Box 16.1 Causes of Collapse with Abdominal Pain

• Acute blood loss from the upper gastrointestinal tract (oesophageal varices and peptic ulceration)
  
• Perforation of a peptic ulcer, sigmoid diverticulum or the appendix
  
• Acute pancreatitis
  
• Leaking aortic aneurysm
  
• Mesenteric infarction
  
• Intra-abdominal sepsis with septic shock
  
• Ruptured ectopic pregnancy
  
• Hypovolaemia from any abdominal cause
  
• Diabetic ketoacidosis
  
• Cardiorespiratory pathology (e.g. myocardial infarction [MI] or pulmonary embolism [PE])

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Further Assessment

Ask About

• Site and speed of onset of the pain
  
• Character and duration of the pain
  
• Exacerbating and relieving factors
  
• Radiation of the pain
  
• Accompanying features such as nausea and vomiting
  
• General health, family and past history, drugs and allergies
  
• Travel abroad.

Think about the patient’s anxieties. If there is a long history, why did the patient choose this moment to present to hospital?

Look For

• Abdominal tenderness and guarding
  
• Rebound tenderness
  
• Rigidity
  
• Bowel sounds
  
• Loin tenderness
  
• Hernias
  
• Perineal signs (→ Boxes 16.2 and 16.3)
  
• Chest disease.

Box 16.2 Rectal Examination

This can provide information about:

• perianal pathology
  
• sphincter tone
  
• the rectal contents (empty, consistency of stool, presence of blood or melaena)
  
• the rectal wall (age >50 years, carcinoma is increasingly common)
  
• pelvic masses or tenderness, including the appendix
  
• the prostate gland

If the presenting symptoms and signs could not be expected to be associated with any of the abnormalities in this list, then there is no indication to undertake a rectal examination.

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Box 16.3 Vaginal Examination

This is a very invasive procedure, particularly in young or nulliparous women. Do not consider undertaking any intimate examination unless you have:

• appropriate training
  
• an experienced chaperone
  
• privacy
  
• the confidence of the patient
  
• reason to believe that the findings of the examination will influence management

Before the examination

• Explain the need for the procedure and what it will entail (including any potential pain or discomfort)
  
• Give the patient an opportunity to ask questions
  
• Obtain the patient’s permission
  
• Give the patient privacy to undress and later on to dress; use sheets to protect the patient’s dignity

During the examination

• Do not make any irrelevant, personal or ambiguous comments
  
• Encourage questions and discussion
  
• Stop if the patient becomes distressed or requests that you terminate the examination

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PAIN AND BLEEDING IN THE OESOPHAGUS AND UPPER ABDOMEN

Oesophageal Pain

Oesophagitis is caused by reflux of gastric contents. It is sometimes associated with a hiatus hernia. The patient is often overweight and experiences burning retrosternal pain on lying flat and bending down. The pain is relieved by antacids and sitting up. Severity of symptoms does not correlate well with endoscopic findings.

Investigations: 

Consider MI → p. 177. A normal ECG does not exclude an MI. A trial of antacids and observation may be helpful.

TX 

Patients in whom MI cannot be excluded must be admitted for observation. However if:

• the history is indicative of oesophagitis
  
• the examination and ECG are normal
  
• the patient responds to antacid

then referral can be made to the GP for further care (weight reduction, small regular meals, stopping smoking, antacids and alginates). A course of a proton pump inhibitor (e.g. omeprazole 20 mg daily for 4 weeks) will give rapid relief of symptoms and promote healing.

Oesophageal Pain and Bleeding after Vomiting

Oesophageal injury may be caused by repeated vomiting, often after excessive alcohol consumption. A small tear of the mucosa may cause bleeding (Mallory–Weiss syndrome, which is usually seen in patients with chronic alcohol problems or after an alcohol ‘binge’). Sometimes this is accompanied by diffuse, intense, retrosternal pain, suggestive of a transmural injury (Boerhaave’s syndrome). Mediastinitis is then a common sequel and may be fatal.

Investigations: 

A plain chest radiograph (CXR) may reveal air in the mediastinum or a foreign body. Radiology after ingestion of contrast medium should be arranged. Oesophagoscopy is hazardous.

TX 

Oral fluids are prohibited and an IV infusion should be commenced. Analgesia and systemic antibiotics are required and the patient should be admitted for observation.

Dyspepsia and Gastritis

Epigastric pain and tenderness are often seen in young adults, especially after alcohol ingestion. Some cases will settle with minimal therapy, whereas others will subsequently prove to result from peptic ulceration. The non-endoscopic diagnosis of gastritis is dependent on the history and the magnitude and duration of the symptoms and signs.

TX 

Most patients with a recent onset of dyspepsia will settle quickly with antacids. However, many GPs will treat undiagnosed dyspepsia in young adults (who have a low risk of gastric malignancy) with a short course of an oral H₂-receptor antagonist. Ranitidine (which can be bought ‘over the counter’ in the UK) is suitable; 150 mg twice daily for a maximum of 14 days should be prescribed. A similar course of a proton pump inhibitor (e.g. omeprazole 20 mg daily) is equally effective. Patients in severe pain will require analgesia and admission for investigation, including barium meal or gastroscopy. The eradication of Helicobacter pylori is now one of the main aims of long-term therapy.

Peptic Ulceration

Dyspeptic pain and tenderness in the epigastrium are the cardinal features of peptic ulceration. Vomiting may also occur, especially with a gastric ulcer. Management depends on the severity and duration of the symptoms and signs. The differentiation between gastric and duodenal ulceration is of little clinical importance in the ED. Gastric carcinoma is associated with profound anorexia, weight loss and anaemia.

There are three other serious acute presentations of peptic ulceration, none of which necessarily follow episodes of dyspepsia:

Gastrointestinal Haemorrhage

The patient with a GI bleed may present with any combination of:

• haematemesis
  
• melaena
  
• passage of bright-red blood per rectum
  
• hypotension, shock and collapse
  
• subacute symptoms (fatigue from anaemia, etc.).

Peptic ulceration is by far the most common cause of serious GI haemorrhage (more than half of all cases) but bleeding may also be seen in:

• gastritis and gastric erosions (e.g. after alcohol or non-steroidal anti-inflammatory drugs [NSAIDs])
  
• oesophagitis
  
• Mallory–Weiss syndrome (oesophageal tear after vomiting) → above
  
• oesophageal or gastric varices → p. 305
  
• diverticulitis (copious melaena or bright red blood)
  
• neoplastic and clotting disorders (variable presentations)
  
• minor conditions of the rectum (e.g. piles → p. 326).

Severe bleeding from the small intestine is rare.

Box 16.4 Patients Most Likely to Die from Upper GI Bleeding

• Age >60 years
  
• Serious concomitant disease
  
• Systolic BP <90 mmHg on admission
  
• Hb <10 g/dL on admission
  
• Evidence of re-bleeding

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TX 

• Protect the airway and give oxygen.
  
• Start immediate volume replacement via two large-bore cannuli. Central venous access may be required. Management of major haemorrhage → Figure 1.2 on p. 8.
  
• Monitor vital functions.
  
• Discuss the patient with the admitting teams (usually both medical and surgical liaison is appropriate).
  
• Take blood for cross-matching (6 units), clotting screen, full blood count (FBC), glucose, urea and electrolytes (U&Es), and liver function tests (LFTs).
  
• Obtain a CXR and an ECG.
  
• Catheterise the bladder and monitor the urine output.
  
• Correct clotting abnormalities (vitamin K₁ or K₂, prothrombin complex concentrate [PCC] or fresh frozen plasma [FFP] → p. 258). Consider acquired haemophilia → p. 257.
  
• In suspected gastroduodenal bleeding, consider an IV infusion of omeprazole (40 mg diluted to 100 mL and given over 20–30 min), although this has not been shown to be effective.

Endoscopic assessment (which should be performed within 24 h of admission) usually precedes any decision to operate and may be life-saving in very severe bleeds.

Variceal Haemorrhage

Haemorrhage from oesophageal (or gastric) varices is a devastating complication of portal hyper­tension that usually occurs in patients with chronic liver disease. The mortality rate is between 33 and 50%. Raised pressure in the portal vein usually develops as a consequence of increased intrahe­patic vascular resistance and increased blood flow through the portal system. Venous collaterals enlarge, in an attempt to decompress the portal system. These varices occur mainly at the portosystemic anasto­moses in the gastro-oesophageal junction and the rectum. Posthepatic causes of portal hypertension include the Budd–Chiari syndrome (hepatic venous obstruction) and constrictive pericarditis.

The diagnosis should be suspected in patients with haematemesis or melaena who have signs of liver disease or a history of alcohol abuse. Unexplained thrombocytopenia may be due to portal hypertension.

TX 

The treatment is that detailed above for GI bleeding with special attention to the inevitable coagulopathy and thrombocytopenia. Management of major haemorrhage → Figure 1.2 on p. 8. Fluid repletion should be cautious, avoiding hypertension and transfusing to a haemoglobin of between 7 and 9 g/dL (over-transfusion increases portal venous pressure). There is no evidence that saline infusions are harmful in the presence of peripheral oedema or ascites. Prophylactic broad-spectrum antibiotics have been shown to reduce mortality (e.g. IV piperacillin with tazobactam or ciprofloxacin). Intensivists and GI specialists should be involved as soon as possible.

Vasoactive drug therapy controls bleeding by reducing portal venous pressure. This is achieved by vasoconstriction of the splanchnic bed, which reduces the blood flow into the portal circulation. Several drugs are used:

• Vasopressin (20 U IV over 15 min) induces vasoconstriction in almost all vascular beds. This causes inevitable side effects including myocardial and cerebral ischaemia. For this reason, nitrates are usually administered concurrently. However, the use of vasopressin has been largely superseded by terlipressin.
  
• Terlipressin (2 mg IV) is a synthetic analogue of vasopressin. It is a prodrug with a slower onset of action, a longer half-life and fewer side effects than the parent drug. It is still contraindicated in the presence of severe coronary heart disease, peripheral vascular disease or pregnancy.
  
• Somatostatin (250 mcg IV bolus followed by an infusion of 250 mcg/h) induces vasoconstriction in the splanchnic vascular bed. It is seldom used in the UK.
  
• Octreotide (50 mcg IV bolus followed by an infusion of 50 mcg/h) is an analogue of somatostatin. It is useful for patients who have contraindications to terlipressin.

Placement of a Sengstaken–Blakemore tube may be required as a temporising measure in continuing severe haemorrhage and is effective in up to 90% of patients. This device has two balloons and two aspiration ports (gastric and oesophageal in both cases). Inflation (with around 200 mL of air) and gentle traction on the gastric balloon alone is usu­ally adequate to control bleeding. (The oesophageal balloon may cause damage, especially post-sclerotherapy.) However, if fresh blood continues to be aspirated from the oesophageal port, then the oesophageal balloon may be inflated to a pressure of 40 mmHg. Variceal tamponade with a Sengstaken–Blakemore tube is most appropriate and safest for patients under general anaesthesia with airway protection.

There are several ways of stopping variceal bleeding more definitively:

• Endoscopy (preferably under general anaesthetic [GA]) should take place within 12 h of the onset of bleeding or much sooner in severe cases. Variceal band ligation may be performed to achieve haemostasis. Injection sclerotherapy (with ethanolamine) is an alternative for oesophageal varices. Gastric varices (present in 20% of patients) are usually injected with cyanoacrylate glue or thrombin.
  
• An intrahepatic portosystemic shunt can be inserted via the transjugular route by an interventional radiologist. This decompresses the portal vein by creating an artificial shunt through the liver.
  
• Surgical interventions include oesophageal transection or creation of a splenorenal shunt.

Pyloric Stenosis

In adults, pyloric stenosis is usually associated with a chronic ulcer history but there is often no recent pain. It presents with episodic projectile vomiting, unrelated to eating. Examination reveals undernourishment and a ‘succussion splash’ emanating from the full stomach. Hypochloraemia, hypocalcaemia and metabolic alkalosis are common. Initial management is directed at the correction of the dehydration and the electrolyte disturbance. The stomach should be emptied by a wide-bore oral tube before endoscopic assessment.

Hepatitis

Hepatitis is caused by the following:

• Viruses with an enteric mode of transmission (hepatitis A and E) → below
  
• Viruses with a parenteral mode of transmission (hepatitis B, C and D) (immunisation against hepatitis B → p. 404)
  
• Weil’s disease (leptospirosis) → below
  
• Drugs.

Leptospirosis or Weil’s Disease: 

this occurs after mucosal contact with water that has been infected by rats’ urine. It is sometimes fatal and should always be considered when a pyrexia and abdominal pain is found in:

• sewage workers
  
• farmers
  
• water board workers
  
• people who have been swimming in fresh water
  
• people who have been sleeping rough.

After an incubation period of about 10 days (range 4–21 days), there is a rapid onset of fever, headache, and limb and back pain. Jaundice occurs in 75% of cases with a purpuric rash and albuminuria.

Infectious Hepatitis: 

hepatitis A is by far the most common cause of hepatitis. Transmission is by the faecal–oral route and the incubation period is 6 days to 6 weeks. Outbreaks may occur in primary schools and in other institutions.

Hepatitis causes a variable degree of:

• anorexia and malaise
  
• nausea and vomiting
  
• abdominal pain and right upper quadrant tenderness
  
• jaundice
  
• dark urine and pale stools
  
• pyrexia
  
• urticaria
  
• hepatomegaly and splenomegaly.

Investigations: 

There is bilirubin and urobilinogen in the urine.

TX 

Admission is required for patients who:

• are significantly jaundiced
  
• are clearly very unwell
  
• have an uncertain diagnosis.

Those with hepatitis A (young, short duration of symptoms and limited signs) can be treated at home and followed up by the GP. Strict hygiene must be observed with a light diet and no alcohol.

Biliary Disease

Biliary pain is usually associated with gallstones, is inevitably recurrent and may be precipitated by a fatty meal, often eaten some hours previously. The classic description of sufferers – female, forty, fat and fertile – is unflattering but, unfortunately, evidence based!

Biliary Colic: 

this is caused by the passage of a gallstone through the bile ducts and presents as sudden, constant (not colicky), epigastric and right hypochrondrial pain radiating to the back. There is tenderness in the right upper quadrant; nausea and vomiting are common. Symptoms may be transitory or last for several hours, with the pain disappearing as suddenly as it started. Impaction of a stone in the common bile duct is unusual but associated with more prolonged symptoms and the gradual appearance of obstructive jaundice. Prolonged obstruction of the cystic duct leads to acute cholecystitis.

Acute Cholecystitis: 

acute inflammation of the gallbladder with or without intermittent obstruction at its neck causes:

• constant right upper quadrant pain, referred to the back
  
• localised tenderness
  
• nausea and vomiting
  
• fever and malaise
  
• a palpable gallbladder with a positive Murphy’s sign (sometimes).

The condition is differentiated from biliary colic by its less abrupt onset, longer duration, more profuse vomiting and the presence of a fever. (In more chronic cases, dyspepsia may be the presenting symptom. Pain is worse after a large, fat-laden meal, and heartburn and belching are common. If these are the only symptoms, then further investigation can be pursued on an outpatient basis.) Rarely, in elderly or diabetic patients, perforation of the gallbladder may occur with subsequent biliary peritonitis.

Cholangitis: 

infection of the biliary ducts is usually seen in elderly patients and is characterised by upper abdominal pain, fever and the develop­ment of obstructive jaundice (Charcot’s triad). Hy­­potension and other signs of severe sepsis are common. Suppuration may lead to hepatic abscesses. Escherichia coli is the most common pathogen. The mortality rate is high (33%).

Investigations: 

Early ultrasound examination visualises the gallstones and the swollen gallbladder and/or bile ducts. Abdominal radiographs may show air in the biliary tree in cholangitis. Inflammatory markers (white cell count [WCC] and C-reactive protein [CRP]) may be raised in acute cholecys­titis and cholangitis, although 50% of patients with infection of the biliary ducts have a normal or reduced WCC. The plasma amylase may be mildly raised.

TX 

Analgesia, IV fluids and admission are required. In the presence of a fever, antibiotics (a cephalosporin, ciprofloxacin or gentamicin) should be prescribed. Patients with cholangitis may have severe sepsis (→ p. 260) and IV piperacillin with tazobactam is appropriate antibacterial therapy.

Pancreatitis

The main predisposing factors are:

• chronic biliary disease (the most common cause in women)
  
• excess alcohol consumption (the usual cause in men).

The pain may begin suddenly but is then constant and very severe. It is accompanied by vomiting and may be relieved by sitting forward. The pain differs from that associated with perforation of a peptic ulcer in that it radiates to the back and extends from the epigastrium bilaterally. There is epigastric tenderness and guarding and decreased bowel sounds (due to ileus). Pyrexia is uncommon but tachycardia is usual. In severe cases the BP falls, cyanosis may be present and the patient is brought in as a ‘collapse’.

Investigations: 

• A serum amylase >1200 IU/mL is considered diagnostic. Lower levels may be caused by other abdominal conditions or by an MI.
  
• The sodium, potassium and calcium are usually low.
  
• The plasma WCC is invariably raised.
  
• The serum bilirubin may be raised.
  
• There may be hypoxia and an effusion on CXR.
  
• ECG may show non-specific abnormalities.

TX 

Initial treatment is nil by mouth, nasogastric aspiration, IV fluids and antibiotics. Analgesia must be given. The patient may require intensive care and laparotomy for peritoneal toilet.

PAIN AND BLEEDING IN THE CENTRAL AND LOWER ABDOMEN

Peritonitis

Generalised peritonitis usually occurs secondary to a perforated viscus following:

• peptic ulceration
  
• appendicitis
  
• diverticular disease
  
• neoplastic or inflammatory bowel disease
  
• trauma
  
• iatrogenic injury.

It causes:

• severe abdominal pain
  
• a rigid (board-like) abdomen
  
• hypotension and shock.

The pain of perforation begins suddenly. After a few minutes, its severity is reduced but the abdomen remains rigid, especially the epigastrium. The pulse is elevated and the patient is pale and anxious but not initially ‘shocked’. Rigidity and pain may decrease after a few hours but bowel sounds remain absent. Symptoms increase again after around 6 h as bacterial peritonitis develops. Vomiting may occur. The patient is often elderly or has a recent history of NSAID ingestion.

Investigations: 

An erect CXR will show gas under the diaphragm in many (but certainly not all) cases. A CT scan of the abdomen is helpful, before laparotomy, to elucidate the cause of the peritonitis.

TX 

Vigorous fluid resuscitation, analgesia and surgical referral are required. Antibiotics may be given: piperacillin with tazobactam (or a cephalosporin and metronidazole) are reasonable first-line choices.

Leaking Abdominal Aortic Aneurysm

Leaking aortic aneurysm is most often seen in an older (>55 years) patient who has generalised vascular disease. Symptoms and signs are variable but include the following:

• Back pain (sometimes with a previous episode a few days before)
  
• Generalised abdominal pain with vague tenderness and fullness (pain may radiate to the groin)
  
• Hypotension
  
• Pallor and sweating
  
• Sudden collapse.

Classic features are often absent; an expansile, pulsatile mass may not be detected and the femoral pulses may be present and not delayed with respect to the radial ones. Pain may not be severe.