Local gastrointestinal causes include acute gastritis and gastroenteritis (especially staphylococcal food poisoning), liver inflammation and cholecystitis.

Migraine is commonly accompanied by vomiting. Other more worrying causes of headache – meningitis, increased intracranial pressure and subarachnoid haemorrhage – are also associated with vomiting, so the symptom itself is of little diagnostic help in this setting. In these situations, other features such as a skin rash or stroke-like symptoms help to clarify the underlying diagnosis.

Vomiting is an important feature that distinguishes the pain of a myocardial infarction from that of angina and is often accompanied by nausea and sweating. In the elderly patient, vomiting may be the only symptom of a myocardial infarction.

Vomiting can be the only symptom of hidden infection, even of frank septicaemia, particularly in the elderly or immunocompromised patient. This is particularly the case in infections in the kidneys and lower urinary tract.

Acute gastric dilatation is important because it is an easily preventable cause of sudden death. In this condition, gross gastric distension leads to upper abdominal swelling associated with nausea, often accompanied by hiccups and belching. These patients are often already unwell and a common outcome is sudden vomiting, aspiration and cardiorespiratory arrest. Factors that can trigger acute gastric dilatation include electrolyte disturbance, bacterial toxins and, most commonly, DKA. Treatment is simple – anticipate the possibility (in DKA, in severe infection and in any critically ill patient), recognise the condition, and prevent aspiration by decompressing the stomach with a nasogastric tube.

Duodenal and gastric ulcers are the causes in half of all cases of acute upper gastrointestinal bleeding. Most ulcers (eight out of ten) stop bleeding of their own accord; the remainder need intervention at endoscopy (injection of the ulcer base with adrenaline (epinephrine)/coagulation with a heat probe or laser/clipping), in the radiology department (embolisation), or possibly by surgery. After a bleed patients require a three week ulcer-healing course of lanzoprazole or omeprazole followed, if the patient has to re-start on NSAIDS or aspirin, by maintenance therapy.

About 60–70% of all gastric ulcers and 80% or more of all duodenal ulcers are caused by H. pylori infection within the stomach (most of the remainder are associated with use of NSAIDs). Eradication of the infection speeds ulcer healing and, of importance to the Acute Medical Unit, if the ulcer has bled, eradication lessens the risk of re-bleeding. Eradication therapy is simple – a week of ampicillin, omeprazole and clarithromycin – and should be started once the patient returns from endoscopy if the patient has a duodenal ulcer and tests on the endoscopic specimens are H. pylori positive. This aspect of management is frequently neglected. The situation with bleeding gastric ulcers is more controversial and in most cases re-endoscopy is advisable 6 weeks after the initial bleed, at which time tests for H. pylori can be performed and eradication therapy given if necessary.

Acute gastric and duodenal erosions are common in patients taking NSAIDs and aspirin. Although they can cause massive blood loss, the bleeding will stop provided the patient survives the initial event. The two major issues are adequate resuscitation and ensuring that the blood loss is not arising from a more serious source such as a chronic ulcer or varices.

Acute oesophageal mucosal tears can be diagnosed from the history: patients retch and vomit several times before noticing that one of their vomits contains a varying amount of fresh blood. The patients are usually young, and acute alcohol intake is often involved. The bleeding can be heavy and the patients can be very alarmed. The outlook is almost universally excellent, with the bleeding stopping of its own accord and the tear healing completely within 24h.

Less common, but more frightening for everyone concerned, oesophageal varices account for around 10% of acute bleeds. Blood loss can be massive and can itself result in death, but more commonly it triggers acute liver failure – in patients whose livers are already performing badly. Varices need active intervention to stop them bleeding and to reduce the risk of a re-bleed. Overall death rates are high, up to 30%. Fortunately, there have been important improvements in the field using endoscopic (injection sclerotherapy and banding) and radiological (transjugular intrahepatic portosystemic anastomosis) techniques. It is to the general relief of many that the Sengstaken tube is now making progressively fewer appearances on the medical ward.

Gastric and oesophageal cancer occur in older patients, and the bleeding is often preceded by a history of weight loss, anorexia and, in the case of oesophageal cancer, swallowing difficulty.

This rare cause of massive bleeding is due to erosion of a congenitally abnormal artery in the lining of the stomach. Emergency surgery is often required.

The consciousness level may be impaired, either as part of shock (poor cerebral blood supply) or because the bleeding has occurred in a patient with liver disease and has triggered liver failure. However, unless the bleeding has taken place, say, as a stress reaction to an acute stroke, the airway is unlikely to be at risk.

Administer high-flow oxygen immediately if the patient is hypotensive or has a pulse over 100 beats/min – on the assumption there has been a major bleed. Monitor the oxygen saturations to assess the response.

Check the patient for any pain: severe abdominal pain is unusual in upper gastrointestinal bleeding and needs urgent medical assessment. In the elderly, blood loss can readily trigger an anginal attack or even cause myocardial infarction.

Anticipate that large-bore i.v. cannulae (e.g. grey Venflons®) will be inserted into both arms and that either immediate saline or polygeline (Haemaccel®) may be needed. If there is haemodynamic disturbance (e.g. pulse 110 beats/min, systolic blood pressure 100mmHg, respiratory rate 30 breaths/min), it would be appropriate to give 2L of isotonic saline rapidly and then, if there is no improvement, consider polygeline (Haemaccel®), as at least 20% of the blood volume will have been lost.

Young patients with minor gastrointestinal bleeding in whom there is no change in pulse or blood pressure can be safely discharged and do not require endoscopy. Most other patients with gastrointestinal bleeding can safely be endoscoped on the next available endoscopy list. Indeed, the risks of emergency endoscopy in an inadequately resuscitated patient in the middle of the night can outweigh the potential advantage. However, urgent endoscopy to establish the site of blood loss, assess the risk of re-bleeding and attempt endoscopic haemostasis is required:

The history is invaluable in assessing blood loss:

The examination adds supporting evidence to the history. However, the patient’s age will influence the signs – a young person can lose 500ml or more of blood before any of the observations change, but a similar loss in an elderly person would have a major impact. The patient with major bleeding characteristically:

• is pale and clammy

• has a tachycardia of more than 100 beats/min

• has a systolic blood pressure of less than 100mmHg

• shows postural hypotension, with a 20+ mmHg fall in the systolic pressure on sitting

Age – is the patient over 60 years of age? The mortality rate in upper gastrointestinal bleeding is 20 times higher in the elderly than in the young:

Amount – small, moderate or large? The initial assessment of pulse, blood pressure and direct observation should be interpreted in combination with the results from the endoscopy. Clearly, the finding of ‘a spurting arterial bleed from the base of a chronic gastric ulcer’ is much more significant than ‘no visible blood in the stomach or duodenum’.

Is there another complicating condition present? The three most important diseases that will influence the chances of recovery are:

Is there an underlying malignancy? This may be the direct source of the bleeding, or the bleeding may be from stress ulceration caused indirectly by a malignancy elsewhere. Upper gastrointestinal bleeding is quite a common problem in terminal malignant disease.

The Rockall Score is used to distinguish between those patients who can be discharged early without endoscopy and those in whom, without emergency intervention, there is a high risk of re-bleeding and death. Patients are scored before and after endoscopy (→Table 5.1).

When the pre-endoscopy score is 0 it is generally safe to discharge the patient early without urgent endoscopy – a higher score requires early endoscopy. A full (post-endoscopy) score of <3 indicates a low risk of re-bleeding or death and these patients can be considered for accelerated discharge.

There are several endoscopic features that predict a high risk of re-bleeding:

Features that indicate re-bleeding are fresh haematemesis or melaena associated with disturbed haemodynamics – a pulse rate over 100 beats/min, a systolic pressure less than 100mmHg, a fall in CVP more than 5cmH₂O or a fall in haemoglobin of more than 2g in 24h. Depending on the underlying diagnosis, patients who re-bleed will need further endoscopic procedures and, if these are unsuccessful, a second re-bleed will almost certainly lead to emergency surgery. Reliable, well-charted observations are critical in the close monitoring of these patients during the first 48h of their admission. The pulse rate is the single most useful measurement, as it is the first to change if the patient re-bleeds (or remains high if bleeding does not stop in the first place). The drop in blood pressure lags behind the increase in pulse rate, although a postural decrease also provides a useful early warning. Halfhourly observations are needed in the first 4h after an acute bleed.

In major bleeds, the CVP provides the most reliable guide to re-bleeding, because it falls before there is any increase in the pulse rate. It is invaluable in the elderly in whom the risks are high and other factors such as betablocker therapy and cardiac arrhythmias render the pulse rate unreliable as a sign of blood loss (→Case Study 5.2).

The patient described in Case Study 5.1 is typical of the type of patient who is commonly admitted to the acute medical wards. He was at high risk because of:

Many personnel were involved, and the patient needed extremely close monitoring. Characteristically, there was uncertainty over the indications and timing of surgery – in circumstances in which a clear management plan from the outset is a fundamental requirement. An early, combined and well-documented consultation between the physicians, surgeons and nursing staff is invaluable in cases such as this, in which the risks of major complications can be anticipated from the moment the patient is first seen.

While difficult management decisions are being considered, it is also critical that the nurse is focused on the immediate condition of the patient:

Intensive monitoring and urgent investigative procedures are likely to lead to disorientation and distress in these elderly patients. Constant reassurance is needed, combined with careful explanations of the various interventions and staff that the patient is suddenly encountering. It will be a great comfort to the patient to be able to identify at least one familiar face among the frenetic activity of the first 12–24h. Patients with significant blood loss are extremely weak and debilitated. If there is frequent melaena, the effort of calling for, and using, a commode at short notice will be exhausting (and often extremely embarrassing) for the patient. Nursing staff have to be readily available to assist the patient and to deal with the distress of melaena or haematemesis with sensitivity and professionalism.

High dose i.v. proton pump inhibitors pantoprazole/omeprazole 80mg stat and 8mg per hour for 72 hours are only used in patients who have had a major bleed from a peptic ulcer. Treatment is started after the patient has returned from endoscopic haemostatic therapy.

Case Study 5.3 illustrates how poor communication can affect a patient’s treatment. This was a very high-risk case due to the bleeding source, the age of the patient and the pre-existing health of the patient. There was good early liaison with the surgeons, but the problems arose because of the quality of the communication. An issue as simple as the orientation of an endoscope photograph had serious consequences and underlines the enormous value of effective communication. In this case, it would have been invaluable to have had a senior member of the surgical team present at the endoscopy.

The nurse is in an ideal position to facilitate the liaison between surgeons and physicians.

The combination of poor liver function and portosystemic shunting means that toxic substances from the gut, in particular ammonia, are either dealt with ineffectively by the liver or bypass it altogether. The result is a toxic encephalopathy with impairment of the consciousness level that can progress rapidly from confusion and agitation to deep coma. When it does, the patient has usually developed cerebral oedema and requires intensive care, preferably in a specialist liver unit. It is useful to assess and follow changes in the hepatic encephalopathy using a standard scoring system (→Box 5.2).

Patients in acute liver failure are at great risk from upper gastrointestinal bleeding due to the combination of varices and impaired clotting. Not only will this cause cardiovascular instability, but blood in the gut provides a source of toxins that can worsen hepatic encephalopathy.

The main problems are hypoglycaemia and renal failure. Hypoglycaemia is important because it will contribute to confusion and can be readily corrected. Patients in liver failure who develop renal failure do particularly badly. At presentation, these patients are often hypovolaemic: careful early fluid replacement (monitored with a CVP line) can improve their renal function. Hypotension unresponsive to fluid replacement will require inotropic support and possibly corticosteroids.

Hepatic encephalopathy is managed according to its severity and its mode of onset. Acute liver failure with grade 3 or grade 4 encephalopathy (confusion or coma) is usually associated with cerebral oedema. The patient needs to be sedated, paralysed and ventilated, as agitation and restlessness increase intracranial pressure. Intravenous mannitol (0.5mg/kg) can be used in the emergency situation to reduce cerebral oedema. Acute on chronic liver failure with encephalopathy (such as may occur in decompensating alcoholic liver disease) can be treated less aggressively: the intake of protein, the main source of ammonia, is reduced and the bowel is cleared using lactulose, which reduces production of ammonia in the bowel and also empties it through its action as a laxative. The dose of lactulose is adjusted until there are between two and four soft stools per day. Oral neomycin, which sterilises the bowel of all ammonia-producing gut bacteria, can also be used.

Bleeding can be minimised by correction of any clotting abnormality. The safest way to monitor bleeding and fluid replacement in the unstable phase is to use a central venous pressure line. There is a fine line between underand over-transfusion in these patients, with the constant risk of pulmonary oedema (particularly when saline is infused) to be balanced against the deleterious effects of under-transfusion on kidney function.

Hypoglycaemia must be avoided by hourly checks on the BM stix and the appropriate use of i.v. 10% or 20% dextrose. Patients with acute on chronic liver disease have often been on diuretics for ascites and may have acutely low potassium levels that need to be corrected. Patients with acute liver failure are ‘hypermetabolic’ – burning up calories and protein – so nasogastric feeding must be considered early. If there is an excessive gastric aspirate it can be reduced using maxalon and clarithromycin (acting as pro-kinetic drugs to aid gastric emptying).

Gallstones usually present with biliary colic – severe upper abdominal pain going through into the back. If they become wedged in the bile ducts there is a risk of infection, either confined to the gall bladder (acute cholecystitis), or spreading up the bile ducts to the liver (ascending cholangitis; →Case Study 5.7). In these situations there is pain, but also signs of sepsis (fever, high white cell count) and, with spreading infection, abnormal liver function tests. Nursing management is focused on assessing the patient’s progress and ensuring that while investigations are in progress there is adequate pain relief. An overall deterioration, continuing or worsening pain and fever that fails to respond to i.v. antibiotics indicate a need for intervention, either by endoscopic attempts to remove the impacted stones (ERCP with sphincterotomy) or a direct surgical approach.

At all times the nurse should ensure the safety of the patient: ABCDE.

To protect staff and patients, infection control must always be instituted in cases of acute diarrhoea until stool cultures are available. Most cases are selflimiting, provided that attention is paid to correct fluid balance. This is particularly the case with the viral diarrhoeas: SRSV and rotavirus. Patients who are most at risk are the elderly and frail. The principle of treatment is to correct fluid deficit and keep up with the loss of fluid in the stool and vomit (→Case Study 5.13). It follows therefore that the fluid balance and stool charts must be accurate. By its nature, diarrhoea will impair the accurate collection and measurement of urine, but the combined volume of stool and urine in a commode or bedpan can be estimated relatively easily. It is critical to keep a reliable stool chart.

Antibiotics are rarely needed unless there are signs of complications:

Ciprofloxacin is the drug of choice except for C. difficile, for which treatment is usually oral vancomycin or metronidazole.

These minimise spread: a single room with an en-suite commode, staff wearing gloves and apron who wash their hands with soap and water (not gel) before entering and before leaving (putting their gloves and aprons in a bin within the patient’s room), liquid soap and disposable wipes for the patient.

Hepatic congestion with stretching of the capsule that surrounds the liver leads to right-sided abdominal pain below the ribs, anorexia and nausea. In extreme cardiac failure the liver can fail, with the development of jaundice and grossly abnormal liver function tests.

Rupture of an aortic aneurysm leads to acute severe abdominal pain and circulatory collapse. Immediate surgical intervention can be life-saving.

Common gastrointestinal-related drug side-effects are warfarin-induced upper gastrointestinal bleeding and the clinical features of digoxin toxicity: nausea, vomiting and anorexia.

Extreme anorexia and weight loss are recognised features of advanced cardiac disease, particularly progressive congestive cardiac failure due to chronic valvular disease. This can be sufficient to mimic the development of a gastrointestinal malignancy, particularly when associated with other gastric symptoms such as abdominal distension (ascites) and the pain from liver congestion.

The pain from diaphragmatic pleurisy can be referred to the upper abdomen and can be confused with biliary colic or peptic ulceration. The clue is that there are usually associated features of pneumonia (cough, breathlessness and fever), and the pain is much worse on inspiration.

Right-sided heart failure in COPD can give rise to hepatic congestion and right upper quadrant pain. In patients with COPD, particularly those who are acutely short of breath, there is often also upper abdominal discomfort, arising from the ribs and diaphragm, that appears to be associated with the extra respiratory effort that these patients have to make.

Patients on long-term oral steroids – chronic asthmatics and those with severe COPD – are prone to gastritis and peptic ulceration. More importantly, as they age these patients are also liable to osteoporotic collapse of their thoracic and lumbar vertebrae. This presents with pain spreading like a girdle from the back around to the front of the abdomen. The pain can be severe and can be confused with an acute abdominal crisis.