The acute abdomen and intestinal obstruction

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12 The acute abdomen and intestinal obstruction

Introduction

The ‘acute abdomen’ is a term used to encompass a spectrum of surgical, medical and gynaecological conditions, ranging from the trivial to the life-threatening, which require hospital admission, investigation and treatment. The primary symptom of the condition is abdominal pain. For the purposes of multicentre studies looking at acute abdominal pain, the definition is taken as ‘abdominal pain of less than 1 week’s duration requiring admission to hospital, which has not been previously investigated or treated’. Acute abdominal pain following trauma is usually considered separately.

The acute abdomen is a very common clinical entity. It has been estimated that at least 50% of general surgical admissions are emergencies and, of these, 50% present with acute abdominal pain. The acute abdomen therefore represents a significant part of the general surgical workload. Furthermore, patients with acute abdominal pain have significant morbidity and mortality. Studies have shown a 30-day mortality of 4% among patients admitted with acute abdominal pain, rising to 8% in those who undergo operative treatment. Not surprisingly, the mortality rate varies with age, being the highest at the extremes of age. The highest mortality rates are associated with laparotomy for unresectable cancer, ruptured abdominal aortic aneurysm and perforated bowel.

Individual conditions presenting with acute abdominal pain will not be dealt with in depth in this chapter, but will be covered elsewhere.

Aetiology

The causes of the acute abdomen may be subdivided into surgical, medical and gynaecological disorders. Surgical causes may be classified according to the organ involved, as well as the underlying pathological process (Table 12.1). The most common causes in any population will vary according to age, sex and race, as well as genetic and environmental factors (Tables 12.2 & 12.3).

Table 12.1 Possible causes of acute abdominal pain

Surgical
Inflammation

Obstruction

Ischaemia

Perforation

Medical
Cardiovascular

Gastrointestinal

Abdominal wall conditions

Genitourinary

Neurological

Haematological

Endocrine

Metabolic

Infective

Gynaecological

Table 12.2 Common causes of acute abdominal pain in UK adults requiring admission to hospital

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

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.

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.

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

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

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

Venous Non-occlusive Shock 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.

Perforation

Spontaneous perforation of an intra-abdominal viscus may be the result of a range of pathological processes. Weakening of the wall of the viscus, which might follow degeneration, inflammation, infection or ischaemia, will predispose to perforation. An increase in the intraluminal pressure of a viscus, such as occurs in a closed-loop obstruction (Fig. 12.2), will predispose to perforation, as will peptic ulceration, acute appendicitis and acute diverticulitis. Other less common causes are carcinoma of the colon, inflammatory bowel disease and acute cholecystitis.

Perforation can also be iatrogenic, and may occur during the insertion of a Verres needle at laparoscopy, because of a careless cut or suture placement during surgery, and during the course of an endoscopic procedure.

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

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