Condition	Approximate incidence (%)
Non-specific abdominal pain	35
Acute appendicitis	30
Acute cholecystitis and biliary colic	10
Peptic ulcer disease	5
Small bowel obstruction	5
Gynaecological disorders	5
Acute pancreatitis	2
Renal and ureteric colic	2
Malignant disease	2
Acute diverticulitis	2
Dyspepsia	1
Miscellaneous	1

Table 12.3 Common causes of acute abdominal pain in UK children

• Acute appendicitis

• Urinary tract infection

• Mesenteric adenitis

• Gastroenteritis

The remainder of this chapter will be concerned principally with surgical conditions, although it should be borne in mind that medical and gynaecological conditions may present with acute abdominal pain.

Pathophysiology of abdominal pain

To be able to make an accurate clinical assessment of the patient presenting with acute abdominal pain, it is necessary to understand the pathophysiology. Abdominal pain can be divided into somatic and visceral types.

Somatic pain

The parietal peritoneum covers the anterior and posterior abdominal walls, the undersurface of the diaphragm and the pelvic cavity. It develops from the somato-pleural layer of the lateral plate mesoderm and its nerve supply is therefore derived from somatic nerves supplying the abdominal wall musculature and the skin (T5–L2). The exception to this is the diaphragmatic portion, which is supplied centrally by afferent nerves in the phrenic nerve (C3–C5), and peripherally in the lower six intercostal and subcostal nerves.

The parietal peritoneum is sensitive to mechanical, thermal or chemical stimulation, and cannot be handled, cut or cauterized painlessly. As a result of its innervation, when the parietal peritoneum is irritated, there is reflex contraction of the corresponding segmental area of muscle, causing rigidity of the abdominal wall (guarding) and hyperaesthesia of the overlying skin.

When the diaphragmatic portion of the parietal peritoneum is irritated peripherally, there will be pain, tenderness and rigidity in the distribution of the lower spinal nerves, but when it is irritated centrally, pain is referred to the cutaneous distribution of C3, 4 and 5 (i.e. the shoulder area, Fig. 12.1). Somatic pain is classically described as sharp or knife-like in nature, and is usually well localized to the affected area.

Fig. 12.1 The shared sensory innervation of the shoulder and diaphragm.

Visceral pain

The visceral peritoneum forms a partial or complete investment of the intra-abdominal viscera. It is derived from the splanchno-pleural layer of the lateral plate mesoderm, and shares its nerve supply with the viscera (i.e. the autonomic nerves). Visceral pain is mediated through the sympathetic branches of the autonomic nervous system, with afferent nerves joining the pre-sacral and splanchnic nerves, which eventually join thoracic (T6–T12) and lumbar (L1–L2) segments of the spinal cord. The visceral peritoneum and the viscera are insensitive to mechanical, thermal or chemical stimulation, and can therefore be handled, cut or cauterized painlessly. However, they are sensitive to tension, whether due to overdistension or traction on mesenteries, visceral muscle spasm and ischaemia.

Visceral pain is typically described as dull and deep-seated. It is usually localized vaguely to the area occupied by the viscus during development, and is referred to the overlying skin of the abdominal wall according to the dermatome level with the sympathetic supply, as mentioned above. Therefore, pain arising from the intestine and its outgrowths (the liver, biliary system and pancreas) is usually felt in the midline. Irritation of foregut structures (the lower oesophagus to the second part of the duodenum) is usually felt in the epigastric area. Pain from midgut structures (the second part of the duodenum to the splenic flexure) is felt around the umbilicus. Pain from hindgut structures (the splenic flexure to the rectum) is felt in the hypogastrium.

Although the division of abdominal pain into visceral and somatic pain is useful, it is important to realize that some pathological conditions will result in a mixed picture. For example, acute appendicitis classically presents with acute abdominal pain that is initially felt in the umbilical area resulting from appendicular obstruction, which gradually localizes to the right iliac fossa and becomes sharper in nature as the overlying parietal peritoneum becomes inflamed.

Summary Box 12.1 Abdominal pain

• Visceral abdominal pain is mediated by the sympathetic nervous system and is typically deep-seated and ill localized to the area originally occupied by the viscus during intrauterine life

• Colic is a form of visceral pain that arises from a hollow viscus with muscle in its walls (e.g. gut, gallbladder, ureter), and results from excessive muscle contraction, often against an obstructing agent

• Patients experiencing colic are usually unable to remain still during the bout of pain but are pain-free between attacks. ‘Biliary colic’ is an exception (and the term colic may be a misnomer), in that pain often waxes and wanes on a plateau and there are no pain-free intervals

• Parietal pain, such as that caused by parietal peritonitis, is mediated by somatic nerves and is localized to the area of inflammation

• Reflex guarding and rigidity of the overlying muscles is usually present, and the patient is reluctant to move for fear of exacerbating the pain

• Some areas of the peritoneum (e.g. the pelvis, posterior abdominal wall) are ‘non-demonstrative’ in that parietal peritonitis may be present without tenderness or guarding of overlying muscles.

Pathogenesis

As one can see from the list of surgical conditions that may present with acute abdominal pain (Table 12.1), there are two main underlying pathological processes involved: inflammation and obstruction. These processes may be triggered by a variety of underlying abnormalities. It is important to realize that in any one patient a combination of abnormalities and processes may be involved.

No matter what the trigger of the inflammation, the subsequent pathological process is the same. There is reactive hyperaemia of the injured tissue as a result of capillary and arteriolar dilatation; exudation of fluid into the tissues as a result of an increase in the permeability of the vascular endothelium; and an increase in filtration pressure. Finally, there is migration of leucocytes from the vessels into the inflamed tissues.

The clinical consequences of the inflammatory process depend upon a multitude of factors, the most important being the underlying condition, its severity and duration, the organ involved, the patient’s age and comorbidity. In general, the patient will complain of abdominal pain and tenderness, which occurs as a result of tissue stretching and distortion and is due to the release of inflammatory mediators, some of which also mediate pain. On general examination, the patient may be pyrexial and have a tachycardia; investigations may reveal a raised white cell count. Examination of the abdomen will reveal tenderness in the affected area, with guarding and rigidity if the parietal peritoneum is involved.

Peritonitis

Inflammation of the peritoneum (peritonitis) may be classified according to extent (either localized or generalized) and aetiology (Table 12.5). In a surgical setting, the most common cause of generalized peritonitis is perforation of an intra-abdominal viscus. Inflammation of the peritoneum results in an increase in its blood supply and local oedema formation. There is transudation of fluid into the peritoneal cavity, followed by the accumulation of a protein-rich fibrinous exudate. In the normal state, the greater omentum constantly alters its position within the abdominal cavity as a result of intestinal peristalsis and abdominal muscle contraction. In the presence of inflammation, the greater omentum will adhere to and surround the abnormal organ. The fibrinous exudate effectively glues the omentum to the inflamed viscus, walling it off and preventing the further spread of inflammation. In addition, the exudate inhibits intestinal peristalsis, resulting in a paralytic ileus which also limits the spread of the inflammation and infection. As a result of the ileus, fluid accumulates within the lumen of the intestine and, along with the formation of large volumes of intra-peritoneal transudate and exudate, this will lead to a decrease in the intravascular volume, producing the clinical features of hypovolaemia.

Table 12.5 Classification of peritonitis

Generalized peritonitis
Primary: infection of the peritoneal fluid without intra-abdominal disease
• Haematogenous spread • Lymphatic spread • Direct spread: usually associated with continuous ambulatory peritoneal dialysis (CAPD) catheters • Ascending infection: from the female genital tract

Secondary: inflammation of the peritoneum arising from an intra-abdominal source

Localized peritonitis
• Usually due to spreading inflammation across the wall of an intra-abdominal viscus

Clinical features

The clinical features of peritonitis will again vary according to a wide variety of factors. The most common symptom is abdominal pain, which is constant and often described as sharp. The pain is usually well localized if it is secondary to inflammation of an intra-abdominal viscus, but may spread to involve the whole peritoneal cavity. Primary peritonitis can present rather more subtly, and as many as 30% of affected individuals may be asymptomatic.

The term ‘peritonitis’ or ‘peritonism detected on clinical examination’ is used to describe the collection of signs associated with inflammation of the parietal peritoneum, and includes ‘guarding’ and ‘rebound’ tenderness. Evidence of inflammation of the parietal peritoneum in association with inflammation of an intra-abdominal viscus is often a strong indication that the patient requires some form of surgical intervention.

Infarction

An infarct is an area of ischaemic necrosis caused either by an occlusion of the arterial supply or the venous drainage in a particular tissue, or by a generalized hypoperfusion in the context of shock (Table 12.6). The typical histological feature of infarction is ischaemic coagulative necrosis. An inflammatory response begins to develop along the margins of an infarct within a few hours, stimulated by the presence of the necrotic tissue.

Table 12.6 Aetiology of infarction

Occlusive

Arterial

• Embolism

• Thrombosis

• Extrinsic compression

Venous

• Thrombosis

• Extrinsic compression

Non-occlusive Shock

• Hypovolaemia

• Cardiogenic

• Sepsis

Vasoconstrictor drugs

The consequences of decreased perfusion of a tissue depend on several factors: the availability of an alternative vascular supply, the rate of development of the hypoper- fusion, the vulnerability of the tissue to hypoxia, and the blood oxygen content. In the context of acute abdominal pain, intestinal infarction is the most common cause. Other organs that may infarct include the ovaries, kidneys, testes, liver, spleen and pancreas.

Obstruction

The term ‘obstruction’ refers to impedance of the normal flow of material through a hollow viscus. It may be caused by the presence of a lesion within the lumen of the viscus, an abnormality in its wall, or a lesion outside the viscus causing extrinsic compression.

The smooth muscle in the wall of the obstructed viscus will contract reflexly in an effort to overcome the impedance. This reflex contraction produces ‘colicky abdominal pain’. The exception to this rule is ‘biliary colic’. The gallbladder and biliary system has little smooth muscle in its wall and attempts at contraction tend to be more continuous than ‘colicky’.

If the obstruction is not overcome, there will be an increase in intraluminal pressure and proximal dilatation. The end result depends on the anatomical location of the obstruction, whether it is partial or complete, and whether the blood supply to the organ is compromised. For example, a urinary bladder calculus causing partial urinary outflow obstruction may result in a dilatation of the ureter and renal pelvis, and subsequent ‘post-renal’ renal failure. An obstructed inguinal hernia, on the other hand, will not only produce proximal dilatation of the intestine (usually associated with vomiting) but may also result in ischaemia of the bowel wall, leading to infarction and perforation.

Clinical assessment

The ability to make an accurate assessment by taking a good history and performing an appropriate examination is a vital skill in the management of the patient with acute abdominal pain. Although an exact diagnosis is often impossible to make after the initial assessment and often relies on further investigations, it is the formulation of an appropriate, safe and effective management plan that is the most important issue. In most cases, it is possible to take a full history and perform a thorough examination, but this is not always so, and occasionally a rapid evaluation followed by immediate resuscitation is required.

History

The main presenting complaint of patients with an acute abdomen is pain. The characteristics of the pain (Table 12.7) give important clues to the likely underlying diagnosis, and these should be explored in depth. However, the importance of a full history cannot be overemphasized and is essential in all patients.

Table 12.7 Characteristics of abdominal pain

• Site

• Nature

• Radiation

• Time and mode of onset

• Severity

• Progression

• Duration

• Exacerbating/relieving factors