestinal metaplasia proximal to the gastro-oesophageal junction, and the implications are unclear.

Features

• Endoscopic evidence, confirmed by biopsy, of columnar-lined oesophagus more than 3 cm proximal to the gastro-oesophageal junction (UK), or intestinal metaplasia proximal to the gastro-oesophageal junction (USA)
• Oesophageal carcinoma develops in 1-5% and dysplasia in 10% over 5 years if Barrett's is > 3 cm in extent, although controversy about the estimated risk persists
• The risk of carcinoma appears to be related to the length of Barrett's oesophagus

Management

• Multiple biopsies every 2 cm are needed to exclude dysplasia at diagnosis
• Prescribe full dose PPI (equivalent to omperazole 40 mg, lansoprazole 30 mg, rabeprazole 20 mg daily). Long-term treatment is indicated, because Barrett's oesophagus is assumed to be a consequence of severe gastro-oesophageal reflux
• Discuss the diagnosis in the context of the individual patient. The risk of cancer is usually small (since most patients are older, or have a short segment of Barrett's) and needless anxiety can be created by generalisations about premalig-nant conditions
• Annual surveillance endoscopy has not been shown to reduce mortality, but cancers detected by surveillance have a better survival than those presenting in the normal course of events. The issues should be discussed with individual patients and a joint decision made. There is no point in surveillance if oesophagectomy is not an option (due to age, comorbidity) if cancer is detected
• Low-grade dysplasia does not necessarily progress. It is reasonable to continue vigorous antisecretory therapy and repeat endoscopy every 6-12 months for as long as patients remain surgical candidates
• High-grade dysplasia also does not always progress to carcinoma, but if confirmed on repeat endoscopy (within 3 months) or multiple foci are detected in young patients, oesophagectomy should be considered
• Photodynamic therapy and ablation of Barrett's epithelium by endoscopic argon beamer remain experimental techniques

Oesophageal ulcers

Features

• Associated with severe oesophagitis or Barrett's oesophagus
• Endoscopy, biopsy and brush cytology are needed to exclude malignancy

Management

• Check that biopsies and brushings for cytology have been taken at endoscopy
• Prescribe full dose PPI (lansoprazole 30 mg or omeprazole 40 mg daily) for 8 weeks
• Repeat the endoscopy, biopsy and brushings after 8 weeks to confirm healing. Do not stop the PPI
• Long-term treatment with a PPI is appropriate for peptic oesophageal ulcers, because these indicate severe reflux with a high recurrence rate
• Refer for surgery if high-grade dysplasia is detected in ulcers that persist despite treatment

Alkaline reflux

Bile, pancreatic enzymes and bicarbonate due to duodenogastric reflux, as well as acid and pepsin, can cause oesophagitis. This occurs particularly after partial gastrectomy. Biliary reflux at endoscopy is normal if the patient is retching.

• Oesophagitis with a pH > 4 at all times during ambulatory monitoring is necessary for diagnosis
• General measures and antacids should be tried. Sucralfate binds bile and may help, but needs to be given four times daily to heal oesophagitis. Dilute hydrochloric acid BP (0.1 mL in 10 mL water) would be logical and is said to be better than placebo for heartburn in pregnancy, but is not in general use
• Surgical (Roux-en-Y) revision is reserved for severe, intolerable symptoms

Dysphagia

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Causes

Acute or progressive dysphagia demands urgent investigation. Oropharyngeal and oesophageal causes are recognised.

Clinical features

A careful history usually distinguishes between oropharyngeal and oesophageal causes. Four questions about the dysphagia are essential: interval, type of food, pattern and associated features.

Interval

• Difficulty in initiating swallowing, repeated attempts at swallowing or dysphagia within a second of starting to swallow characterise oropharyngeal dysphagia
• Dysphagia a few seconds after starting to swallow indicates an oesophageal cause
• Where the patient points to is no help in locating the site of the lesion

Type of food

• Ask if dysphagia is for liquids (usually pharyngeal), solids (mechanical oesophageal cause likely) or both (oesophageal dysmotility more likely)
• Exacerbation by hot or cold liquids is common in oesophagitis

Pattern

• Progressive dysphagia indicates an organic cause, such as carcinoma, benign stricture or achalasia
• Intermittent symptoms are common in oesophageal dysmotility, diverticula, web or ring
• Short (< 3 months), progressive history indicates malignancy
• A 'lump in the throat' as the only symptom is unlikely to have a mechanical cause

Associated features

• Weight loss confirms that an organic cause is probable, but lack of weight loss is of no diagnostic value
• A history of heartburn suggests a peptic stricture, although when a patient presents with dysphagia, heartburn may no longer be present
• Cough indicates spillover into the bronchial tree, commonly due to oropharyngeal dysphagia, or achalasia when at night. Very rarely it is due to an oesophagobronchial fistula
• Odynophagia (pain during swallowing) often accompanies dysphagia in oesophagitis, achalasia, or diffuse oesophageal spasm
• Examine the mouth and teeth or dentures, and feel for supraclavicular nodes (from carcinoma of the cardia)
• Look for signs of systemic disease (anaemia, systemic sclerosis, or neurological disorders)

Urgent investigations

• Indicated when dysphagia is for solids alone, when symptoms are progressive or when there is associated weight loss
• Consult the radiologist or gastroenterologist to arrange urgent investigation
• Chest X-ray—look for a hilar tumour, mediastinal fluid level, absent gastric bubble or right lower lobe consolidation (aspiration)
• Barium swallow—within 48 h. A smooth, tapering stricture is often benign. Irregularity or asymmetry suggests malignancy
• Endoscopy—after a barium swallow. Allow 12 h for barium to clear: it can block the endoscope
• Blood tests—anaemia may be due to malignancy, poor nutrition, bleeding, or Plummer-Vinson syndrome. A high urea usually reflects dehydration

Elective investigations

• Barium swallow, chest X-ray and endoscopy can be performed electively in patients with intermittent dysphagia without weight loss, or when symptoms suggest oesophageal motility disorders
• Cine or bread/marshmallow barium swallow, or oesophageal manometry is usually appropriate if the barium swallow is normal
• ENT assessment is indicated for most pharyngeal causes of dysphagia
• Pulmonary function tests (spirometry and oxygen-diffusing capacity) establish a baseline in patients with systemic sclerosis

Acute hepatic failure

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Acute hepatic failure occurs in a previously normal liver and is either acute or late onset (subacute). The time of onset and mortality distinguish the two types, although other features and management are similar.

The main differential diagnosis is between acute and acute-on-chronic liver failure. The potential for complete recovery distinguishes acute failure, although it has a worse prognosis.

Clinical features

Hyperacute hepatic failure

• Encephalopathy within 7 days of the onset of jaundice (after paracetamol/acetaminophen)
• Encephalopathy includes all stages from personality change to coma. The grade may change rapidly
• Paradoxically, this group has the highest likelihood of recovery with medical management

Acute liver failure

• Encephalopathy develops 8-28 days after the onset of jaundice (viral or drug-induced)
• This group has a high mortality and marked prolongation of prothrombin time

Subacute liver failure

• Encephalopathy after an interval of 4-12 weeks after the onset of jaundice (any cause)
• Less marked prolongation of prothrombin time, but mortality remains high

Associated features

• Fetor hepaticus—characteristic smell of 'pear-drops' (acetone) in breath
• Jaundice—may be minimal in the early stages
• Liver size—usually small, due to hepatic necrosis. If enlarged, acute-on-chronic liver failure or Budd-Chiari syndrome is more likely
• Spleen—usually not palpable
• No single feature entirely discriminates between acute and acute-on-chronic hepatic failure. The history is the best guide

Causes

• Acetaminophen/paracetamol overdose and cryptogenic are the commonest
• Acetaminophen/paracetamol—presentation a few days after apparent recovery from poisoning is typical
• Cryptogenic (or non-A-non-B-non-C viral hepatitis, NANBNC)—the commonest cause after acetaminophen/paracetamol
• Viral—hepatitis B or D (8 agent). Rare after hepatitis A, C or E (community-acquired non-A, non-B), yellow fever or leptospirosis
• Drugs—acetaminophen/paracetamol (especially associated with alcohol), halothane, isoniazid
• Alcohol—occasionally without underlying liver disease, but usually acute-on-chronic
• Wilson's disease—haemolysis is a feature
• Budd-Chiari syndrome—ascites and abdominal pain are often prominent
• Fatty liver of pregnancy—third trimester
• HELLP syndrome (haemolysis, elevated liver enzymes and low platelet count)—a severe complication of pre-eclampsia in pregnancy

Investigations

Blood tests

• Coagulation studies, glucose and potassium immediately and creatinine as soon as possible
• Full blood count, group and save, bilirubin, albumin, AST, amylase
• Hepatitis serology (including hepatitis B core IgM), acetaminophen/paracetamol levels, serum copper and caeruloplasmin (24 h urinary copper if Wilson's suspected Acetaminophen/paracetamol is often undetectable by the time acute liver failure presents

Other

• Chest X-ray
• Ultrasound of liver and pancreas. Hepatic vein Doppler studies if Budd-Chiari syndrome is suspected
• Blood cultures—even if afebrile
• EEG—may be diagnostic when there is doubt, but is seldom necessary

Management General

• Intensive care nursing
• Insert a central venous line early to ensure good hydration. Aggressive early rehydra-tion appears to improve outcome. Patients drink little because of nausea or encephalopathy. Hypovolaemia impairs hepatic and renal perfusion
• Monitor urine output, blood glucose and vital signs, every hour
• Check serum potassium and coagulation studies twice daily for the first 48 h, then daily with full blood count, creatinine and albumin
• Avoid giving FFP as prothrombin time/INR are the best guide to liver function, severity and outcome
• Reassess the grade of encephalopathy, ascites and fluid balance once or twice daily

Specific therapy

• Commence N-acetyl cysteine infusion for significant acetaminophen/paracetamol poisoning and continue infusion until coagulation returns to normal
• Inotropic support if hypotensive

Encephalopathy

• Avoid sedation if possible, but chlordiazepoxide is appropriate for alcohol withdrawal
• Protect the airway as encephalopathy progresses beyond grade 2
• Intracranial pressure monitoring is appropriate in grade 4 encephalopathy (usually when the patient has been transferred to a liver unit). Mannitol 0.3-1.0 g/kg is given when intracranial pressure is increased provided not anuric. Oxygen and inotropic support are also necessary. Phenytoin decreases subclinical seizure activity and cerebral oedemaHypoglycaemia and hypokalaemia
• 10% dextrose 100 mL/h with KCl 40 mmol/L, but 20-50% dextrose may be needed if hypoglycaemia is severe
• Empirical antibiotics (see below)

Bleeding

• Avoid arterial punctures
• FFP if clinically significant bleeding occurs
• Acid suppression (omeprazole 20 mg orally, or sucralfate 2 g three times daily) is often given to reduce stress-induced gastric erosions, but the evidence of benefit is debated

Renal failure

• Over 50% develop renal impairment. Good hydration is the key to preventing renal failure, but hepatotoxic drugs may be directly nephrotoxic. Hepatorenal syndrome may be defined as doubling of serum creatinine to > 200 |lmol/L in < 2 weeks, together with a low urinary sodium (< 5 mmol/L), in the absence of hypovolaemia. Although two types (early and late) are described, the differences are largely semantic
• Serum urea is falsely low in severe liver disease, so creatinine should be measured, but a bilirubin > 200 |lmol/L interferes with creatinine assay
• Hepatorenal syndrome has a dreadful prognosis, although terlipressin, where available, has an increasing therapeutic role. The optimum dose, duration and amount of additional albumin are still being assessed. Terlipressin 0.5 mg twice daily (less than for variceal bleeding), with 20% albumin 1 g/kg (i.e. 60 kg man = 300 mL 20% albumin) is appropriate. Increase terlipressin to 1 mg four times daily if no fall in creatinine after 48 h
• Haemofiltration or dialysis is rarely indicated because the prognosis of established renal and liver failure is so poor. Discussion between consultant hepatologist and renal physician is appropriate

Infection

• Meticulous care of intravenous and urinary catheters
• Blood, urine and catheter cultures are essential and must be performed before starting antibiotics
• Antibiotics are recommended, because patients are critically ill and signs of sepsis are commonly absent. Intravenous cefuroxime 750 mg three times daily is appropriate, until culture results are available

Indications for transplant

Deciding when the chance of spontaneous recovery is less than the risks of a liver transplant is difficult. Discuss the situation with the nearest transplant centre at an early stage.

Transfer is generally recommended in the following circumstances

• The prothrombin time (measured in seconds) at the time of referral is greater than the interval (hours) between poisoning and referral
• Prothrombin time exceeds 50 s
• Metabolic acidosis at presentation
• All patients with established encephalopathy. Alcohol abuse is a relative, but not absolute, contraindication to transplantation
• In one study 17/92 patients admitted to a liver unit with paracetamol poisoning were listed for transplantation. 70% of those transplanted survived compared to 14% who were listed but not transplanted. The overall mortality was 32%

Take into account

• Age (< 60 years)
• Previous liver function (should have been normal)
• Ability to cope with post-transplant regimen

Before and during transfer

• Insert a central venous line if the prothrombin time exceeds 30 s (INR 2.0) or if there is renal dysfunction. Good hydration and circulation improve outcome
• Give 10% glucose 100 mL/h with 40 mmol/L KCl to prevent hypoglycaemia or hypokalaemia
• Give 20% mannitol 20 mL/h if encephalopathic before transfer
• Intubate and ventilate patients with advanced encephalopathy before transfer, because cerebral oedema is exacerbated by movement

Prognosis

Factors

• Grade of encephalopathy—15% survival without transplant, when grade 3-4
• Age:
• > 40 years 15% survival
• < 30 years 40% survival
• Albumin:
• > 35 g/L 80% survival
• < 30 g/L 20% survival
• Cause—drug reactions and non-A-non-B (hepatitis C) induced failure have a worse prognosis than other causes
• Onset—late onset has a worse prognosis than fulminant failure

Transplant in acute liver failure

• 65% survive, but this is improving
• Auxiliary liver transplantation until the original liver recovers has proved disappointing
• The role of Molecular Adsorbant Recirculating System (MARS) in hepatorenal syndrome and as a bridge to transplantation is being evaluated

Toxic dilatation of the colon

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Dilatation of the colon with signs of systemic upset ('toxic') is becoming less common as acute attacks of ulcerative colitis are recognised and appropriately treated. The danger if surgery is inappropriately delayed is colonic perforation, which still carries a high mortality.
Clinical features

• Colitis—usually caused by severe ulcerative colitis, but can occur in Crohn's colitis, and rarely in ischaemic, or infective, colitis.
• Fever > 37.8°C
• Neutrophils > 10 X 109/L
• Tachycardia > 90 b.p.m.
• Radiological colonic dilatation
• Clinical appearance can be deceptive due to steroids

Management

Patients presenting with dilatation should start intensive medical treatment (see below) and the response should be carefully assessed after 24 h. About half respond, but a decision to continue for a further 24 h or proceed to emergency colectomy must be made by a senior gastroenterologist in consultation with a colorectal surgeon. Patients who recover continue treatment as for severe colitis. When dilatation develops during intensive medical treatment for colitis, colectomy is indicated without further delay.

Diagnosis

• Always take a plain abdominal X-ray on admission in patients with severe colitis. Mucosal islands, in addition to dilatation indicate very severe ulceration and predict the need for colectomy. The presence of three or more distended loops of small bowel is also associated with the need for colectomy. The X-ray should be repeated daily until clinical improvement or surgery occurs
• Stool culture and faecal Cl. difficile toxin assay
• Blood cultures
• Flexible sigmoidoscopy and rectal mucosal biopsy to confirm colitis, but colonoscopy or barium enema are dangerous and should be avoided

Supportive therapy

• Vigorously correct fluid and electrolyte imbalance with intravenous fluids and KCl supplements (serum K 4.0-4.5 mmol/L)
• Nil by mouth
• Involve the surgeons as soon as the diagnosis is made
• 4-hourly observation of pulse, temperature and BP, as well as fluid balance and meticulous stool chart, since nursing observations are essential prognostic factors when deciding the timing of colectomy
• Examine the patient at least twice daily (check pulse, abdominal tenderness, temperature and stool chart)
• Monitor daily full blood count, C-reactive protein, electrolytes and maximum colonic diameter on plain abdominal X-ray

Specific therapy

• Stop antidiarrhoeal agents, opiates and anticholinergic drugs
• Intravenous hydrocortisone 100 mg four times daily or methylprednisolone 20 mg three times daily, for ulcerative colitis or Crohn's disease
• Rectal hydrocortisone 100 mg in 100 mL twice daily
• There is no evidence that antibiotics alter outcome

Indications for emergency colectomy

The decision is usually difficult, but prolonged medical treatment increases mortality, even in young patients. If objective signs (pulse, temperature) are improving after 24 h, a further 24 h trial of medical treatment may be justified. This decision should be taken by a senior physician, jointly with the surgeons. Indications for colectomy in the presence of a dilated colon are:

• Failure to improve clinically (no change in stool frequency, tachycardia or temperature) or radiologically within 24 h
• Signs of perforation (may be minimal, due to steroids)
• Mucosal islands as well as dilatation (because such severe ulceration is very unlikely to respond to steroids)
• Severe ulcerative colitis without colonic dilatation is slightly different, but early decision-making on surgery is still essential. If, after 3 days' intravenous treatment, the stool frequency is > 8/day, or the frequency is 3-8/day together with a C-reactive protein > 45 mg/L, then there is 85% chance that colectomy will be needed on that admission

Alimentary Emergencies: Intestinal obstruction

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Look for mucosal oedema, the site that luminal gas disappears, displacement of bowel loops by a mass, and air in the bowel wall or biliary tree. An occasional fluid level on an erect film is normal. On an erect chest X-ray, look for air under the diaphragm. It remains the investigation of choice

• CT scan—often helpful in determining the site and likely cause of partial bowel obstruction
• Blood tests—look for hypokalaemia or high urea. Leucocytosis suggests strangulation. Crossmatch 2 units prior to surgery
• Arterial gases—metabolic alkalosis occurs with severe vomiting

Management

• Nasogastric suction
• Replace fluid and electrolytes—5 L 0.9% saline and 200 mmol KCl may be needed in the first 24 h. Sequestered fluid in obstructed bowel is not measured, so adjust infusion rate according to the urine output and central venous pressure in very sick patients
• Assess concomitant medical problems—drugs may not have been absorbed
• Relieve the obstruction—the site governs the type of operation. Suspicion of strangulation demands urgent surgery. Non-operative manoeuvres are initially indicated for ileus, pseudo-obstruction, volvulus, or intussusception
• Monitor:
• urine output
• nasogastric aspirate
• central venous pressure in the shocked or elderly
• daily electrolyteslleus
• Nasogastric suction, maintaining serum potassium at 4.0-4.5 mmol/L, intravenous fluids and patience are usually sufficient
• Check that anticholinergic drugs are not prescribed and decrease opiate analgesia to a minimum
• Try metoclopramide 10 mg intravenously three times daily, or erythromycin 500 mg four times daily (as a motilin agonist), as prokinetic agents
• Consider parenteral nutrition if resolution is delayed for longer than 72 h
• Exclude mechanical obstruction by contrast radiology, if ileus persists after a few days

Volvulus

• Sigmoid volvulus—common in developing countries, elderly males and the mentally handicapped. Plain X-ray shows massive sigmoid distension. Colonoscopy is more effective than a deflating rectal tube and should be attempted before surgery
• Caecal volvulus—obstruction is often incomplete initially but recurs without surgery, so laparotomy is advisable
• Gastric volvulus—associated with diaphragmatic eventration, visible on plain chest and abdominal X-rays. Distinguish from 'acute gastric dilatation', which is a misnomer for gastric ileus, caused by poor attention to nasogastric suction and electrolyte balance. Surgery is needed for gastric volvulus, with repair of the diaphragm
Intussusception
• Usually idiopathic in infants; due to a Meckel's diverticulum in adolescence; or a polyp or carcinoma in adults
• Intermittent pain, rectal bleeding, small intestinal fluid levels and an absent caecal gas shadow suggest the diagnosis. Facial pallor during pain occurs in infants
• Ultrasound in experienced hands is diagnostic and the recommended initial investigation, although barium enema may be both diagnostic and therapeutic in the early stages

Pseudo-obstruction

• Clinical features of intestinal obstruction without a mechanical cause. The motility disorder commonly affects the whole gastrointestinal tract, although it is colonic distension that is often most prominent
• Consider the diagnosis in the elderly and mentally handicapped, or when obstruction is associated with other disorders (myocardial infarction, pneumonia, Parkinson's disease)
• An urgent single contrast barium enema is often necessary to distinguish pseudo-obstruction from mechanical obstruction, and occasionally has a therapeutic effect
• Stop causative drugs (opiates, phenothiazines, tricyclics, clonidine) and treat associated disease
• Do not allow the patient to remain supine, but ensure mobility or turning regularly, including into the prone or head-down position as this may help deflation
• Intravenous neostigmine 2 mg, repeated if necessary, may have a dramatic effect in relieving pseudo-obstruction. There is usually a relative contraindication (other drugs, cardiovascular, or respiratory disease), but liase with an experienced anaesthetist and monitor for bradycardia
• Erythromycin 2 g daily as a prokinetic (motilin-like activity), stimulant laxatives (e.g. senna) rarely help, and lactulose may increase intraluminal gas. Enemas should be used with care as perforation can occur
• Repeat plain abdominal X-ray after 24 h to monitor caecal diameter
• 90% resolve spontaneously, but colonoscopic decompression is warranted if pain is severe, or the caecum > 10 cm. Surgery should be avoided if at all possible, but caecostomy is appropriate if two attempts at colonoscopic decompression fail and symptoms persist
• Chronic intestinal pseudo-obstruction is a feature of systemic sclerosis, neuromuscu-lar diseases and amyloidosis amongst others. Severe dysmotility syndrome causes severe abdominal pain and episodes of functional intestinal obstruction. It is usually associated with previous surgery for functional disease (e.g. slow transit constipation), opioid dependence and may cause intestinal failure requiring home parenteral nutrition. Referral to a specialist centre is appropriate

Acute cholecystitis

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Distinguishing features

• Fever and persistent pain distinguish acute cholecystitis from biliary colic or chronic cholecystitis
• Impaction of a gallstone in the cystic duct causes > 90%
• Typical pain occurs in < 50%
• Pain may be provoked by a fatty meal and builds up to a peak over 60 min, unlike the short spasms of biliary colic
• Fever develops after 12 h due to bacterial invasion and pain then becomes continuous
• Murphy's sign is sensitive, but not specific
• Calcified calculi (15%) and very rarely gas within biliary tree due to gasforming organisms or a spontaneous choledochoduodenal fistula may be visible on plain abdominal X-ray

Complications

• Recurrence (50%)
• Cholangitis due to associated common duct stones (10%)
• Mucocoele, empyema or gangrene of the gall bladder (1%)
• Biliary peritonitis (0.5%, with a mortality of 50%)
• Mirizzi's syndrome (obstructive jaundice due to external pressure on the common bile duct from inflammation around a stone impacted in the cystic duct)

Conservative management

• Confirm the diagnosis by ultrasound. Tenderness under the ultrasound probe in the presence of gallstones and a thickened gall bladder wall is effectively diagnostic. Isotope—hepatobiliary iminodiacetic acid (HIDA)—scans are also accurate, but not universally available
• Analgesia (intramuscular pethidine/meperidine 100 mg and hyoscine 20 mg, but not morphine, which can increase the pain)
• Intravenous fluids
• Nasogastric suction may be helpful, to alleviate vomiting if present
• Antibiotics (intravenous amoxycillin 500 mg three times daily and gentamicin 5 mg/kg once daily)
• Cholecystectomy at the earliest opportunity (see below)

Surgical management

• Optimum treatment is surgery on the same admission, on the next available list. Morbidity, total hospital stay, costs and mortality from complications of acute cholecystitis are lower compared to delayed cholecystectomy. Early surgery is especially appropriate in elderly patients or diabetics, because septic complications are more common
• Laparoscopic cholecystectomy is safe during acute cholecystitis in experienced hands. Cholecystostomy or percutaneous drainage of an empyema may be more appropriate in very sick elderly patients, but is rarely necessary
• The longer the interval between cholecystitis and surgery, the greater the risk of a recurrent attack: concern about an increased surgical complication rate 7-14 days after an acute attack is probably unfounded
• Other indications for surgery include signs of peritonitis and uncertainty about the diagnosis (when perforation or retrocaecal appendicitis cannot be excluded)

Appendicitis

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Biliary colic

Distinguishing features

• Biliary colic typically causes a few minutes of right upper quadrant pain, with intervals of 1 h, and subsides after several hours. The pain may be exclusively high epigastric in location. Recurrent colic is a feature of chronic cholecystitis
• Fever, leucocytosis or pain lasting more than 12 h is likely to be due to acute cholecystitis
• Murphy's sign (tenderness in the right upper quadrant on inspiration) is positive in acute cholecystitis
• Flatulence, distension, fat intolerance and nausea are frequent but non-specific, and occur in other common conditions, especially irritable bowel syndrome (IBS) or non-ulcer dyspepsia
• Daily pain is unlikely to be due to biliary colic, even if gallstones are present

Management

• Ultrasonography will detect gallstones, although difficult in the obese and those with a fibrosed gall bladder. Repeat ultrasound after a fatty meal is a test of gall bladder function, and is abnormal (no contraction) in acute or chronic cholecystitis
• Other laboratory investigations are usually unhelpful, but a transient (<48 h) elevation in aspartate transaminase (AST) may occur in uncomplicated biliary colic
• Cholecystectomy is appropriate if symptoms are typical.

Acute abdominal pain

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Clinical diagnostic accuracy is about 50%. Metabolic and extraintestinal causes should be considered if the diagnosis is in doubt.Discriminating questions

• Site

• Duration
• Severity
• Radiation
• Aggravating factors

Also ask about

• Vomiting (if it precedes pain, a surgical cause is less likely)
• Time last ate or drank
• Bowel disturbance
• Urinary frequency
• Date of last menstrual period
• Previous abdominal surgery

Specifically examine for

• Distension
• Visible peristalsis
• Rebound tenderness, guarding or rigidity
• Pulsatile mass and peripheral pulses
• Hernial orifices
• Rectal and pelvic tenderness or masses
• Bowel sounds
• Epigastric bruit (normally audible in about 10% of thin patients)
• Fever (> 39°C with rigors suggests pyelonephritis, cholangitis or pneumonia)

Investigations

Every patient with acute abdominal pain should have on admission:

• Full blood count—leucocytosis may be absent in the elderly
• Electrolytes and creatinine
• Amylase—but many causes of slight elevation other than acute pancreatitis
• Group and save serum
• Urine examination—including pregnancy test if doubtful
• Erect chest X-ray—look for basal atelectasis and gas under diaphragm
• Supine abdominal X-ray—look for biliary and renal calculi, dilated bowel (> 2.5 cm small intestine, > 6.0 cm colon), air in the biliary tree
• ECG
• Blood cultures—if febrile
• Abdominal ultrasound—the most discriminating investigation to identify appendicitis, cholecystitis, renal, or pelvic inflammatory disease
• Abdominal CT scan is indicated when ultrasound is technically difficult (often due to bowel gas or obesity) or does not identify a specific cause for acute abdominal pain. It is the initial imaging procedure of choice for suspected pancreatitis

Management—general principles

• Analgesia—do not withhold opiates for severe pain 'pending a surgical opinion', if the diagnosis is clear
• Perforation, peritonitis, or obstruction needs emergency surgery
• Observation overnight often clarifies a difficult diagnosis
• Nil by mouth until a decision about surgery has been made
• Specific management of common causes of abdominal pain are discussed below

Acute bleeding: upper gastrointestinal tract

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The aims of management in upper gastrointestinal bleeding are to stabilise the patient, stop active bleeding and prevent recurrent bleeding. There are about 90 admissions per 100 000 adults annually in the UK, with an overall mortality of 14% unless patients are admitted to a specialised bleeding unit, where a mortality of about 5% can be expected. Most bleeds from peptic ulcers stop spontaneously and about 25% can be identified who have no risk of rebleeding and can be rapidly discharged. The task is to distinguish the 20% who rebleed in hospital and who may need surgical intervention. A standard
clinical approach is recommended for every patient, so that patients at highest risk of rebleeding and death are identified early

Clinical approach

• Assess severity
• Resuscitate
• Establish the site of bleeding
• Liaise with the surgical and intensive care teams on call
• Medical intervention
• Early surgery when appropriate

Assessment

The aim is to identify patients at high risk of rebleeding and death, by clinical and endoscopic examination. The Rockall score is an independently validated risk assessment score that is simple to apply and recommended. All patients with haematemesis or melaena must be treated actively until a stable baseline has been established. There is no room for complacency.

Document the following

In addition to a record of the assessment of the patient:
• Preceding symptoms (dyspepsia, vomiting, weight loss)
• Drug and alcohol ingestion
• Presence or absence of melaena on rectal examination
• Signs of chronic liver disease

Investigations and management

Resuscitation on arrival
• Ensure a patent airway
• Insert one 14- or two 18-gauge intravenous cannula
• If pulse > 100b.p.m., give 500-1000 mL colloid (such as Haemaccel, Gelofusin, Pentaspan or pentastarch) over 30-60 min and repeat if necessary whilst waiting for blood
• Transfuse blood until haemodynamically stable in the first few hours, because initial haemoglobin is a poor indicator of the severity of the bleed. Subsequently transfuse up to haemoglobin of 10 g/dL
• Synthetic colloid or crystalloid will cause haemodilution: 1000 mL decreases the pre-transfusion haemoglobin by about 10%
• Reserve group O rhesus negative blood for dire emergencies (such as continuing massive bleeding and systolic BP < 80 mmHg despite 1000 mL intravenous colloid), when the risk from hypotension exceeds that from uncrossmatched blood
• Insert a urinary catheter in patients who need a central venous line, to monitor urine output for information regarding fluid balance
• Ensure that the patient remains nil by mouth until endoscopy
• Do not insert a nasogastric tube, because this increases the risk of haemorrhage from gastric and oesophageal lesions
• Admission to a designated specialised unit for gastrointestinal bleeding reduces mortality to 5% or less. If this is not available, consider admission of patients with a predicted mortality > 10% (initial Rockall score > 3) to a critical care unit and contact surgical colleagues as soon as the patient is resuscitated
Initial investigations
• Full blood count, crossmatch, coagulation studies and electrolytes
• Crossmatch 4 units of blood for patients with > 10% mortality risk (Rockall > 3), but group and save alone for lower risk patients. Note that this is a practical application of the Rockall score, but it has not been validated for this purpose
• Haemodynamic status is a better guide to transfusion requirements than measured haemoglobin
• Arterial gases in those with cardiorespiratory disease
• ECG in high-risk patients
• Chest X-ray in high-risk patients (abdominal films rarely help)

Indications for a central venous line

• Signs of major haemorrhage (pulse > 100 b.p.m., systolic BP < 100 mmHg). Reasons for not inserting a central line in patients with a high (> 10%) predicted mortality (p. 9) must be carefully considered
• Rebleed during the same admission
• Inadequate peripheral venous access
• If a central venous line is needed, monitoring in a critical care area is advisable

Establish site of bleeding

• Arrange endoscopy after resuscitation, ideally within 12-24 h. Mucosal lesions and stigmata for rebleeding are otherwise missed. Ensure that the presence or absence of stigmata is recorded
• Indications for emergency endoscopy are continued bleeding, a rebleed in hospital, or if the patient is being considered for surgery
• Profuse haemorrhage may obscure the bleeding site. Gastric lavage to remove clots rarely alters management and can be hazardous. Repeat endoscopy after a further 12 h resuscitation is recommended. Immediate surgery should be a joint decision between surgeons and physicians
• Interpret the endoscopy report intelligently: it should identify stigmata of recent haemorrhage (predicts risk of rebleeding), state whether there has been intervention (e.g. sclerotherapy of ulcers) and describe the position of ulcers (posterior duodenal ulcers overly a branch of the gastroduodenal artery that can rebleed vigorously)

Monitoring and discharge
• Pulse, BP, central venous pressure and urine output hourly, until stable
• Re-examine after 4 h
• Coagulation studies if > 4 units transfused
• Daily full blood count, urea and electrolytes for patients being transfused and for 2 days after
• Keep 2 units in the blood bank for 48 h after bleeding has stopped
• Patients who do not have endoscopic stigmata of high rebleeding risk and who have not had endoscopic intervention can safely start eating and drinking immediately after endoscopy and be discharged at any time thereafter, as long as there is adequate support at home
• Patients who have had endoscopic intervention should be kept in hospital for 72 h after bleeding has stopped

Medical intervention

These measures are not an alternative to surgery if an operation is indicated, but may help stop bleeding or reduce the risk of rebleeding. Endoscopic intervention is indicated for patients with a peptic ulcer and active bleeding or non-bleeding visible vessel.

• Endoscopic intervention: all techniques halve the risk of rebleeding, but depend on local expertise and may not be available. Injection of adrenaline (up to 10 mL 1 : 10 000) around peptic ulcers, thermocoagulation and laser photocoagulation all have similar efficacy. Sclerosant (ethanolamine) is best avoided as necrosis and perforation have been reported. A combination of adrenaline (1 : 10 000) and thrombin (1000 U/mL) may be more efficacious at preventing rebleeding
• Intravenous omeprazole or pantoprazole (20-80 mg in 250 mL saline infused over 1 h, then 8 mg/h for 72 h) is only indicated after endoscopic intervention for bleeding peptic ulcers. It halves the risk of rebleeding and surgery and reduces mortality by one-third
• Ranitidine, oral omeprazole or other acid-suppressing drugs have no place in the initial treatment of bleeding. They should be reserved for treatment once a peptic ulcer has been diagnosed
• Tranexamic acid (1 g intravenously, three times daily for 72 h) has been shown on meta-analysis to reduce rebleeding and mortality. In the absence of a previous thromboem-bolic event, it is a reasonable adjunct in the treatment of high-risk patients until further trials are available. It also reduces the risk of recurrent bleeding from angiodysplasia
• Determination of Helicobacter pylori status should be done at the time of emergency endoscopy, using a biopsy urease (Campylobacter-like organism, CLO) test in patients with a bleeding ulcer. Eradication therapy for H. pylori-positive patients is indicated as soon as oral feeding is restarted
• Terlipressin (Glypressin) 2 mg bolus, then 2 mg every 4 h is indicated for varices (below); Glypressin may not be available in all countries
• Other drugs (octreotide, vasopressin) do not have a proven role in the management of acute non-variceal gastrointestinal bleeding. A combination of ethinyloestradiol (50 |lg) and norethisterone (1 mg/day) may decrease episodes of recurrent acute bleeding from angiodysplasia (such as hereditary telangiectasia)

Rebleeding

Rebleeding greatly increases mortality. Patients at high risk of rebleeding need to be recognised and the surgeons told of their admission. Patients are best admitted to a critical care area, where signs of rebleeding should be detected early. Signs of rebleeding are:

• Rise in pulse rate (a sensitive and early sign)
• Fall in central venous pressure
• Decrease in hourly urine output
• Haematemesis or continued melaena
• Looking at the patient (pallor, pulse, postural pressure drop and poor peripheral circulation) is as important as looking at the charts

Indications for surgery

Contact surgical colleagues at the outset, before an operation is necessary rather than when it is inevitable. Delay increases mortality. When the following criteria are met, surgery may be appropriate. Any decision not to operate should only be taken after discussion with the consulting surgeon.

Oesophageal varices

Cirrhosis is the commonest cause of portal hypertension and oesophageal varices in the UK and North America. Whilst oesophageal varices can be found at endoscopy in almost 50% of patients with cirrhosis, less than one-third of these will bleed from their varices. Mortality during an acute bleed depends on the severity of liver disease on admission. Mortality according to Child's grade A is 10%, grade B is 25% and grade C is 50%, but 60-80% of all patients who bleed from varices will be dead within 4 years.

Assessment

• Bleeding from oesophageal varices is a complex clinical emergency for which control of bleeding is only one aspect
• Attention to infection, control of ascites, encephalopathy, alcohol withdrawal and nutrition are vital for a successful outcome

Acute bleeding

• Resuscitate and monitor. Colloids (synthetic, albumin or blood) are indicated and saline can be used in the acute situation. Avoid 5% dextrose if hyponatraemic
• 30% with known varices have another source of haemorrhage
• During active bleeding, correct disordered coagulation to international normalized ratio (INR) < 1.5 or prothrombin time < 22 s with fresh frozen plasma (FFP). However, FFP is contraindicated in the absence of bleeding, because this increases intravascular volume and variceal pressure, which may precipitate haemorrhage. Platelet transfusion may be necessary for thrombocytopenia (platelet count < 60 X 109/L). Discuss with the haematologists
• Arrange urgent endoscopy for banding or sclerotherapy by an experienced endoscopist
• Control of the airway, with endotracheal intubation if necessary, is extremely important when carrying out emergency endoscopy in a patient with an active variceal bleeding
• Give oral lactulose, starting at 90 mL/day or phosphate enemas if nil by mouth to prevent/treat hepatic encephalopathy, intravenous vitamins and ben-zodiazepine, as necessary, for alcohol withdrawal.

If endoscopic therapy is not available, or massive bleeding continues:

• Insert a Sengstaken tube until sclerotherapy/banding can be performed or repeated after 12 h
• Start splanchnic vasoconstrictors such as Glypressin (2 mg bolus, then 2 mg every 4 h, for up to 96 h). Glypressin rarely can be associated with ischaemic complications
• For recurrent bleeding after two attempts at endoscopic therapy the alternatives are tran-sjugular intrahepatic portosystemic shunt (TIPSS) or oesophageal transection (see below)
• Where a stent is inserted between the hepatic and portal vein under radiological control, TIPSS can only be performed by experienced interventional radiologists, but is probably the procedure of choice where bleeding is not controlled by other means. Control of bleeding is excellent (approaching 100%), but 1 month mortality is still high (30-40%) owing to liver failure. Late complications (blocked stent, encephalopathy) are common
• Oesophageal transection has a mortality of 50% and should only be considered for patients without other organ failure, who were admitted in Child's group A or B. Splenectomy and proximal gastric devascularisation are needed to prevent subsequent bleeding from gastric varices
• Bleeding gastric varices are one cause of failed endoscopic haemostasis. TIPSS should be considered, but preliminary reports suggest that endoscopic injection of bovine thrombin (2-10 mL of 1000 U/mL) or histoacryl (mixed with 1 : 1 lipiodal, 1-2 mL injected) controls active bleeding, although varices are not eradicated. Histoacryl has the potential to glue up the endoscope and should only be used by experienced endoscopists

Balloon tamponade

• Indicated for uncontrolled variceal bleeding, or recurrent haemorrhage despite scle-rotherapy or banding
• To be inserted by experienced operators only
• Sedation, or a general anaesthetic to insert an endotracheal tube and secure the airway, may be necessary
• Insert a cooled, lubricated Sengstaken or Minnesota tube beyond 45 cm. The tube can usually be stiffened by inserting a well-lubricated pair of paediatric endoscopic biopsy forceps down the central lumen
• Inflate the gastric balloon with 300 mL tap water containing 50 mL of any intravenous X-ray contrast medium or 300 mL of air. Ensure gastric balloon channel is double-clamped
• Tie a 250 mL bag of saline to the tube to provide traction at the gastro-oesophageal junction, but be very careful to protect the mouth to prevent pressure necrosis
• Aspirate gastric and oesophageal ports (if present) hourly, and connect to a bag for continuous drainage
• It is rarely necessary to inflate the oesophageal balloon. If necessary because of persistent bleeding, inflate the oesophageal balloon to 30 mmHg with air, measured by manometer. Deflate for 5 min every hour.
• X-ray to check position
• Active bleeding is arrested in 90%. Continued bleeding usually means that the tube is misplaced or that there are gastric varices
• Deflate the oesophageal balloon after 6 h and the gastric balloon after 12-24 h to allow further endoscopic sclerotherapy or banding
• Complications include tracheal intubation, oesophageal rupture from inflating the gastric balloon in the oesophagus, or mucosal necrosis from leaving the balloon inflated for too long

Prevention of rebleeding from varices

• The highest risk of rebleeding is in the first 6 weeks
• Most gastroenterologists repeat endoscopic therapy at 1-2-week intervals until varices are obliterated
• Varices recur after obliteration in 40%, usually within 1 year
• Propranolol 40 mg three times daily decreases the risk of bleeding, can be used following initial endoscopic therapy and in this situation is as effective as repeated endo-scopic therapy.
• Portal hypertensive gastropathy may cause bleeding after variceal obliteration. The gastric mucosa (usually fundal) has a characteristic 'snakeskin' appearance at endoscopy. Propranolol is the treatment of choice
• Surgical or percutaneous TIPSS are indicated for recurrent bleeding, especially in non-cirrhotic portal hypertension

Mallory-Weiss tears

A mucosal tear at the oesophagogastric junction due to forceful vomiting results in haematemesis. The typical features are:

• Initial vomitus does not contain blood
• Vomiting has often been provoked by alcohol
• 90% settle with conservative treatment
• Acid-suppressing drugs are unnecessary
• Continued bleeding can be controlled by endoscopic injection or thermocoagulation. Surgery is very rarely needed
• Bleeding after forceful vomiting may also be caused by prolapse of the gastric mucosa resulting in a focal area of haemorrhagic gastropathy ('hernia gastropathy') opposite the gastro-oesophageal junction
Acute gastric erosions and haemorrhagic gastropathy

Erosions are diagnosed endoscopically, but may be obscured by oozing from haemor-rhagic gastropathy (gastritis is a misleading term that should be reserved for a histo-logical diagnosis). Major haemorrhage from superficial gastric injury is unusual and the cause is often readily apparent.

Causes

• Non-steroidal anti-inflammatory drugs (NSAIDs)
• Alcohol
• Stress (trauma, major surgery or patients in intensive care)

Specific treatment

• A PPI (any) is usually given for 1-4 weeks, depending on the cause
• Persistent bleeding is treated with intravenous tranexamic acid 1 g three times daily, in addition to a PPI (e.g. omeprazole or pantoprazole), which can be given intravenously
• Total gastrectomy is the last resort for continued bleeding after all medical treatment has been vigorously applied for 24-48 h, and should only be performed by an experienced surgeon
• It should be noted that despite the fact that antacids, ranitidine or sucralfate may prevent stress erosions in intensive care patients, there is almost no evidence that they reduce clinically significant bleeding or mortality

Gastric ulcer

• Consider provoking causes (such as NSAIDs)
• Appropriate endoscopic haemostasis reduces rebleeding and mortality
• Give a PPI (lansoprazole 30 mg, omeprazole 20 mg, pantoprazole 40 mg, rabeprazole 20 mg daily) for 4 weeks once bleeding has stopped, together with H. pylori eradication therapy if endoscopic biopsies confirm infection
• For patients with NSAID-associated ulcers who cannot stop NSAIDs, concomitant PPI therapy (lansoprazole or omeprazole) has replaced misoprostol in healing ulcers and preventing recurrence
• Arrange a repeat endoscopy after 8-12 weeks, to biopsy and take brushings for cytology from the ulcer site
• If surgery is needed for continued bleeding, a Billroth 1 gastrectomy is usually performed. Undersewing with a vagotomy and pyloroplasty is a simpler operation, but the ulcer cannot be examined histologically to exclude cancer. Wedge resection removes the ulcer and has the lowest morbidity in high-risk elderly patients, but long-term acid suppression is then necessary because it does not prevent recurrent ulceration

Duodenal ulcer

• Combine ulcer healing with eradication of H. pylori
• The optimum treatment is triple, or quadruple eradication therapy
• Repeat endoscopy is unnecessary, except in special circumstances (e.g. patients needing warfarin)
• Always confirm that eradication of H. pylori has been successful after an ulcer has bled, preferably by an isotope breath test
• Successful eradication of H. pylori significantly reduces the risk of rebleeding and the risk of bleeding from another ulcer to an extent similar to acid suppression. It is also cheaper in the long term and provides a cure
• Risk of repeat haemorrhage without eradication or maintenance therapy is 20% over 5-10 years, but is higher if associated with NSAIDs
• NSAID-associated ulcers heal with PPIs even if NSAIDs have to be continued, but are not directly associated with H. pylori
• Maintenance acid suppression (lansoprazole 15 mg, omeprazole 10 mg daily) is only indicated for patients at high risk of dying from the complications of recurrent ulcer-ation when eradication therapy has been unsuccessful, or when NSAIDs have to be continued

This is common (up to 20% acute bleeding) and can produce difficult management problems. Possible causes are:

• Lesion missed on endoscopy
• Mucosal lesion healed before patient endoscoped:
• erosions
• Mallory-Weiss tear
• Dieulafoy's lesion (bleeding vessel with no surrounding ulceration, usually high on the greater curve)
• Bleeding from third part of the duodenum, or beyond:
• jejunum (ulcerative jejunitis)
• Meckel's diverticulum
• colon
• Other:
• nose bleed
• rare causes of bleeding

Management

• Reassess the patient—no further action is necessary for low-risk patients
• Repeat endoscopy in patients with a predicted mortality > 10%
• Investigate rare causes of bleeding (recheck coagulation, discuss small bowel radiology, endoscopic retrograde cholangiopancreatography (ERCP), 99Tc sulphur colloid red cell scan or 99Tc pertechnate scan with radiologists)
• Selective angiography during active bleeding (which must be at a rate of 1 U/4 h) is indicated after two negative endoscopies, preferably in a specialist unit
• Small bowel enteroscopy, including video capsule endoscopy may be available in specialist units, but referral is necessary, and other procedures (mesen-teric angiography, small bowel enema) will normally be repeated in the specialist unit
• Laparotomy, careful examination of the whole bowel with a bright light (e.g. sigmoi-doscopy light source) and peroperative endoscopy is the ultimate procedure for recurrent episodes of active bleeding from obscure origin, but may still not identify the source and it is usually wise to refer to a specialist unit if this is contemplated

Aortoenteric fistula

Consider this rare diagnosis in every patient with an aortic graft and gastrointestinal bleeding. Exsanguination at the first bleed is uncommon. Small 'herald' bleeds occur for up to 2 weeks. Urgent abdominal CT scan, the diagnostic procedure of choice, may show haematoma around the graft. Endoscopy, if performed, should be to the fourth part of the duodenum, but surgery should not be delayed if hypotension has occurred. Aggressive surgery is needed as soon as the diagnosis is made, preferably in a specialist unit.
Acute bleeding: lower gastrointestinal tract

Bleeding from the colon is recognised by the passage of fresh red or reddish-brown altered blood per rectum. It is usually readily differentiated from upper gastrointestinal bleeding, because it has neither the smell, nor the tarry-black appearance of melaena. Upper tract bleeding rapid enough to cause red rectal bleeding is uncommon, and invariably associated with haemodynamic disturbance.

Clinical approach

• Resuscitate
• First episode, or recurrent (obscure) bleeding
• Establish the site of bleeding
• Specific treatment

Investigations—first episode

Severe bleeding

• Full blood count, coagulation studies, crossmatch and check electrolytes
• Urgent colonoscopy after full bowel preparation (within 24-48 h) is safe and effective, although some prefer flexible sigmoidoscopy after phosphate enema preparation
• Gastroscopy—particularly in those with haemodynamic disturbance, to exclude brisk upper gastrointestinal haemorrhage
• Mesenteric angiography—if bleeding continues in excess of 1 U/4 h

Slight/moderate bleeding

• Blood tests as above
• Colonoscopy once the bleeding has stopped
• Small bowel enema—better than a follow-through for identifying mucosal lesions
• Video capsule endoscopy
• 99Tc sulphur colloid red scan—care must be taken not to overinterpret the scans, which may indicate the wrong area because blood accumulates in the colonic lumen. Early phase scans are the most helpful in localising the site of bleeding
• 99Tc pertechnate Meckel's scan—at an early stage in young patients, but sensitivity is < 80%
• Angiography—during a subsequent episode of brisk bleeding (1 U/4 h)
• Self-induced rectal trauma is a rare cause of recurrent bleeding

Management

Severe bleeding stops spontaneously in 80% of cases after adequate blood replacement. Treatment of the cause is then needed. In the remainder, bleeding is continuous or recurs, sometimes frequently, over many months. Identifying the site of persistent or recurrent bleeding is one of the most difficult problems in acute gas-troenterology. Once the site is identified, surgical resection is indicated. If the site cannot be found, treatment depends on the pattern of bleeding.

Continuous bleeding

Referral to a specialist unit is advisable if bleeding persists after replacement of 6 units of blood and the source cannot be found. Surgery is an alternative and depends on local expertise. The options are:

• Laparotomy with peroperative colonoscopy after lavage through an appendicostomy. The physician is well advised to attend the laparotomy, but the difficulty of performing colonoscopy in these circumstances should not be underestimated
• Segmental resection if the site can be identified
• 'Blind' hemicolectomy can rarely be justified. If the site cannot be found and surgery is essential to stop bleeding, a subtotal colectomy should be performed

Intermittent bleeding

Referral to a specialist gastroenterology unit is advisable if the site of bleeding cannot be identified after three episodes of bleeding.

Rectal bleeding in children

The differential diagnosis is:

• Intussusception—commonest at 6-12 months
• Meckel's diverticulum
• Ulcerative colitis
• Foreign body
• Juvenile polyps—usually in the descending colon
• Intestinal haemangiomas
• Child (sexual) abuse

Caustic oesophageal injury

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Ingestion of caustic cleaning fluids can cause progressive and devastating injury to the oesophagus and stomach. Most occur as accidents in children under 5 years. Symptoms and the appearance of the pharynx do not correlate with the extent of oesophageal or gastric injury.

Clinical features

• There may be no symptoms initially, but diagnosis is not difficult if an accurate history is obtained
• Identify the specific fluid ingested
• Hoarseness and stridor indicate pharyngeal or laryngeal injury
• Painful dysphagia or haematemesis indicate oesophageal oedema and ulceration. This may occur rapidly or be delayed for several hours
• Respiratory distress and shock occur when mediastinitis develops due to oesophageal necrosis
• Acute symptoms may resolve, to be followed by dysphagia after several weeks or months as scar tissue causes an oesophageal stricture

Investigations

• Chest X-ray—look for mediastinal air or oedema
• Direct laryngoscopy and endoscopy—to record the extent of injury. This should be performed under general anaesthetic, since sedation is unsatisfactory in children anddoes not allow adequate views of the larynx or hypopharynx. Circumferential burns lead to strictures

Management

Resuscitation

• Nil by mouth
• Establish the airway by intubation or tracheostomy if respiratory symptoms or stridor are present
• Intravenous fluids
• Do not give neutralising agents

Minor, non-circumferential burns

• Allow liquids and then a light diet if tolerated
• Arrange psychiatric assessment if ingestion was a suicide attempt

Deep ulcers or circumferential burns

• Remain nil by mouth for 48 h
• Monitor for chest pain or fever, indicating delayed perforation or mediastinitis. If these occur, give intravenous antibiotics, liaise with thoracic surgical colleagues and start nasojejunal feeding
• Allow liquids and a light diet if asymptomatic after 48 h
• Omeprazole 40 mg daily, lansoprazole 30 mg daily, rabeprazole 20 mg daily or equivalent PPI for 4 weeks may reduce the rate of late stricturing, but steroids have no effect

Late complications

• Oesophagogastric strictures occur in about 25%, but almost invariably in those with deep ulcers or circumferential burns
• Review patient after 4 weeks and at 3, 6 and 12 months
• Arrange a barium swallow if dysphagia occurs, before oesophageal dilatation
• Repeated dilatation is frequently necessary. Shortening of the oesophagus may promote gastro-oesophageal reflux, so omeprazole 40 mg daily, lansoprazole 30 mg daily or equivalent PPI is reasonable to reduce restricturing
• Attention to nutrition is vital
• Surgery is indicated if patients cannot tolerate repeated dilatation
• The risk of carcinoma of the oesophagus is substantially increased

Oesophageal rupture

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Sudden chest pain after forceful vomiting is the cardinal symptom when the distal posterior oesophageal wall tears longitudinally in spontaneous perforation (Boerhaave's syndrome). Traumatic perforation after instrumentation or chest injury is more common than spontaneous rupture.

Differential diagnosis

Perforation presents with chest pain, respiratory distress, painful swallowing or subcutaneous emphysema. Early diagnosis is crucial to survival. Failure to consider the possibility is the commonest reason for misdiagnosis.

• Myocardial infarction (ECG, cardiac enzymes)
• Dissecting aneurysm (pulses, chest X-ray, urgent CT scan)
• Perforated peptic ulcer (rigid, silent abdomen, erect chest X-ray)
• Acute pancreatitis (amylase more than fourfold elevated)
• Spontaneous pneumothorax (chest X-ray in expiration)

Investigations

Confirm the diagnosis and site of perforation.

• Chest X-ray—look for mediastinal or subdiaphragmatic gas, or a hydro/pneumo-thorax
• Gastrografin swallow—in spontaneous rupture, tears are usually large and leak contrast; after instrumental rupture, tears are often small and do not leak contrast. Upper oesophageal perforations tend to leak into the mediastinum; mid-oesophageal perforations into the mediastinum and right pleura; and distal oesophageal perforations into the mediastinum, left pleural cavity or abdomen

Management

Oesophageal perforation is a potentially lethal condition. Conservative management is confined to highly specific situations. If the perforation has involved the pleural cavity, or has been contaminated by saliva, gastric contents or food, then surgery is mandatory.

Resuscitation

• Intravenous fluids

• Analgesia—intravenous morphine 2.5-5 mg every hour until pain is relieved, then every 4 h

• Involve thoracic surgical colleagues at an early stage

Spontaneous rupture

• Nil by mouth

• Surgical repair and drainage is almost always needed and should occur within 24 h

• Antibiotics (intravenous metronidazole 500 mg and cefuroxime 750 mg three times daily for 5 days)

• Enteral nutrition through a jejunostomy fashioned at the time of surgery is best Instrumental rupture

• Small tears (with minor symptoms and no leakage of contrast) may be managed conservatively in conjunction with the surgeons. Large tears that leak contrast are managed as for spontaneous rupture

• Nil by mouth

• Nasogastric aspiration for 3 days

• Intravenous fluids

• Antibiotics as above

• Indications for surgery are a persistent fever, or pneumothorax after 48 h

• When perforation complicates palliative treatment of a malignant stricture, patients who are unfit for surgery may be managed by endoscopic insertion of a cuffed oesophageal tube.

Complete oesophageal obstruction: Clinical feature, Prevention, Management, Investigations,

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Bolus obstruction causes sudden, complete dysphagia for solids and liquids, with inability to swallow saliva. Food impacted against a benign or malignant stricture is the usual cause. Occasionally the presentation is delayed for a few days in the mentally handicapped or severely debilitated. The obstruction must be relieved urgently.

Clinical features

Ask about and look for:

• Duration of symptoms preceding obstruction
• Predisposing disease (stricture, carcinoma, Schatzki's ring)
• Triggering factors (steak, toast, fibrous foods, tablets)
• Dehydration
• Weight loss (suggests malignant obstruction)
• Supraclavicular nodes (from a carcinoma of the cardia)
• Complications (aspiration pneumonia, perforation)

Investigations

The endoscopist should be contacted as a priority.

• Full blood count—anaemia suggests carcinoma
• Serum electrolytes—high urea indicates dehydration
• Chest X-ray—look for a mediastinal fluid level (obstruction), absent gastric air bubble (obstruction) or right lower lobe consolidation (aspiration)
• Urgent endoscopy—must be performed by an experienced endoscopist
• A barium swallow risks aspiration and is inappropriate, unless the diagnosis is in doubt. This is not the same as in dysphagia without obstruction.

Management

• Intravenous fluids
• Endoscopic removal of the obstructing bolus

• Endoscopic dilatation can be done immediately after disimpaction

• Carbonated drinks occasionally disimpact fibrous debris, but endoscopy is needed when a food bolus is stuck for a few hours

• Fine-bore nasogastric feeding, or nutritional supplements are needed if dilatation is delayed after removal of the bolus. Endoscopic placement of the tube is awkward, but indicated if it cannot be inserted in the normal way.

• Intravenous metronidazole 500 mg and cefuroxime 750 mg three times daily for 5 days, if aspiration pneumonia is present

Prevention

Simple measures decrease the risk of acute obstruction in patients with oesophageal strictures or prosthetic oesophageal tubes.:

• Avoid fibrous food (apples, oranges), steak and toast

• Wear dentures if edentulous

• Chew all solids well

• Carbonated drinks with meals

• Avoid oral potassium supplements, salicylates and large tablets>

• A proton-pump inhibitor (PPI; e.g. omeprazole 20-40 mg, lansoprazole 30 mg or rabeprazole 20 mg daily) delays or prevents restricturing in most patients and heals associated oesophagitis. PPIs should be continued indefinitely

Swallowed foreign body: Management and Treatment

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Toddlers, the mentally disturbed and the elderly most commonly swallow foreign bod-

ies. If no history is available, look for excessive salivation, regurgitation, choking or dis-

tress. Objects impact in the pharynx, lower end of the oesophagus, or pylorus. Pain or

fever suggests perforation. Once through the pylorus, spontaneous passage is the rule,

but perforation can occur in the ileocaecal region.

All cases

Look in the mouth
If the object is impacted in the fauces, call the ENT surgeon
X-ray the chest and abdomen, but failure to visualise an object does not exclude its presence
Look for surgical emphysema, mediastinal and subdiaphragmatic gas on X-ray
Barium or Gastrografin examination is not indicated and may hinder endoscopy
Address the underlying issues to avoid repeated ingestion, especially in prisonersor the mentally disturbed who may have ingested foreign bodies for individual gain

Bones, pins, glass and batteries

Chest pain suggests perforation, and a small haematemesis may herald perforation of a major vessel. In either case, contact the thoracic surgeon urgently
Sharp objects should be removed by an experienced endoscopist, unless they have passed the duodenum. A plastic sleeve over the endoscope helps prevent trauma during withdrawal. If possible, the endoscopist should practice snaring or grasping a similar object before starting the procedure in order to determine the best means of retrieval
After endoscopic removal, further chest pain may indicate delayed perforation
Batteries, especially small alkaline batteries ingested by toddlers, should be retrieved immediately if in the oesophagus. Corrosive perforation or heavy metal intoxication has been reported. Once in the small intestine, safe passage is the rule

Coins, beads and blunt objects

Almost always pass spontaneously unless more than 5 cm long or 3 cm in diameter
Reassure the patient or parents and advise them to check stools for 3 days
Repeat abdominal X-ray after 36 h if there is doubt about progress. Documented arrest by X-rays for 72 h is an indication for surgical exploration

Body-packing (ingested packets of drugs)

Smuggled packets of drugs may be swallowed, or secreted per rectum
Intact packets can cause intestinal obstruction and if packets do not pass within 72 h, surgical removal is advisable
Endoscopic removal is contraindicated because of the risk of rupturing the bags
Packets may burst spontaneously and cause life-threatening overdose
Heroin overdose causes constricted pupils, bradypnoea or coma. Hypoglycaemia or non-cardiogenic pulmonary oedema may occur later. Give intravenous naloxone 0.8 mg rapidly, to a maximum of 2.4 mg if necessary
Cocaine causes dilated pupils, tachycardia and agitation. Convulsions, metabolic acidosis or coma may occur. Sedate with intravenous midazolam 5–10 mg and give oral propranolol 40 mg three times daily for a few days
Severe overdose of any narcotic is an indication for ventilation and surgical removal of the packets, to stop drug absorption
The doctor’s immediate duty is the treatment of the patient if body-packing is discovered. Once treatment has been initiated, the appropriate authorities should be notified according to local legal regulations
Questioning of the patient must wait until the patient is fit, and be sanctioned by the most responsible physician