Position of pain	Nature or type of pain
Generalised Localised, e.g.: • epigastric; • right upper quadrant; • central (periumbilical); • right iliac fossa; • left iliac fossa; • lower abdominal (hypogastric).

Constant
Peritoneal
Colicky

Clinical evaluation is performed with the knowledge that many of the patients who present with acute abdominal pain have a short-term, self-limiting illness for which nothing more than symptomatic and supportive treatment is required. Selection bias results in this proportion being small in patients admitted to hospital, larger in patients presenting to emergency units and largest in general practice. A list of causes of non-trauma-related abdominal pain seen in an English hospital is shown in Table 4.2.

Table 4.2 Causes of abdominal pain seen at a hospital emergency unit

Cause	Percentage
Non-specific abdominal pain	34
Acute appendicitis	28
Acute cholecystitis	10
Small bowel obstruction	4
Acute gynaecological disease	4
Acute pancreatitis	3
Renal colic	3
Perforated peptic ulcer	2
Cancer	2
Diverticular disease	1
Miscellaneous	9

From de Dombal FT. Diagnosis of acute abdominal pain. 2nd edn. Edinburgh: Churchill Livingstone; 1991, with permission.

Clinical features are discussed under specific categories later in this chapter. It is important to consider that abdominal signs may be diminished or absent in patients with particular comorbidities. These would include patients with diabetes or who are immunosuppressed. Immunosuppressed patients include those on long-term steroids or other immunosuppressive medication, patients on chemotherapy or those with some specific haematological disorders, including AIDS.

Radiological investigations are frequently used to augment clinical assessment and, increasingly, Computed tomography (CT) scanning is the investigation of choice for the investigation of acute abdominal pain. Provided the patient has normal renal function, the abdominal CT scan to assess acute abdominal pain should have intravenous (IV) contrast and be done in the precontrast, arterial and venous phases to provide the most information. Oral contrast should also be administered in order to outline the gastrointestinal tract, unless there is a specific contraindication, such as severe vomiting.

Generalised Abdominal Pain

The common causes of generalised acute abdominal pain are listed in Table 4.3. The first issue to address is whether or not the patient has an abdominal catastrophe. On most occasions, differentiation of a patient with an abdominal catastrophe from one with non-specific abdominal pain is relatively straightforward. As indicated in Table 4.3, the patient with an abdominal catastrophe usually has generalised peritonitis, with generalised tenderness, guarding, rebound tenderness and absence of bowel sounds. However, there may be few signs initially to accompany a mesenteric embolus or thrombosis while the bowel is still viable. Further, the abdominal signs associated with acute pancreatitis may be mild.

Table 4.3 Causes and clinical features of conditions producing generalised acute abdominal pain

Cause	Abdominal signs	Associated signs
Non-specific abdominal pain	Nil or mild	Nil
Perforated appendix	Generalised peritonitis, more tender in the right iliac fossa	± shock
Perforated diverticulum	Generalised peritonitis, possibly more tender in the left iliac fossa	± shock
Ruptured ectopic pregnancy	Generalised peritonitis	± shock
Ruptured pathological solid organ	± mass/organomegaly	± shock
Ruptured aortic aneurysm	Tender pulsatile mass	Shock
Strangulated bowel	Focal or generalised peritonitis	Bowel obstruction ± sepsis ± shock
Superior mesenteric thrombosis or embolus	Initially few or no signs (pain out of proportion to signs)	Atrial fibrillation or myocardial infarction ± shock
Ischaemic colitis	Often not severe unless there is transmural infarction	Bloody diarrhoea, atrial fibrillation or myocardial infarction
Pancreatitis	May be few signs (pain can be out of proportion to signs)	± shock

There are commonly signs of shock if there has been blood loss or dehydration. These include tachycardia, hypotension, oliguria and peripheral vasoconstriction (cool blue peripheral tissues and a thready pulse). Pallor may be indicative of blood loss. Dehydration is suggested by a dry tongue, reduced skin turgor, decreased eye turgor and postural hypotension. The signs of gram-negative shock are slightly different. Rather than the signs of peripheral vasoconstriction there may be peripheral vasodilatation, evidenced by a bounding pulse and a warm periphery as well as clamminess.

The previous history and associated signs that may be of help in distinguishing the various catastrophes are listed in Table 4.4.

Table 4.4 Clinical clues to establish the cause of the abdominal catastrophe

Abdominal catastrophe	Previous history	Possible differentiating signs
Perforated peptic ulcer	Dyspepsia or proven peptic ulcer	Lack of liver dullness to percussion Signs maximal in the epigastrium

Perforated appendix Initial history consistent with appendicitis

Signs maximal in the right iliac fossa

Perforated diverticulum Preceding history of diverticular disease

Lack of liver dullness to percussion

Signs maximal in the left iliac fossa

Ruptured aneurysm Recent backache
Other history of vascular disease Tender pulsatile midabdominal mass
Vascular disease elsewhere Ruptured ectopic pregnancy Missed period

Signs maximal in the lower abdomen

Tender pelvic mass on per vagina examination

Ruptured pathological organ Organ specific Organ specific Strangulated bowel Hernia
Previous abdominal surgery Tender hernia
Abdominal scars Mesenteric thrombosis or embolus Atrial fibrillation
Myocardial infarction
Other vascular disease Vascular disease elsewhere Ischaemic colitis Other vascular disease
Recent period of low cardiac output
Irritable bowel syndrome symptoms Bloody diarrhoea
Signs maximal on the left side Acute pancreatitis Alcoholic binges
Gallstones Periumbilical or renal angle blood staining of subcutaneous fat

The management of an abdominal catastrophe includes urgent admission to hospital, cardiopulmonary resuscitation, some simple investigations depending on the gravity of the situation and early operative intervention on most occasions. Conditions for which early operative intervention might not be undertaken include ischaemic colitis and acute pancreatitis.

The investigations that are usually performed are listed in Table 4.5. They include tests aimed at establishing the diagnosis and tests to assist resuscitation. Air under the diaphragm suggests a perforated viscus. It is most commonly present with a perforated peptic ulcer (80% of cases), less commonly present with a perforated diverticulum (20%) and rarely present with a perforated appendix. An amylase and lipase estimation is essential in all patients with generalised abdominal pain to avoid an inadvertent laparotomy for acute pancreatitis.

Table 4.5 Investigations for patients with acute generalised abdominal pain

Investigation	Possible findings
Routine
Erect chest x-ray	Gas under the diaphragm Atelectasis
Erect and supine abdominal x-ray	Distended small or large bowel Thickened bowel Gas in bowel wall Calcified aneurysm
Haemoglobin	Anaemia Haemoconcentration
White cell count with differential	Leucocytosis with left shift
Electrolytes	Unexpected hypokalaemia
Urea and creatinine	Unexpected renal failure
Serum amylase Serum lipase	Hyperamylasaemia and hyperlipasaemia are suggestive of pancreatitis; marginal elevation seen in small bowel obstruction, acute cholecystitis and mesenteric infarction
Under appropriate clinical circumstances
Limited gastrograffin meal	Confirmation of duodenal perforation if conservative treatment is contemplated
Beta human chorionic gonadotropin	Elevated in ectopic pregnancy
Abdominal ultrasound	Confirmation of ruptured aneurysm only if diagnosis in doubt and condition is stable;demonstration of intraabdominal fluid
CT scan	Confirmation of ruptured aneurysm only if diagnosis in doubt and condition is stable; confirmation of pancreatitis if doubt exists; confirmation of perforated bowel to plan intervention
Limited gastrograffin enema	‘Thumb printing’ due to mucosal oedema

Specific management of conditions causing generalised abdominal pain

Local resection is required if the loop of bowel remains non-viable after it is released intraoperatively (Fig 4.1). Bowel that is pink in colour and exhibits spontaneous peristalsis or peristalsis when stimulated is viable. Further, there should be pulsatile flow of bright red blood through feeding vessels.

A ruptured pathological organ

Presentation and treatment is dependent on the underlying pathology. A delayed splenic rupture due to recent trauma, for example, will usually require splenectomy. A splenectomy is required for a spontaneous rupture of an abnormal spleen. A ruptured ovarian cyst may require ovarian cystectomy or oophorectomy. A ruptured liver cell adenoma requires a liver resection. Often the underlying problem will become apparent only at laparotomy.

Small bowel ischaemia

This is caused by a superior mesenteric artery thrombosis or embolism. It initially presents with severe constant abdominal pain of non-peritoneal type in an elderly patient with risk factors for vascular disease or a patient with risk factors for arterial embolism (e.g. atrial fibrillation or recent myocardial infarction). Early on, when the bowel is still viable, there are minimal abdominal signs. Clinical suspicion in an elderly patient with associated atrial fibrillation, vascular disease elsewhere or a low cardiac output state is the key to early treatment. The diagnosis must be considered in an elderly patient if the pain is out of proportion to the signs as the abdominal signs are not marked and there are no specific diagnostic signs on plain abdominal radiology. A triple phase CT scan may be diagnostic and saves valuable time in the lead-up to surgery.

Revascularisation of the bowel may be achieved with percutaneous therapeutic procedures that involve clot dissolution and possible stenting of the superior mesenteric artery. This would then be followed by an urgent laparotomy to assess the viability of the bowel.

At laparotomy, if the bowel is viable and does not require resection, a second laparotomy is performed 24 hours later. If, at the laparotomy, there are segments of the bowel that are not viable these are resected and may be anastamosed. Once again, a relook laparotomy is performed at 24 hours to assess the ongoing viability of the residual bowel. The extent of bowel ischaemia depends on whether the main trunk of the superior mesenteric artery or a branch is occluded. When the main trunk is occluded, a variable length of proximal jejunum supplied by collaterals from the coeliac artery and a variable amount of the right hemicolon supplied by collaterals from the inferior mesenteric artery remain viable.

There are two initial therapeutic options for extensive small bowel infarction:

1. resection with re-anastomosis of the viable ends.Thereafter the patient receives anticoagulation treatment to prevent extension of the thrombotic process. A ‘second-look’ laparotomy is usually performed after 24 hours to assess the viability of the remaining bowel.

2. diagnostic laparotomy only. There are some elderly and frail patients who have no realistic chance of returning to an enjoyable lifestyle after extensive small bowel resection. For these, a decision against massive resection may be made.

After initial surgical recovery, there is gut adaptation and hypertrophy sufficient to allow maintenance of nutrition by oral means if the residual small bowel length is greater than 45 cm. Patients with shorter residual lengths usually require long-term parenteral nutrition (Ch 17).

Superior mesenteric venous thrombosis usually results in a more subacute presentation. There can be associated ascites. The demonstration of a venous filling defect on the CT scan confirms the diagnosis (Fig 4.5). Management is determined by whether the affected bowel is viable or not. If the diagnosis can be made by CT scan and there are no signs of peritonism, the patient can be managed by anticoagulation and observation. Prior to commencement of anticoagulation therapy a predisposing cause is sought. Predisposing causes include the oral contraceptive pill, factor V Leidin mutation, antiphospholipid syndrome, antithrombin III deficiency, and protein S and protein C deficiency.

Figure 4.5 CT scan demonstrating a clot in the superior mesenteric vein (SMV) In this case there was no infarction of the small bowel and the patient was managed non-operatively with anticoagulation.

Ischaemic colitis

This condition is associated with severe central and lower abdominal pain, in association with risk factors for vascular disease and is often associated with bloody diarrhoea. There may be localised signs in the left iliac fossa or generalised signs of diffuse tenderness. The clinical diagnosis is supported by the finding of gross oedema and ‘thumb printing’ in the left colon on plain abdominal x-ray examination (see Fig 4.6) or CT scan. If there is uncertainty, colonoscopy can be helpful. Ischaemic colitis often settles with non-operative treatment. If during close observation, however, the abdominal signs become more marked or the patient develops systemic signs of sepsis, laparotomy is required to exclude an occult perforation and resect the ischaemic segment as a Hartmann’s procedure. Reanastomosis is then delayed until after full recovery. Anticoagulation treatment is contraindicated early because of the risk of massive colonic haemorrhage.

Figure 4.6 Plain abdominal x-ray showing gangrenous large bowel and thumb printing due to ischaemic colitis.

Pancreatitis

This is discussed below under ‘Acute epigastric pain’.

Acute Abdominal Colic

Colicky pain is felt in the midline. It is associated with forceful smooth muscle contraction. It has a characteristic repetitive pattern. There is intense pain for a few minutes, followed by complete relief of pain for a few minutes. It is associated with gastric, small and large intestinal and uterine disorders. Gastric (foregut) colic is experienced in the epigastrium; small bowel and right hemicolon (midgut) colic periumbilically; and left hemicolon (hindgut) and uterine colic suprapubically. So-called ‘biliary colic’ is a continuous rather than intermittent pain experienced in the epigastrium or the right upper quadrant.

The causes of acute abdominal colic are listed in Box 4.1. The common causes are acute gastroenteritis, food poisoning, constipation and uterine disorders. The life-threatening causes are small and large bowel obstruction.

Hernia:

– abdominal wall;

– internal.

Neoplasm:

– benign (e.g. leiomyoma);

– malignant (e.g. carcinoid tumour, adenocarcinoma).

Stricture:

– ischaemic;

– radiation;

– inflammatory (e.g. Crohn’s disease).

Volvulus Intussusception:

– tumour (e.g. Peutz-Jegher’s syndrome, gastrointestinal stromal tumour).

Superior mesenteric artery syndrome Intraluminal bolus:

– gallstone;

– bezoar.

• Large bowel obstruction:

– colon cancer;

– diverticular disease;

The initial clinical question is: does this patient have an innocent or a serious cause of abdominal colic? Acute gastroenteritis is usually of viral origin, is associated with diarrhoea and is infectious so that it is likely to have affected others in the household. Food poisoning can usually be related to ingestion of a particular meal. The specific management of the problems that cause abdominal colic with diarrhoea is covered in Chapter 13. Simple analgesics are part of the management.

Constipation of recent origin can often be related to ingestion of drugs (e.g. codeine-containing analgesics) or a change in dietary pattern (Ch 11). It is managed with simple analgesics, elimination of an identifiable cause and use of a bulking agent.

Uterine causes are associated with vaginal bleeding and menstrual irregularities. Their management is beyond the scope of this book.

Some patients with a non-specific cause may be difficult to distinguish from patients with early bowel obstruction. When there is doubt after the initial clinical evaluation, the patient should have simple investigations, such as plain abdominal radiology, looking for a bowel obstruction. Continued clinical uncertainty may be managed best by close observation in hospital.

Bowel obstruction

The four cardinal symptoms of uncomplicated complete bowel obstruction are colicky abdominal pain, vomiting, abdominal distension and absolute constipation, which includes failure to pass flatus (obstipation) as well as faeces. If the obstruction is incomplete, one of the cardinal symptoms, constipation, may be replaced by diarrhoea. The differential diagnosis of incomplete bowel obstruction is acute gastroenteritis. The degree of abdominal distension is high with colonic obstruction and low with high small bowel obstruction. In contradistinction, the severity of vomiting is less and occurs late with colonic obstruction, and is greater and occurs earlier with proximal small bowel obstruction. The vomitus, although initially bile-stained, becomes feculent as the obstruction progresses. If the obstruction continues untreated, a paralytic ileus may supervene and then the hypermotility of the bowel proximal to the obstruction (and the colicky pain) will subside. Alternatively, the unrelieved obstruction may become complicated by strangulation or perforation. These complications are also associated with paralytic ileus. However, rather than the pain settling, it becomes constant and peritoneal in type.

The most common cause of small bowel obstruction is adhesions from a previous laparotomy. The next commonest cause is hernia, usually inguinal or femoral hernia (Ch 21). As well as eliciting the symptoms of obstruction, it might be possible to elicit the cause from the history (see Box 4.1).

Physical examination is directed to the demonstration of:

• signs of obstruction (abdominal distension, hyper-resonant abdomen, increased bowel sounds);

• cause of the obstruction (e.g. a previous laparotomy scar raising the possibility of adhesions; an irreducible hernia; an intraabdominal mass caused by a tumour, intussusception, Crohn’s disease, or an appendiceal or diverticular inflammatory phlegmon; or blood mixed with mucus on rectal examination from an intussusception);

• degree of dehydration, so that fluid resuscitation can commence promptly; and

• signs that the obstruction has become complicated (localised peritonism, tenderness in an irreducible hernia), or signs of systemic sepsis (fever and tachycardia).

Specific investigations include the following:

• Plain abdominal radiology reveals distended loops of small bowel with fluid levels and absence of colonic gas (see Fig 4.4). Occasionally the cause will be evident, as in Figure 4.7.

• Leucocytosis, particularly if there is a left shift, may indicate ischaemic bowel.

• An abdominal CT scan will show a small bowel obstruction earlier than plain radiology. It will often show the point of obstruction with a transition from dilated bowel to collapsed bowel. The cause may also be evident.

Figure 4.7 Radio-opaque stones in the gall bladder (a) and the common bile duct (b).

Treatment is as follows. After initial fluid resuscitation and gastric decompression with a nasogastric tube, an urgent laparotomy may be required. Factors in favour of early laparotomy include:

• evidence of strangulated bowel (constant pain, focal tenderness, unexplained tachycardia [over 100 beats/min], fever [over 37.8°C], and leucocytosis [over 16,000]); and

• no history of previous surgery that may have caused adhesions.

If a trial of non-operative treatment is selected, frequent re-evaluation is imperative lest clinical deterioration be overlooked. If there is no evidence of resolution after 48 hours laparotomy is required, as it is unlikely that spontaneous resolution will occur beyond this time. The duration of the non-operative trial may be extended if the cause is thought to be radiation enteritis, Crohn’s disease, involvement of small bowel in a diverticular mass or known peritoneal metastatic disease.

There are three common causes of large bowel obstruction: colon cancer (75% of cases), diverticular disease (15%), and sigmoid and caecal volvulus (5%).

When managing a patient with an apparent large bowel obstruction on clinical and simple radiological grounds, it is important to be sure that the diagnosis is not simple constipation or acute pseudo-obstruction of the colon, as these conditions are treated non-operatively.

Constipation is associated with a loaded rectum, whereas the rectum should be empty with obstruction. If constipation is the likely diagnosis, bowel washouts from below with enemata should resolve the dilemma. If doubt persists, a limited gastrograffin enema will be conclusive.

Acute colonic pseudo-obstruction (also called Ogilvie’s syndrome) occurs most often in patients in hospital secondary to conditions such as sepsis, acute pancreatitis, electrolyte imbalance, renal failure, spinal cord injury, hip fractures, hip replacement surgery or postoperatively.

If acute pseudo-obstruction is the clinical diagnosis, a gastrograffin enema will confirm the diagnosis and exclude a mechanical obstruction. A gastrograffin enema may produce a return of bowel activity because of its cathartic action.

Colonic pseudo-obstruction may mimic organic obstruction if acute pseudo-obstruction is the clinical diagnosis. Acute colonic pseudo-obstruction usually resolves within 48 to 96 hours with non-operative treatment. This includes fluid resuscitation, correction of electrolyte abnormalities, withdrawal of medications (such as narcotics and antidepressants) that might be contributing, stimulation of colonic motility with intravenous neostigmine under cardiac monitoring, and colonoscopic decompression if needed.

Continued competence of the ileocaecal sphincter prevents retrograde decompression of obstructed large bowel into the small bowel in more than 50% of patients, effectively producing a closed loop. Colonic distension proximal to the site of obstruction is greatest in the caecum and ascending colon. Perforation is usually heralded by localised overlying tenderness. The other useful marker of imminent perforation is colonic distension greater than 10 cm as assessed by plain abdominal x-ray examination (Fig 4.8). A sigmoid or caecal volvulus is also a closed loop that may perforate if neglected.

Figure 4.8 Plain abdominal x-ray demonstrating a large bowel obstruction with grossly distended caecum. There is an acute cut-off in the region of the junction of the descending colon and sigmoid (arrow).

Diagnosis and management of large bowel obstruction

Colon cancer is discussed in detail in Chapter 22. Presentation with complete obstruction is usually preceded by fluctuating incomplete obstruction for several weeks. The tumour is more commonly in the sigmoid or descending colon. The patient may also have noted rectal bleeding. The level of the obstruction may be evident on plain abdominal radiology (see Fig 4.9). Further management is dependent upon whether the obstruction is left-sided or right-sided. An obstructing cancer in the right hemicolon can be resected with immediate re-anastomosis. An obstructing left-sided colon cancer may be managed initially with an endoscopically placed expanding metal stent (Fig 4.9) to decompress the colon. The patient is then assessed for definitive care (Ch 22). If stenting is not available the bowel can be resected with immediate re-anastomosis if all the proximal colon is resected. If a more limited resection is to be performed in mechanically unprepared bowel, and an anastomosis is performed, either a covering colostomy or ileostomy, or an intraoperative antegrade colonic washout is required. Another approach is to resect the tumour and exteriorise the proximal end as a colostomy (Hartmann’s procedure). If the tumour is associated with extensive distant metastases, a colonoscopically delivered expanding metal stent may be the definitive treatment.

Figure 4.9 Radiological imaging of an expandable metal stent that was inserted endoscopically across a carcinoma of the sigmoid that presented with acute large bowel obstruction. This stent allowed for emergency decompression of the colon. The patient was able to be worked-up further and proceeded to an elective colonic resection 3 weeks later.

The patient with diverticular disease has usually had previous episodes of diverticulitis (see below) prior to the onset of obstruction. Whether or not the patient has a sigmoid colon cancer that is the cause of the obstruction, as well as diverticular disease, can be resolved with colonoscopy. Local colonic resection is reserved for those with an obstruction that fails to settle with antibiotic therapy and bowel rest.

The typical patient with a sigmoid volvulus is elderly, has chronic constipation and is institutionalised. The patient usually has gross abdominal distension but little vomiting and abdominal pain. The clinical diagnosis is confirmed with a plain abdominal x-ray examination, which has a typical appearance (see Fig 4.10). The single loop based in the left iliac fossa can extend to the right upper quadrant. The volvulus is decompressed using either a rigid or flexible sigmoidoscope by gently passing a soft rectal tube under direct vision through the point of the rotation at the level of the brim of the pelvis. The torted colon usually reduces spontaneously over 2–5 days, after which the rectal tube can be removed. As the condition is commonly recurrent, an elective resection of the redundant colon on its long mesentery is advisable unless contraindicated by other medical problems.

Figure 4.10 Plain abdominal x-ray showing sigmoid volvulus. Note the large ‘coffee-bean’ shape gas-filled structure represents the distended, involved portion of the sigmoid colon with the apex in the left iliac fossa. This is the classic appearance of this abnormality.

A caecal volvulus involves the caecum, the ascending colon and the terminal ileum, which rotate on a long mesentery. Typically it affects younger and fitter patients. Radiologically the volvulus extends from the right iliac fossa towards the splenic flexure (Fig 4.11). The volvulus cannot be reduced radiologically, but may be reduced using the flexible colonoscope. Operative reduction and right hemicolectomy can then be performed electively.

Figure 4.11 Plain abdominal x-ray demonstrating a caecal volvulus, which can be seen as a large distended loop of bowel emanating from the right iliac fossa.

Gastric outlet obstruction

The dominant symptom is profuse vomiting. Pathognomonic features of the vomitus are the presence of foodstuffs consumed several days previously, lack of bile staining and a small amount of old blood (coffee ground vomitus). Epigastric pain, particularly colicky postprandial pain, may be a feature. When pain is present, it is relieved by vomiting. Weight loss may be marked.

The main causes of gastric outlet obstruction are distal gastric malignancy, malignancy of the pancreatic head or proximal duodenum (rare), and oedema or scarring due to chronic peptic ulceration. In the latter case, there will often be a history of long-standing dyspepsia.

The clinical diagnosis may be supported by demonstrating a gastric succussion splash. This is done by listening to the abdomen while shaking the patient from side to side.

Initial management includes intravenous fluid replacement, correction of any electrolyte and acid–base disturbance and nasogastric decompression. There are several points that are salient during resuscitation:

• Gastric fluid losses that need replacement may be as high as 3 L/day.

• Gastric fluid losses may have resulted in a hypokalaemic, hypochloraemic metabolic alkalosis. These are corrected with normal saline and potassium supplements.

• Total parenteral nutrition may be appropriate if weight loss is greater than 10% (Ch 17).

• Blood transfusion may be required for severe iron deficiency anaemia.

After gastric decompression the cause should be defined by upper gastrointestinal endoscopy. If active peptic ulceration is found, the gastric outlet obstruction is potentially reversible. Healing the ulcer with parenteral acid suppression may result in resolution of oedema around the ulcer and restitution of luminal patency. Otherwise, the stomach needs to be drained surgically. If the cause is peptic ulceration, this is done by vagotomy and distal gastric resection or gastroenterostomy depending on the position of the ulcer. If the cause is gastric malignancy, this is done by distal gastric resection if the tumour is potentially curable, or gastroenterostomy or insertion of an expanding metal stent if it is not curable (see Ch 17). When the cause is a pancreatic or duodenal malignancy resection should be considered. When the lesion is not resectable resolution of the obstruction may be achieved with an endoscopic expanding metal stent or operative gastroenterostomy.

Acute Epigastric Pain

Acute epigastric pain is a common complaint. Often the pain is short-lived and no organic cause is found. A list of causes is shown in Box 4.2. On the basis of an initial clinical evaluation the clinician must decide if:

• the patient requires hospitalisation; and

• further specific investigations, such as upper gastrointestinal endoscopy and/or upper abdominal ultrasound, are needed.

The first of those decisions is difficult and requires clinical experience. It will depend on whether it is considered likely that there is a specific cause and the likely natural history. Factors that assist the clinician to decide include:

• the severity, duration of the symptoms and response to the treatment to date;

• associated systemic symptoms and signs; and

• the results of initial non-invasive investigations.

There are few features that assist in differentiating specific from non-specific causes. The severity tends to be greater and continuous with organic causes. Radiation of pain to the back is supportive of pancreatitis or biliary stone disease. Migration to the right upper quadrant suggests cholecystitis. Migration around the side to the scapula or through to the back also suggests gallstones. Associated jaundice may indicate a stone in the common bile duct (Ch 23).

On many occasions deep epigastric tenderness is the only abdominal sign. If there is focal epigastric peritonism, or more generalised peritonism, a perforated peptic ulcer or acute pancreatitis becomes more likely. The abdominal signs with acute pancreatitis may be unimpressive. Right upper quadrant tenderness or mass suggests a biliary cause for the epigastric pain.

Associated signs of hypovolaemia or gram-negative sepsis (discussed above under generalised abdominal pain) suggest a perforated peptic ulcer, acute pancreatitis or cholangitis.

Initial investigations

A routine initial screen includes plain radiology of the chest and abdomen, a blood film looking for anaemia and leucocytosis, liver function tests looking for evidence of hepatobiliary disease, and serum amylase and lipase. A marginal elevation of serum amylase (100–400 U/L) is not specific for pancreatitis. While an elevated lipase is more sensitive in acute pancreatitis it is also elevated in many other acute abdominal conditions and therefore is a less specific test for acute pancreatitis. Some uncommon but significant radiological signs are listed in Table 4.6. Basal pulmonary consolidation may rarely present with abdominal pain.

Table 4.6 Specific radiological findings to be looked for in acute epigastric pain

Sign	Possible cause	Figure
Gas under the diaphragm	Perforated peptic ulcer	4.2
Radio-opaque gallstones	Biliary disease	4.7
Colonic cut-off sign	Acute pancreatitis
Sentinel loop	Acute pancreatitis
Pancreatic calcification	Chronic pancreatitis	4.12

Further investigations

The need to proceed with further investigation as either an inpatient or an outpatient depends on the degree of clinical suspicion that an organic cause will be found. For many, symptomatic treatment with antacids or antispasmodics or just simple analgesics is sufficient. The next tier of investigations includes upper gastrointestinal endoscopy and upper abdominal ultrasound. The order in which they are performed depends on the clinical features. The management of abnormalities found on upper gastrointestinal endoscopy is discussed under dyspepsia (see Ch 6). Hepatobiliary abnormalities found on ultrasound examination are discussed in the next section on right upper quadrant pain and also in Chapter 26.

Acute Pancreatitis And Its Complications

Aetiology

The causes of acute pancreatitis are listed in Table 4.7. The most common causes are passage of gallstones down the common bile duct and alcohol abuse. Pointers towards gallstones as the cause include female gender, older age and abnormal liver function tests.

Table 4.7 Aetiology of acute pancreatitis

Cause	Incidence
Gallstones	50–60%
Alcohol	30–40%
Idiopathic	10%
Post-ERCP	2%
Medications, e.g. azathioprine, 6-mercaptopurine, frusemide. hydrochlorothiazide, tetracycline, sulfonamides, oestrogens, sodium valproate, L-asparaginase	Uncommon
Major abdominal trauma	Variable
Mumps	Rare
Hyperlipidaemia	Rare
Hypercalcaemia	Rare
Hereditary (familial)	Rare
Pancreatic tumours	Rare

ERCP = endoscopic retrograde cholangiopancreatography

It is not uncommon for those with alcohol as the cause to deny alcohol abuse, at least initially. If no cause is apparent, check serum triglycerides, calcium levels and IgG4 (immunoglobulin G4) for autoimmune pancreatitis during convalescence, along with a three-phase CT scan to re-evaluate the pancreas.

Diagnosis

Detection of elevated serum amylase levels is the usual means of diagnosis. The level rises within 12 hours of the onset of pain and gradually returns to normal over the next week. This test has a number of false positive and false negative results. False positive results include perforation of stomach or small bowel, small bowel obstruction, mesenteric ischaemia, acute cholecystitis or common bile duct obstruction, morphine, chronic pancreatitis, pancreatic carcinoma, end-stage renal failure and chronic alcoholism. Minor elevations can occur with parotitis, tumours (lung, oesophagus, ovarian and breast carcinoma), acute or chronic liver disease, diabetic ketoacidosis and HIV infection. Macroamylasaemia is rare; there are macromolecular aggregates of amylase or IgA and amylase that are not filtered by the kidneys so that the amylase-creatinine clearance is abnormally low.

False negative results may occur in hypercholesterolaemia and recurrent alcoholic pancreatitis. If there is doubt, the diagnosis can be confirmed by CT scan, which shows swelling of the pancreas and peripancreatic oedema.

In most centres, serum lipase in addition to amylase is used as the biochemical marker of pancreatitis due to its greater specificity. Its rise and fall after acute pancreatitis occur after the same changes in serum amylase.

Assessment of severity

The height of the peak in serum amylase or serum lipase levels provides no useful measure of the severity of an attack of pancreatitis. Severity is scored by a combination of predominantly laboratory measurements (see Table 4.8) during the first 48 hours of hospitalisation, and this provides prognostic guidance. Severe pancreatitis is present if there are three or more poor prognostic factors. The mortality rate in cases of mild pancreatitis (less than three poor prognostic factors) is less than 1%, whereas the mortality with severe pancreatitis is greater than 50%.

Table 4.8 Poor prognostic factors for acute pancreatitis according to the Glasgow scoring system

Factor	Critical value
Age	> 55 years
AST/ALT	> 200 IU/L
White cell count	> 15 × 10⁹/L (15,000/mm³)
Serum glucose	> 10 mmol/L
Blood oxygen (PaO₂)	< 60 mmHg
Blood pH	< 7.35
Serum urea	> 16 mmol/L
Serum albumin	< 32 g/L
Serum calcium	< 2 mmol/L
Serum lactic dehydrogenase	> 600 U/L

ALT = alanine aminotransferase; AST = aspartate aminotransferase.

Initial management

Non-operative management is supportive and directed towards the prevention and treatment of complications. The complications of acute pancreatitis, the timeframe of their development and methods for prevention or treatment are listed in Table 4.9.

Table 4.9 Complications of acute pancreatitis

The important early complications are acute renal failure due to inadequate fluid resuscitation, and respiratory embarrassment due to a combination of inadequate analgesia and physiotherapy, fluid overload and adult respiratory distress syndrome. Some of the causes are at least partly preventable. Patients at risk because of three or more poor prognostic signs, or because of other diseases, must be managed in a high-dependency or intensive care unit where fluid resuscitation can be managed aggressively with appropriate monitoring. Nasogastric suction to prevent tracheal aspiration, a respiratory complication of paralytic ileus, is required only if the patient is vomiting due to ileus.

Severe pancreatitis

The mortality and the morbidity in acute severe gallstone pancreatitis, as defined by the presence of three or more poor prognostic factors (see Table 4.8), can be reduced by urgent endoscopic retrograde cholangiopancreatography (ERCP) and sphincterotomy. Thus an abdominal ultrasound is performed early in the admission to diagnose gallstones and if the pancreatitis is rated as severe an ERCP is performed urgently.

Pancreatic necrosis

The chance of failure of early resolution of pancreatitis, and of development of complications, rises if pancreatic necrosis develops. This complication is usually apparent within 5 days of the onset of the attack if it is going to occur. Pancreatic necrosis is a radiological diagnosis made on a contrast-enhanced CT scan and is evident as unperfused tissue (see Fig 4.12). Its incidence is high in patients who present with three or more poor prognostic signs. It should also be suspected in patients whose pancreatitis fails to settle clinically within a week. Pancreatic necrosis takes 5–10 days to develop so, unless otherwise indicated, a CT scan to establish the presence of necrosis should be performed after the seventh day of the illness, unless otherwise indicated.

Figure 4.12 Dynamic enhanced CT scan showing early pancreatic necrosis (arrow), which is demonstrated as an unperfused portion of the head and neck of the pancreas compared to the perfused portion of the body and tail.

The incidence of the four common major local complications (infected pancreatic necrosis, acute fluid collection, pancreatic pseudocyst and pancreatic abscess) is much higher in patients who have had pancreatic necrosis. These various complications can co-exist.

Infected pancreatic necrosis

The most life-threatening complication of pancreatic necrosis is infection of the necrotic pancreatic and peripancreatic tissue. This complication should be suspected if clinical signs of sepsis develop, usually beyond the second week after the onset of the illness, or if there is increasing abdominal pain, tenderness and swelling, or if unexplained deterioration occurs in another organ system (e.g. cardiac or respiratory). Previously, a suspicion of infected pancreatic necrosis can be confirmed by a positive culture from a CT-guided pancreatic fine needle aspirate. Infected pancreatic necrosis will usually require surgical intervention to remove the infected necrotic material. Previously, this was done with early and repeated laparotomy and debridement of the pancreas and necrotic retroperitoneal tissue. Currently, the operative intervention is delayed for as long as possible, in order to develop clear delineation between the necrotic tissue and viable tissue. The intervention is now performed, where possible, using minimally invasive techniques, as opposed to an open laparotomy. If the minimally invasive techniques are unsuccessful a laparotomy may be required to debride the infected necrosis.

Acute fluid collection

This is a collection of fluid without a fibrous capsule occurring in the lesser sac in the first 6 weeks after the onset of pancreatitis. It is often asymptomatic, being diagnosed by a CT scan (Fig 4.13). It may be associated with slow resolution of the symptoms and signs of acute pancreatitis. It may resolve spontaneously or persist to develop a capsule, when it is defined as a pseudocyst. Alternatively, the collection may become infected, or produce gastric outlet obstruction, in which case it should be drained percutaneously under CT or ultrasound guidance. Otherwise, the collection should be monitored by serial CT or ultrasound scans.

Figure 4.13 CT scan 4 weeks after an episode of acute pancreatitis. Note that there is an incomplete wall to this collection along the posterior and left sides, differentiating this from an established pseudocyst.

Pancreatic pseudocyst

This is an acute fluid collection that has developed a fibrous capsule over 6 or more weeks. It may be asymptomatic, or be associated with ongoing abdominal pain, nausea and vomiting. It may be complicated by infection, haemorrhage or rupture. It may be evident as an abdominal mass (see Ch 19). If it is asymptomatic, it can be followed by serial scans (Fig 4.14). Smaller pseudocysts (under 5 cm) may resolve spontaneously; larger pseudocysts (over 5 cm) will persist and eventually need cyst-enteric drainage. Cyst-enteric drainage is also required for symptomatic pseudocysts (including infected pseudocysts). Cyst-enteric drainage involves draining the pseudocyst into the adjacent gastrointestinal tract lumen. This may be the stomach, duodenum or small bowel. The stomach and duodenum are used when the cyst abuts against these organs. The small bowel is used where the pseudocyst is distant from either the stomach or duodenal walls. Cyst-enteric drainage needs to be continued until the cavity of the collection shrivels. It can be performed percutaneously through the stomach under CT control, endoscopically through the posterior wall of the stomach, or transgastrically at laparoscopic or open operation. Where a pseudocyst cannot be drained into the stomach or adjacent duodenum an open operation is performed, and the pseudocyst joined to a loop of small bowel, in order to achieve cyst-enteric drainage.

Figure 4.14 CT scan demonstrating a large pseudocyst posterior to the stomach. Note that this has a complete wall surrounding the pseudocyst. This pseudocyst is much larger than 5 cm and required surgical intervention.

Pancreatic abscess

A pancreatic abscess is a collection of pus in the peripancreatic tissues. It is not an infected pseudocyst. Clinically, the patient is usually septic and has persistent upper abdominal pain and tenderness. Initial treatment is by percutaneous CT-guided drainage and broad-spectrum antibiotics. Operative drainage is required if the sepsis does not settle after percutaneous drainage.

A pancreatic fistula may develop as a consequence of operative debridement of pancreatic necrosis and the management of such fistulae are described in Chapter 19.

Subsequent management

Attention should be directed towards prevention of further attacks of acute pancreatitis. This involves laparoscopic cholecystectomy and operative cholangiography for patients with gallstones. Only 25% of these cases are found to have persistent stones in the common bile duct (Fig 4.16), which can be removed intraoperatively by exploration of the common bile duct or postoperatively by ERCP. Abstinence from alcohol should be recommended for patients with alcohol abuse and the patient referred to a drug and alcohol specialist for ongoing management.

Figure 4.16 Abdominal ultrasound demonstrating gallstones in the gall bladder.

Severe acute pancreatitis with associated pancreatic necrosis may be complicated by the development of diabetes mellitus or malabsorption due to pancreatic endocrine and exocrine insufficiency, respectively (Ch 14).

Right Upper Quadrant Pain

Common causes of acute right upper quadrant pain are listed in Box 4.3.

Initial assessment involves making a decision about whether the patient has an immediately life-threatening condition. This view would be supported by finding symptoms and signs of systemic sepsis or shock. Such signs might be attributable to gram-negative sepsis from cholangitis or cholecystitis, to haemorrhage from a liver cell adenoma or a hepatocellular carcinoma, or one of the life-threatening problems that more commonly cause epigastric pain, such as a perforated peptic ulcer and pancreatitis. Such patients need to be managed in hospital.

Management involves haemodynamic resuscitation and investigation aimed at rapidly identifying the underlying problem. These same investigations are relevant for patients with life-threatening conditions that cause generalised abdominal or epigastric pain as discussed above. They include plain x-ray examinations of the

Figure 4.15 Endoscopic retrograde cholangiopancreatography showing gallstones in the common bile duct.

abdomen and chest, a white cell count, liver function tests and serum amylase and lipase tests. If there are features of gram-negative sepsis, blood cultures should be performed and parenteral broad-spectrum antibiotics commenced. The second line of investigation should include an upper abdominal ultrasound looking for cholelithiasis, thickening of the gallbladder wall, dilatation of the biliary tree, air in the wall of the gallbladder or the biliary tree, and intraabdominal fluid. Even though these life-threatening conditions are uncommon, they require prompt, appropriate management.

Most patients who present with acute right upper quadrant pain are not systemically ill. They require analgesia (often narcotic) for the relief of pain. If the pain persists, hospitalisation enables the regular administration of narcotic analgesics and intravenous fluids.

Gallstones

Gallstones are of two major types: cholesterol-containing stones and pigment stones. Cholesterol-containing stones are much more common. Cholesterol and mixed stones occur in patients with bile secreted from the liver that is supersaturated with cholesterol. Cholesterol-supersaturated bile results from either enhanced cholesterol secretion (e.g. obesity, pregnancy or fasting) or decreased bile acid secretion (e.g. small bowel disease). Gallbladder hypomotility (e.g. fasting, pregnancy or hyperalimentation) also predisposes to gallstone formation. Pigment stones occur in patients with excessive haemolysis such as occurs in haemolytic anaemia.

Biliary pain (colic)

Biliary colic is severe pain of gradual onset, over 5–10 minutes, which reaches a peak that may be sustained for minutes to hours and then resolves slowly. It is more commonly experienced in the epigastrium than in the right upper quadrant, and may be in the lower chest and imitate an acute myocardial infarction type pain. The pain can be severe enough to cause agitation and a secondary tachycardia. It may radiate around the side to the right scapula or through to the back. The pain will often occur in the evening and may wake the patient from sleep. It can be associated with nausea and vomiting. If the patient has had the pain previously, gallstones may already have been demonstrated by upper abdominal ultrasound (Fig 4.16). As well as upper abdominal ultrasound, the following investigations are also performed:

• a white cell count looking for a leucocytosis, which suggests the development of cholecystitis;

• a serum amylase and lipase test so that pancreatitis is not overlooked; and

• liver function tests, looking for evidence of choledocholithiasis.

Once the diagnosis of biliary colic is confirmed, initial management depends upon whether the pain is adequately controlled and whether the development of acute cholecystitis or evidence of stones in the common bile duct has complicated the attack of biliary colic. The complications of gallstones are listed in Box 4.4.

Acute cholecystitis

Obstruction of the outlet of the gallbladder by a gallstone initially causes biliary colic. The obstruction eventually results in chemical inflammation of the gallbladder, which may be complicated by secondary bacterial infection. The pathological process takes about 24 hours to develop. The pain of acute cholecystitis is peritoneal in type. There may be associated fever. Abdominal examination reveals right upper quadrant peritonism. Usually the tenderness is too great to allow detection of a gallbladder mass, even if one is present at this stage. As the attack resolves, and the gallbladder swelling settles, the gallbladder with residual inflammation may be evident as a tender area beneath the costal margin during deep inspiration. This sign is called Murphy’s sign.

An attack of acute cholecystitis may settle within 24–48 hours. Recovery is assisted by the use of broad-spectrum antibiotics administered parenterally. Resolution of the attack is associated with dislodgment of the obstructing gallstone from the gallbladder outlet. The diagnosis of cholecystitis is confirmed, if necessary, by demonstrating a thick-walled gallbladder on ultrasound.

Failure of acute cholecystitis to resolve leads to one of five complications:

1. Empyema of the gallbladder is an ‘abscess of the gallbladder’. Clinically, the patient remains septic and has continuing right upper quadrant pain of peritoneal type, tachycardia, high spiking fever, and marked right upper quadrant peritonism, with an underlying grossly thickened, inflamed gallbladder surrounded by an omental phlegmon. The mass may not be evident on clinical examination because of overlying guarding but will be apparent on ultrasound. Antibiotics alone are not enough to produce resolution. Definitive management may be required, with cholecystectomy, which may be done laparoscopically or open. If cholecystectomy is contraindicated or not possible, drainage of the intravesical pus is required either percutaneously under ultrasound (or CT) guidance, or by operative cholecystostomy or cholecystectomy. Clinical neglect may result in perforation of the gallbladder, septicaemia, a right subphrenic, subhepatic abscess or an intrapatic abscess.

2. Gangrenous cholecystitis (Fig 4.17) may be indistinguishable from empyema of the gallbladder on clinical grounds; the pathological diagnosis is made at operation when patchy areas of necrosis are found as the gallbladder is shelled out of its omental phlegmon. The diagnosis may be made radiologically or by ultrasound on the basis of gas in the gallbladder wall from anaerobic organisms. The treatment is as for empyema. Perforation is more common here than with empyema.

3. If the gallbladder outlet remains obstructed and the contents do not become infected, a mucocoele of the gallbladder develops over several weeks. The bile is absorbed and the gallbladder distends with mucus secreted by the gallbladder mucosa. Clinically, an avocado-sized, slightly tender mass is evident in the right upper quadrant. Ultrasound will reveal a distended, thick-walled gallbladder with a stone impacted in Hartmann’s pouch. The treatment is cholecystectomy.

4. The resolution of acute inflammation without the development of an empyema or mucocele results in fibrosis of the gallbladder wall. This produces a thick and contracted gallbladder wall. This may occur after a single or multiple attacks and results in a small, contracted, fibrotic gallbladder with little or no bile in the lumen (chronic cholecystitis).

5. Cholecystoduodenal fistula is recognised only after it has occurred. The fistula forms when a gallstone trapped in the neck of the gallbladder slowly erodes through into the second part of the duodenum. This might be recognised after the event by the presence of air in the biliary tree. It may become evident after a large gallstone impacts in the terminal ileum causing small bowel obstruction (gall stone ileus).

Figure 4.17 Operative photograph demonstrating gangrene of the gall bladder.

Acute acalculous cholecystitis

This is a rare form of cholecystitis usually seen in the intensive care unit, where it occurs in debilitated patients, following major trauma, burns, recent major surgery or severe sepsis. Some of these patients are so unwell that they are unable to complain of right upper quadrant pain. If the patient complains of pain, diagnosis is by ultrasound. If there are no complaints of pain the diagnosis is made after clinical suspicion, with either ultrasound or CT scan. The alternative way of making a diagnosis is at surgery (when the clinical diagnosis has not been considered) performed as a result of unexplained deterioration thought to have an abdominal cause. Where the diagnosis is suspected and confirmed on ultrasound or CT scan, it may be managed with percutaneous transhepatic cholecystostomy and drainage of the gallbladder. When diagnosed at laparoscopy a cholecystostomy, rather than a cholecystectomy, may be required because of the patient’s poor physical state.

Definitive management of cholelithiasis

The definitive treatment of gallstones is cholecystectomy. If possible, the procedure is performed laparoscopically because this has a lower morbidity and more rapid recovery time than open cholecystectomy. Routine operative cholangiography is performed at the same time to ensure that unsuspected stones are not left behind in the common bile duct and that the common bile duct has not been injured during cholecystectomy. The risk of unsuspected choledocholithiasis at cholecystectomy is 3–7%. This possibility becomes more likely if one or more of the risk factors listed in Box 4.5 are present.

Box 4.5 Preoperative risk factors for common bile duct stones

• History of obstructive jaundice

• History of pancreatitis

• Elevated hepatic transaminases

• Elevated alkaline phosphatase

• Elevated bilirubin

• Dilated common bile duct on ultrasound (over 6 mm)

In the management of cholecystitis the timing of cholecystectomy has been controversial. Previously, cholecystectomy may have been delayed for 6–12 weeks to allow an acute inflammatory process to resolve, in the belief that the operation can more often be completed laparoscopically without the need to convert to open operation. However, randomised controlled trials have demonstrated that there is no benefit in delaying the operative management in acute cholecystitis. Therefore, unless surgery is contraindicated, acute cholecystitis should be managed with an urgent (within 72 hours) laparoscopic cholecystectomy. Where there is a contraindication to surgical intervention (e.g. a recent myocardial infarction) the episode may be managed non-operatively, with a view to doing elective cholecystectomy when the patient is fit. If the episode of acute cholecystitis were not to resolve in this situation, the gallbladder should be drained with a percutaneous transhepatic cholycystostomy, in a similar fashion to acute acalculus cholecystitis in a sick intensive care patient.

Currently, other treatments of cholelithiasis have an extremely limited use. Extracorporeal lithotripsy, even when combined with dissolution therapy (e.g. ursodeoxycholic acid), fails to completely remove stones from the gallbladder in over 50% of patients with asymptomatic gallstones. This therapy is not recommended for symptomatic stones. Dissolution therapy alone will work only in a functioning gallbladder with stones that contain no calcium. It may take several years for successful dissolution. All non-resectional therapies result in recurrent stones, unless the patient is on long-term dissolution therapy, which has its own complications and problems.

Acute right upper quadrant pain and jaundice

Most patients with both acute right upper quadrant pain and jaundice have a stone obstructing the common bile duct. If they have pain, jaundice and fever they have biliary obstruction with secondary infection or cholangitis. This triad of symptoms is known as Charcot’s triad (Ch 23). Initial management involves resuscitation and treatment of associated gram-negative sepsis. An urgent ultrasound examination should reveal cholelithiasis, a dilated common bile duct and sometimes a stone in the common bile duct. ERCP with sphincterotomy should be performed urgently if the signs of sepsis are severe, or early if they do not settle rapidly with parenteral antibiotics or the jaundice persists.

If the jaundice settles promptly, the underlying cause of the jaundice still needs to be treated during that hospital admission. This would be with a laparoscopic cholecystectomy and exploration of the common bile duct.

If the ultrasound examination does not demonstrate gallstones, other causes must be sought. In a small subset of patients, as discussed below, the explanation is apparent on the ultrasound of the liver. As mentioned above, normal serum amylase and lipase levels essentially eliminate unsuspected acute pancreatitis. Peptic ulceration is diagnosed by upper gastrointestinal endoscopy. For the remainder, no further investigation is required if the pain resolves without recurrence.

If the biliary colic recurs, the ultrasound examination should be repeated because small stones may be missed in up to 5% of cases. If the cause is still not apparent, a cholecystokinin-diethyl iminodiacetic acid (CCK-DIDA) test should be performed. This is a test of gallbladder function. Initially, DIDA is taken up by the liver, excreted in the bile and concentrated in the gallbladder. If the gallbladder is non-functional or contains tiny stones, it contracts minimally in response to cholecystokinin. If the cystic duct is obstructed by a small stone, the gallbladder will not be outlined (Ch 26).

Differential diagnosis of biliary colic

Occasionally, a patient with a clinical picture suggestive of acute biliary colic has an alternative explanation, which is apparent on ultrasound examination. More usually the pain is less severe in degree and more prolonged in duration. On review, there may be other clinical clues, which are summarised in Table 4.10.

Table 4.10 Causes of right upper quadrant pain other than gallstones found on ultrasound examination

Diagnosis	Ultrasound findings	Clinical clues
Hepatic metastases	Multiple solid lesions	Previous carcinoma Irregular hepatomegaly

Pyogenic liver abscess Cystic lesion(s)

Amoebic liver abscess Cystic lesion(s)

Spiking fevers

Anorexia

Loss of weight

Recent travel to endemic area

Right-sided cardiac failure Dilated hepatic veins

Hepatic adenoma/focal nodular hyperplasia Solitary solid lesion

Young woman

Oral contraceptive pill

Hepatocellular carcinoma

Solid lesion

Satellite lesions

Risk of hepatitis B or C

Known cirrhosis

Ascites

Hydatid cyst Cystic lesion with daughter cysts or calcified wall Rural exposure Budd-Chiari syndrome

Caudate lobe hypertrophy

Ascites

Hepatic metastasis

Haemorrhage into a liver metastasis, rapid growth or necrosis of a metastasis can produce a dull ache in the right upper quadrant. The primary tumour is usually gastrointestinal and, on questioning, the patient may reveal symptoms attributable to it. Occasionally the primary tumour is in the breast or the lung or is a melanoma.

On ultrasound examination, usually multiple solid lesions are found throughout the liver. A CT scan is used to confirm the ultrasound findings and to assess the pancreas. Management of metastatic liver disease is covered in Chapter 26.

Hepatic abscess

In a patient with a hepatic abscess (Fig 4.18) the symptoms of sepsis (spiking fevers, night sweats, poor appetite and loss of weight) tend to overshadow the right upper quadrant pain.

Figure 4.18 CT scan of a hepatic abscess in a 36-year-old male. This was managed with multiple percutaneous drains. Microbiology examination revealed infection to be due to Streptococcus faecalis. No underlying cause for this abscess was found.

Hepatic abscesses are of two types: amoebic and pyogenic. An amoebic abscess is caused by the protozoan Entamoeba histolytica, which invades the colonic mucosa, and is carried to the liver via the portal circulation. Infestation is rare in Western societies and usually follows a visit to an endemic area. Confirmation that the abscess is amoebic is usually made serologically. Treatment with metronidazole should result in resolution of the abscess. Percutaneous drainage is indicated if the diagnosis is uncertain, the abscess is likely to rupture or there is no clinical improvement after 48 hours.

Management of pyogenic abscesses has two components:

1. drainage of the abscess, usually percutaneously, using ultrasound or CT guidance and broad-spectrum parenteral antibiotics;

2. elucidation and treatment of the underlying cause.

The causes of pyogenic abscesses are listed in Table 4.11.

Table 4.11 Aetiology of pyogenic liver abscesses

Mechanism of infection	Examples
Cholangitis	Biliary obstruction from stone or malignancy Bile duct instrumentation

Portal pyaemia

Acute/subacute diverticular disease

Appendiceal abscess

Direct spread

Penetrating duodenal ulcer

Systemic bacteraemia

Intravenous drug abuse

Subacute bacterial endocarditis

Secondary infection of primary liver lesion

Traumatic haematoma

Necrotic hepatic metastasis

Hydatid cyst

Amoebic abscess

Hepatic adenoma and focal nodular hyperplasia

The benign liver tumours, hepatic adenoma and focal nodular hyperplasia, can cause right upper quadrant pain by intraperitoneal rupture, by bleeding into the lesion or expansion of the lesion. Their diagnosis is discussed in Chapter 26. Symptomatic and complicated lesions are usually managed by liver resection.

Hepatocellular carcinoma

As with hepatic adenoma and focal nodular hyperplasia, hepatocellular carcinoma can cause right upper quadrant pain as a result of rupture, haemorrhage or expansion. The lesion usually arises in a cirrhotic liver, so that the patient may also have signs of chronic liver disease, portal hypertension or ascites. The diagnostic features on scanning are discussed in Chapter 26.

Hydatid cyst

This lesion may be asymptomatic or cause a dull ache in the right upper quadrant. It is caused by Echinococcus granulosus (rarely Echinococcus multilocularis). The appearance of the liver cyst on ultrasound examination is often diagnostic. In a living cyst, usually there are also daughter cysts. Calcification of the wall of the cyst indicates that the contents are no longer viable (Ch 26). The diagnosis is confirmed serologically, with an enzyme-linked immunosorbent assay (ELISA) and a complement fixation test. Viable cysts need to be removed to prevent complications such as intraperitoneal rupture. Intraperitoneal spillage needs to be avoided during intraoperative clearance of the live cyst contents to avoid the risk of anaphylaxis and intraabdominal seeding with infective material. Preoperative therapy for several weeks with anthelmintics, such as albendazole, reduces the risk of recurrence.

Budd-Chiari syndrome

Hepatic vein thrombosis or Budd-Chiari syndrome that develops acutely is a rare cause of right upper quadrant pain. Ultrasound examination will show ascites and caudate lobe enlargement. The venous drainage of the caudate lobe is directly into the inferior vena cava, so that this segment hypertrophies as it is not affected by the hepatic vein thrombosis. CT scanning and Doppler flow studies are useful but liver biopsy may be necessary to confirm the diagnosis. Management is by treatment of the underlying cause (e.g. anticoagulation) and usually a portal systemic venous shunt (Ch 24).

Right heart failure

Severe or acute right heart failure may cause right upper quadrant pain by venous engorgement of the liver and stretching of the capsule. The symptoms and signs of cardiac failure are gross and dominate the clinical picture. Palpation of the liver may show it to be pulsatile.

Right upper quadrant pain after previous cholecystectomy

Recurrence of biliary pain after cholecystectomy occurs in 5–20% of patients. The cause may be due to a biliary or a non-biliary cause. Biliary causes include a retained or recurrent stone in the common bile duct or sphincter of Oddi dysfunction. Non-biliary causes include peptic ulceration, pancreatitis, irritable bowel syndrome or non-ulcer (functional) dyspepsia.

As discussed above for right upper quadrant pain without prior cholecystectomy, the initial question is whether the patient has an immediately life-threatening illness.

Patients with life-threatening conditions such as acute cholangitis are managed along the lines discussed above. Thereafter, investigation is first aimed at exclusion of common duct stones as the cause. The finding of a dilated common bile duct (with or without a stone on ultrasound examination) or abnormal liver function test results supports the diagnosis of choledocholithiasis, which needs to be confirmed or excluded by CT cholangiography or magnetic resonance cholangiopancreatography. Choledocholithiasis after previous cholecystectomy is managed by ERCP and sphincterotomy.

If choledocholithiasis is not found, the cause may be sphincter of Oddi dysfunction. This is a syndrome characterised by biliary-type pain following cholecystectomy. There are two types:

• Type 1 is characterised by a demonstrable stricture of the sphincter with a dilated duct on ultrasound examination, elevated liver function test results in association with episodes of pain, and relief of symptoms after endoscopic sphincterotomy in 90–95% of patients;

• Type 2 is characterised by a non-dilated duct, variable abnormalities in liver function test results during episodes of pain and a less certain response to endoscopic sphincterotomy; 60–65% of patients have resolution.

Findings of a normal diameter bile duct with normal liver function test results make a biliary cause for right upper quadrant pain less likely.

Right Iliac Fossa Pain

The exact cause of acute right iliac fossa pain may remain undetermined. The pain may resolve spontaneously after a short period and does not recur. Patients, on the other hand, have a different perspective. They commonly believe that they have acute appendicitis and require urgent appendicectomy.

The causes of right iliac fossa pain are listed in Box 4.6. Differentiation between the various causes is not always possible on clinical grounds, and investigations frequently do not help. Acute appendicitis remains largely a clinical diagnosis; CT scanning is useful where clinical uncertainty exists. Right iliac fossa pain seldom represents an intraabdominal catastrophe.

The initial aim of the clinician is to determine whether there is sufficient clinical evidence of localised peritonitis to require surgery. A patient with a typical history of periumbilical pain that shifts to the right iliac fossa, together with a low grade temperature, and localised and rebound tenderness maximal over McBurney’s point in the right iliac fossa, is likely to have acute appendicitis and should proceed to appendicectomy. Other signs of acute appendicitis are listed in Table 4.12. If the clinical picture is not clearly one of appendicitis, the next priority depends upon the gender of the patient. In women, consideration must be given to possible gynaecological causes of right iliac fossa pain (Box 4.6), some of which require surgical intervention. A history of abnormal or missed periods or a vaginal discharge is sought. A vaginal examination and speculum examination may demonstrate localised tenderness, a mass or a purulent discharge. Relevant investigations include a pregnancy test and pelvic ultrasound. Laparoscopy may be required to confirm a gynaecological diagnosis and/or deliver definitive treatment.

Table 4.12 Other signs of acute appendicitis

Name	Sign
Jump tenderness	Jumping or hopping induces pain. Useful in children
Cough tenderness	Cough produces localised pain over McBurney’s point
Psoas sign	Pain on elevating right leg (due to inflammation adjacent to psoas muscle)
Rovsing’s sign	Tenderness felt in the right iliac fossa while palpating the left iliac fossa
Rectal tenderness	Tenderness palpable on the right side accentuated by bimanual palpation

Those patients of the cohort without evidence of localised peritonitis are observed and reviewed. Most are afebrile and have a normal white cell count. If the clinical signs progress and become more suggestive of appendicitis, surgery is indicated. If the pain resolves spontaneously, no further investigations or follow-up are required.

Other inflammatory conditions of the terminal ileum and caecum may mimic acute appendicitis. Such conditions include mesenteric adenitis or terminal ileitis. These conditions frequently have no clinical clues and are often diagnosed at surgery. Terminal ileitis may be due to Yersinia enterocolitica infection and this is confirmed using acute and convalescent serology. Follow-up of patients with terminal ileitis needs to consider the possibility of Crohn’s disease, although this is uncommon. Mesenteric adenitis is common in childhood and adolescence and is a self-limiting illness of probable viral aetiology.

Occasionally there are clinical clues that indicate that the localised peritonitis is not due to appendicitis. An elderly patient may have a right iliac fossa mass, suggesting a caecal carcinoma or a complication of a diverticulum. If a mass is found, the presence of tumour or pus within it should be ascertained by CT scanning. An appendix abscess, if diagnosed preoperatively, can be drained percutaneously with ultrasound or CT control, avoiding urgent surgery. The appendix may then be removed electively, after a 3–6 month interval, if the abscess and associated acute inflammation resolve with drainage. A caecal carcinoma is treated by right hemicolectomy. The principles of treatment of right colonic diverticulitis or caecal diverticulum are the same as for left-sided diverticulitis if the diagnosis is known. Often, however, the diagnosis is established only after the affected colon is removed.

A patient with acute right iliac fossa pain and diarrhoea may have acute terminal ileitis. Recurrent right iliac fossa pain and diarrhoea or previous episodes of perianal sepsis may suggest Crohn’s disease.

Specific management

Acute appendicitis

The treatment for acute appendicitis is appendicectomy. Traditionally this is performed open through a muscle-splitting incision. That approach is still best for children. In adults the operation is commonly performed laparoscopically for several reasons:

• The accuracy of the clinical diagnosis is relatively low in adult women (53–78% of cases); it is higher in men (85–90%). The inaccuracy relates to gynaecological diseases that mimic acute appendicitis.

• If the cause is gynaecological, laparoscopy is a more accurate diagnostic tool than laparotomy through an incision in the right iliac fossa.

• Laparoscopic appendicectomy is associated with a more rapid postoperative recovery.

Terminal ileitis

Some patients with a clinical diagnosis of acute appendicitis are found to have terminal ileitis. Diarrhoea will have been a feature of the disease. The usual cause is Yersinia enterocolitica (Ch 13). This should be confirmed by convalescent serology. Occasionally, terminal ileitis that is not due to a bacterial cause is the first manifestation of Crohn’s disease.

Mesenteric adenitis

Mesenteric adenitis is quite common in children and adolescents. It is presumed to be a viral illness with enlargement of the mesenteric lymph nodes. There is often a preceding history of a viral-like illness. This is a self-limiting condition that resolves without specific therapy. There is no specific test to establish this diagnosis prior to surgery. It presents with a similar clinical picture to acute appendicitis and is often diagnosed at operation.

Meckel’s diverticulum

A Meckel’s diverticulum is a congenital remnant of the vitelline duct. It is a true diverticulum that occurs on the antimesenteric border of the terminal ileum, 45–60 cm from the ileocaecal sphincter. It occurs in 2% of the population and complications are unusual. If the base of the diverticulum is narrow, the diverticulum can become obstructed and present with an appendicitis-like illness. Other complications include:

• bleeding from peptic ulceration caused by ectopic gastric mucosa; and

• small bowel obstruction due to a congenital adhesion to the umbilicus.

These complications are managed by local resection of the diverticulum.

Crohn’s disease

The management of Crohn’s disease diagnosed prior to surgery is covered in Chapter 15. When a segment of Crohn’s disease is found at operation for presumed appendicitis, a resection needs to be performed only if there is a local complication (perforation, fistula or obstruction).