The acute abdomen and acute gastrointestinal haemorrhage

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The acute abdomen and acute gastrointestinal haemorrhage

Introduction

The term acute abdomen is widely understood but is difficult to define precisely. Typically, the symptoms are of acute onset and strongly suggest an abdominal cause; abdominal pain is almost always a prominent feature. The illness is of such severity that admission to hospital appears essential and operative surgery is a likely outcome. Many of the disorders causing an ‘acute abdomen’ are serious and potentially life-threatening unless treated promptly. On the other hand, simple and relatively trivial conditions such as constipation can produce acute and severe symptoms mimicking the early stages of an acute abdomen.

Major gastrointestinal haemorrhage is also a common reason for acute surgical referral, and is manifest by vomiting of blood (haematemesis) or profuse rectal bleeding or the passage of melaena. Many such patients are initially referred to a general (internal) physician or gastroenterologist, especially if the presumptive diagnosis is bleeding from a peptic ulcer or oesophageal varices.

Acute surgical emergencies constitute about 50% of all general surgical admissions. About half of these are for abdominal symptoms, predominantly pain, and half of those in this group resolve without operation.

Basic principles of managing the acute abdomen

The first goal is to resuscitate the patient with intravenous fluids and give analgesia. The next is to make a broad diagnosis on the history, examination, laboratory tests and imaging (Box 19.1). All help decide if an operation is necessary, and its urgency, and clarify any non-surgical treatment, e.g. antibiotics for diverticulitis or conservative measures for acute pancreatitis. The differential diagnosis encompasses the likely pathophysiological phenomena responsible.

Box 19.1 Plain radiology in the acute abdomen—what to look for

Five main image densities are detectable on radiographs:

• White—metallic objects

• Off white—calcified structures

• Medium shades of grey—most soft tissues

• Dark grey—fat

• Black—gas

How to review an abdominal X-ray:

1. Check name is correct and date is current

2. Note type of X-ray, i.e. plain or contrast, erect or supine

3. Is the image of adequate diagnostic quality, i.e. appropriate density? Does it show the whole abdomen?

4. Bowel gas and bowel wall—note distribution and dilatation (small bowel diameter less than 3 cm, most large bowel less than 5 cm, caecum less than 9 cm). Absence of gas may indicate a displacing mass, ascites (central) or acute pancreatitis (ground glass appearance). Faeces appear mottled; ‘faecal loading’ may mean constipation or obstruction. Rigler’s sign is strongly suggestive of bowel perforation

5. Non-bowel gas—free intraperitoneal gas, e.g. subphrenic gas in perforation of bowel, gas within bowel wall in necrosis, gas in biliary tree after sphincterotomy or fistula into bowel

6. Calcification—aortic wall in aneurysm, pancreas, renal and ureteric stones, gallstones, pelvic phleboliths (calcified old venous thrombi), teratomas, and fetus. Bones of spine and pelvis—osteoarthritis, metastases (lytic or sclerotic), Paget’s disease, fractures

7. Soft tissues. Thickened bowel wall. Check outline of kidneys (are both present?; length equal to three or more vertebral bodies) and psoas muscles (obscured in retroperitoneal inflammation)

8. Artefacts—artificial objects placed by medical personnel—central venous line, nasogastric tube, metal vessel or Fallopian tube clips, biliary, vascular or bowel stents, inferior vena caval filter, intrauterine contraceptive device

— foreign bodies—embedded bullets, glass fragments, objects inserted rectally

— projection of buttons, safety pins, rings on hand, coins, body piercing

In patients with an acute abdomen, always review chest X-ray for the following:

• Hiatus hernia

• Lung fields

• Pneumothorax

• Diaphragms: relative height; gas under

• Bony changes

• CVP line position

Disorders and diseases causing the acute abdomen

Intestinal obstruction

Pathophysiology of intestinal obstruction

Any part of the gastrointestinal tract may become obstructed and present as an acute abdomen. Gastric outlet obstruction, however, presents differently and is described in Chapter 21. The causes of intestinal obstruction are many and varied, as outlined in Figure 19.1.

Fig. 19.1 Mechanical causes of bowel obstruction

Obstruction leads to dilatation of bowel proximally and disrupts peristalsis. The manner of presentation depends on the level of obstruction in the GI tract (i.e. stomach, proximal or distal small bowel or large bowel) and on the completeness of obstruction. The most acute presentation is upper small bowel obstruction. This manifests within hours of onset because the large volume of gastric and pancreaticobiliary secretions is prevented from progressing, so it regurgitates into the stomach and is vomited. In contrast, distal large bowel obstruction is more chronic and may be present for days or a week before the patient seeks treatment.

Symptoms of intestinal obstruction

Symptoms and physical signs are summarised in Box 19.2.

Box 19.2 Clinical features of bowel obstruction and strangulation

• Vomiting—time of onset and nature of the vomitus suggest the level of obstruction

• Absolute constipation (i.e. no flatus or faeces passed rectally)—pathognomonic of complete obstruction (but not present in partial obstruction)

• Abdominal pain—usually colicky in character, often mild in uncomplicated obstruction and more severe in strangulation

• Dehydration—caused by vomiting, lack of fluid intake and fluid sequestration in obstructed bowel

• Abdominal distension—due to gas-filled loops of bowel. The more distal the obstruction, the greater the distension

• Visible peristalsis—uncommon finding; usually encountered in a very thin patient with prolonged but incomplete distal small bowel obstruction

• Abdominal tenderness—important feature distinguishing bowel strangulation from uncomplicated obstruction

• Central resonance to percussion with dullness in the flanks—gas within dilated bowel loops rising to the uppermost point in the abdomen

• Abnormal bowel sounds—exaggerated, lapping, sloshing, perhaps high-pitched or tinkling. Bowel sounds are absent or normal in adynamic obstruction

Vomiting: Bowel obstruction eventually leads to vomiting; the more proximal, the earlier it develops. Vomiting can occur even if nothing is taken by mouth because saliva and other GI secretions continue to be produced and enter the stomach. At least 10 litres of fluid are secreted into the GI tract each day. The nature of the vomitus gives clues about the level of obstruction. For example, vomiting of semi-digested food eaten a day or two earlier suggests gastric outlet obstruction. Copious vomiting of bile-stained fluid suggests upper small bowel obstruction. If the vomitus becomes thicker and foul-smelling (faeculent), more distal obstruction is likely and this change is often an indication for urgent operation. The term faeculent is a misnomer as the vomitus contains altered small bowel contents rather than faeces.

Pain: Fluid and swallowed air proximal to an obstruction plus continuing peristalsis cause pain. The general area of the pain gives clues to the embryological origin of the affected bowel: upper, middle or lower abdominal pain originates in foregut, midgut or hindgut respectively. In obstruction, pain is not usually the most prominent symptom. It is usually colicky, occurring in short-lived bouts as peristalsis attempts to overcome the obstruction. In small bowel, the peristaltic action often increases for 24–48 hours after the onset of obstruction and then fades.

Constipation: Absolute constipation, i.e. no faeces or flatus passed rectally, is pathognomonic of obstruction. The longer the duration, the more noteworthy it becomes in the diagnosis of obstruction.

Effects of the competence of the ileocaecal valve: Symptoms develop more gradually in large bowel obstruction because of the large capacity of colon and caecum and their absorptive capability. However, if the ileocaecal valve remains competent, no retrograde flow of accumulating bowel contents occurs and the thin-walled caecum progressively distends and eventually ruptures; operation is clearly more urgent in these cases. The ileocaecal valve becomes incompetent in about half the cases of large bowel obstruction. This allows the small bowel to distend, delaying the onset of obstructive symptoms and perhaps their acuteness.

Incomplete obstruction: If bowel is partially obstructed, clinical features are less distinct. Vomiting may be intermittent and the bowel habit erratic. Chronic incomplete obstruction leads to gradual hypertrophy of bowel wall muscle proximally and strong peristaltic activity causes bouts of colicky pain, often more severe than in complete obstruction. In thin patients, the pain is often accompanied by visible peristalsis, the hallmark of incomplete obstruction. The most common cause is a slowly progressively obstructing colonic cancer. Incomplete obstruction should not be called subacute obstruction as the term is misleading.

Physical signs of intestinal obstruction

General examination: Vomiting, diminished fluid intake and sequestration of fluid in the small bowel lead to dehydration. Gas-filled loops of bowel proximal to the obstruction produce abdominal distension; the more distal the obstruction, the greater the distension. Examination may also reveal signs of anaemia or lymphadenopathy attributable to the primary disorder.

Groin examination: It is essential that the groins are examined for hernias as the resultant bowel obstruction will not settle with conservative treatment. An obstructed femoral hernia is usually very small and rarely causes local symptoms or signs, even when strangulated. Hence it is easily missed if not specifically sought. Instead it produces the symptoms and signs of small bowel obstruction. This is an important clinical point—an obstruction due to an irreducible hernia will not settle with the usual conservative treatment.

Abdominal examination: On inspection, scars of previous operations provide a map of previous surgical disease, and raise the possibility of adhesive obstruction. On palpation, the most striking feature is the lack of abdominal tenderness except when strangulation has occurred. Obstruction with tenderness must be diagnosed as strangulation or perforation, necessitating urgent operation after fluid resuscitation. Note that a large obstructing abdominal mass may be palpable.

On percussion, the centre of the abdomen tends to be resonant and the periphery dull because bowel gas rises to the most elevated point, mimicking ascites. On auscultation, obstructive bowel sounds are traditionally described as loud and frequent, high-pitched and tinkling; in practice, bowel sounds may or may not be increased but have an echoing, cavernous quality or else can sound like the lapping of water against a boat. A succussion splash, heard on gently shaking the patient’s abdomen from side to side, may be heard in gastric outlet obstruction.

Radiological investigation of suspected bowel obstruction

The most useful initial investigation is a plain supine abdominal X-ray (see Figs 19.2 to 19.4). The pattern and distribution of bowel gas often indicates the approximate site of obstruction. In small bowel obstruction, fluid levels may be visible on an erect or decubitus X-ray. Measuring the bowel diameter on X-ray gives the degree of distension. (See Box 19.1 for norms.)

Fig. 19.2 Radiological appearances of obstructed bowel
(a) Supine abdominal film in a man of 67 presenting with vomiting and abdominal distension. The film shows mid small bowel obstruction. Dilated small bowel fills the upper left quadrant and centre of the abdomen, and can be identified by the valvulae conniventes (plicae circulares P) which extend across the whole width of the lumen. The small bowel distal to the obstruction is collapsed and is not visible on this film. The large bowel is also collapsed, with faecal loading of the ascending colon (F) and only a small amount of gas in the sigmoid colon (S). Note also the metallic tip of the nasogastric (NG) tube and the incidental radiopaque gallstone.
(b) Erect film showing multiple loops of dilated small bowel and multiple fluid levels. The obstruction was caused by a small carcinoma of the medial wall of the caecum encroaching upon the ileal opening. Note: erect abdominal films are rarely taken nowadays

Case History

Fig. 19.3 Radiological appearances of obstructed bowel
(a) Supine abdominal X-ray in a middle-aged man with several days of symptoms of small bowel obstruction. The abdomen is filled with grossly dilated small bowel loops. In addition, the small bowel wall is thickened, as shown by the apparent space between loops of bowel (arrowed); this is a characteristic feature of prolonged obstruction.
(b) ‘Instant’ contrast enema showing contrast filling the normal colon Co and distal ileum I which abruptly terminates at the obstruction (arrow). The obstruction proved at laparotomy to be caused by a band adhesion resulting from an operation for appendicitis 25 years previously

Case History

Fig. 19.4 Radiological appearances of obstructed bowel
Supine film of an elderly man showing gross caecal dilatation with loss of haustration (surface folds). In large bowel obstruction, this typically occurs if the ileocaecal valve remains competent—a condition that carries a high risk of perforation. In this case, the transverse colon T is dilated with gas and there is complete absence of colonic gas on the left side of the abdomen where the descending and sigmoid colon lies. From this, it can be deduced that the colon is obstructed near the splenic flexure. In fact, this patient had an obstructing carcinoma at the splenic flexure and the caecum had perforated, as shown by the presence of gas G in the extra-peritoneal tissues

Profound large bowel dilatation without small bowel distension is seen on X-ray in large bowel obstruction where the ileocaecal valve remains competent; this is a key determinant of the likely rate of deterioration of the patient. When the caecum reaches 10 cm, it is in imminent danger of rupture and an operation is needed urgently.

In large bowel obstruction of less acute onset, radiology helps demonstrate the site and nature of the obstruction (including sigmoid volvulus) and distinguish mechanical from pseudo-obstruction (see below). This may be a contrast enema but CT scanning is increasingly employed. CT scanning gives an indication of the level of obstruction but may not always give the precise diagnosis. Other useful information such as the presence of hepatic metastases may radically influence management, for example using a bowel stent to relieve the obstruction rather than operating.

The adynamic bowel

This is covered in Chapter 12.

Pseudo-obstruction of the colon

A form of adynamic bowel disorder peculiar to the large bowel is pseudo-obstruction although no mechanical obstruction is present. It can be caused by a range of apparently unrelated conditions that impair bowel peristalsis. These include retroperitoneal inflammation or haemorrhage, neurological conditions, biochemical abnormalities, certain drugs (e.g. anticholinergics), pregnancy and delivery, orthopaedic injuries or surgery (particularly in the elderly) and prolonged recumbency.

Physical signs are similar to those of mechanical obstruction except that bowel sounds are normal or inaudible. The diagnosis is based on the clinical findings and is confirmed if no mechanical obstruction is found on imaging.

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