Read Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice Online
Authors: Simon Paterson-Brown MBBS MPhil MS FRCS
Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice (44 page)
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developed pancreatic infection compared with seven patients in the control group (
P
= 0.023).
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Peter Lamb
Acute disease of the small bowel, from which appendicitis is considered separately, contributes substantially to the workload of the general surgeon and often patients will present as emergencies. There are many causes of acute small-bowel disease and disease in any intra-abdominal organ or the peritoneum may involve the small bowel secondarily. The pattern of acute small-bowel disease varies with the age of the patient: some conditions are more common in young people, others in an older population. The incidence of acute surgical small-bowel pathology is difficult to estimate but is probably second to appendicitis as the site of disease requiring urgent surgical intervention. Acute small-bowel disease manifests itself in one of three main ways: (i) obstruction, (ii) peritonitis and (iii) haemorrhage. These categories are not mutually exclusive and more than one type of process may exist in each clinical episode. Treatment of small-bowel disease may be operative or conservative, and the timing of surgical intervention requires as much consideration as the causes and specific treatment of small-bowel disease.
Although there are many causes of small-bowel obstruction (
Box 9.1
), the commonest cause in the developed world is adhesions secondary to previous surgery (approximately 60% of episodes), followed by malignancy. By comparison, in the developing world the most common cause is hernia. A large retrospective study using Scottish National Health Service data estimated that 5.7% of all hospital admissions following abdominal and pelvic surgery over a 10-year period were directly related to adhesions.
1
In order to avoid unnecessary surgery and to ensure the correct surgical approach is employed, an attempt should be made to diagnose the cause of the obstruction preoperatively where possible, or at least to eliminate conditions that might require special treatment. In practice, however, the cause of the obstruction is often diagnosed at operation. A retrospective study of 102 patients undergoing surgery for adhesive small-bowel obstruction carried out between 1987 and 1992, and followed up for 14 years, reported that a total of 273 further episodes of obstruction occurred, requiring 237 hospital admissions.
2
Nearly half of these further episodes resulted in more surgery.
Box 9.1
Causes of small-bowel obstruction
Within the lumen
Gallstone
Food bolus
Bezoars
Parasites (e.g.
Ascaris
)
Enterolith
Foreign body
Within the wall
Tumour
Primary
Small-bowel tumour
Carcinoma
Lymphoma
Sarcoma
Carcinoma of caecum
Secondary
Inflammation
Crohn's disease
Radiation enteritis
Postoperative stricture
Potassium chloride stricture
Vascultides (e.g. scleroderma)
Outside the wall
Adhesions
Congenital
Bands
Acquired
Postoperative
Inflammatory
Neoplastic
Chemical (e.g. starch, talc)
Pharmacological (e.g. practolol)
Hernia
Primary
Congenital (e.g. diaphragmatic)
Acquired (e.g. inguinal, femoral, etc.)
Secondary
Incisional hernia
Internal postoperative hernia (e.g. lateral space, mesenteric defect)
The small bowel responds to obstruction by the onset of vigorous peristalsis. This produces colicky pain, usually in the central abdomen, as the small bowel is of midgut embryological origin. As the obstruction develops, the proximal intestine dilates and fills with fluid, producing systemic hypovolaemia. Further fluid is lost through vomiting, which occurs early if the obstruction is proximal. As the process continues the risk of complications increases and if the blood supply is compromised, infarction and perforation will occur. If the blood supply remains intact and the bowel is readily decompressed by vomiting and subsequent nasogastric drainage, peristalsis will eventually stop, leaving grossly dilated, non-functioning bowel. In the former scenario the pain, initially colicky, will become continuous, whereas in the latter even the colicky pain may cease as peristalsis stops.
The typical clinical presentation of small-bowel obstruction is central abdominal colicky pain, vomiting (often bile stained), abdominal distension and a reduction or absence of flatus. Vomiting may be less of a feature and a greater degree of abdominal distension observed if the blockage is in the distal ileum – in which case the vomiting often becomes ‘faeculant’ as the stagnant small-bowel contents become degraded by bacterial colonisation. Bowel sounds increase and may be audible to the patient. Localised peritonitic pain and tenderness may develop and this suggests incipient strangulation. In some patients there may be an obvious causative feature such as an irreducible hernia. The presence of surgical scars is important, as is any history of previous intra-abdominal pathology.
Although small-bowel obstruction can occur without the development of abdominal pain, the absence of this symptom should be viewed with caution. This is particularly the case in postoperative patients, where small-bowel obstruction and intestinal ileus can be difficult to differentiate. The history and examination of the patient should be sufficiently detailed to allow a diagnosis of small-bowel obstruction and to determine possible causes. Complicated small-bowel obstruction, with ischaemia or perforation, should be readily detectable by marked abdominal tenderness. It is essential to assess the patient's general state, particularly the degree of dehydration and its effect on the patient, so that adequate resuscitation is undertaken prior to any planned surgical treatment.
The aim of management is to adequately resuscitate patients, confirm the diagnosis and to identify possible bowel strangulation before gangrene and perforation occurs, so that early surgery can be arranged. There is less urgency in the recognition of non-strangulating obstruction, and a period of decompression and intravenous fluid resuscitation may allow resolution to occur without surgery. However, failure of the obstruction to resolve after 48–72 hours is usually an indication for surgical intervention.
The first step in management is fluid resuscitation and patients often require several litres of normal saline with potassium supplementation or Hartmann's solution in the first few hours after admission. Patients with a long history are likely to be severely dehydrated, with an alkalosis and associated hypokalaemia, the former due to loss of hydrogen ions in the vomit and the latter from renal compensation. Urinary catheterisation is essential to monitor response to resuscitation and measurement of central venous pressure can be helpful in the elderly, particularly those patients with coexisting morbidity. Adequate fluid replacement should be given before any surgical intervention is planned and can be given rapidly if required, even in the elderly, provided appropriate monitoring is used (see also
Chapter 16
).
Decompression of the stomach with a nasogastric tube will reduce vomiting in most patients, help to decompress the bowel and reduce the risk of airway contamination from aspiration. Fluid lost from the nasogastric tube should be replaced with additional intravenous crystalloids (normal saline or Hartmann's solution) and potassium supplements. Analgesia should be given early and in adequate doses, with opiates the most commonly used. This will not mask signs of peritonitis and there is no justification for withholding adequate analgesia while waiting for further clinical assessment
3
(see also
Chapter 5
). However, the analgesia requirement should be reviewed regularly, especially in the early stages of management, as a persistent requirement for increasing amounts of opiate analgesia is a strong sign that underlying strangulation is a possibility and surgery indicated. Again, as in all emergency patients, antithromboembolic prophylaxis should be commenced early and continued until resolution (see
Chapter 14
).
The investigations undertaken in patients with small-bowel obstruction are aimed at:
assessing the general state of the patient;
confirming the diagnosis of small-bowel obstruction;
identifying which patients should undergo early surgery (those with a high risk of strangulation) and those in whom a non-operative approach is appropriate.
Radiological investigations are discussed in detail in
Chapter 5
. Contrast-enhanced computed tomography (CT;
Fig. 9.1
) is increasingly used in the early assessment of patients with small-bowel obstruction, both to identify the underlying cause (particularly malignancy) and to identify features of possible strangulation. CT features of intraperitoneal free fluid, mesenteric oedema and lack of the ‘small-bowel faeces sign’, in combination with a history of vomiting, have been reported to be highly predictive of requiring operative intervention.
4
There is also evidence to support the role of oral contrast studies, with the passage of contrast to the colon at 4 hours being a good predictor that obstruction will resolve with non-operative treatment.
5
The current view is that, although these tests may aid management, identifying patients with possible strangulation remains difficult, and the surgeon must base much of the decision-making on clinical assessment.
Figure 9.1
Multislice CT scan with intravenous contrast demonstrating small-bowel obstruction.
With thanks to Dr Dilip Patel, Consultant Radiologist, Royal Infirmary, Edinburgh.
Intravenous fluids and nasogastric aspiration are the two components of the ‘drip and suck’ regimen, which is the first-line treatment for most patients with obstruction, particularly when the underlying cause is thought to be adhesions, as spontaneous resolution will occur in the majority. As mentioned earlier, this treatment plan should be abandoned at the first suggestion of underlying strangulation. Although non-operative management can be continued for several days in the absence of any suggestion of strangulation, surgical exploration is generally indicated if the obstruction fails to resolve after 48–72 hours. In some patients with known extensive adhesions from multiple previous explorations, it might be worth waiting longer and if so attention should be paid to nutritional support, sometimes necessitating insertion of a central line for parenteral feeding (see
Chapter 17
).
In the absence of clinical or CT signs (free fluid, mesenteric oedema, small-bowel faeces sign, devascularised bowel) of strangulation, or patients with partial obstruction, initial non-operative management is appropriate. These patients are good candidates for a trial of water-soluble contrast medium with both diagnostic and therapeutic purposes. The appearance of water-soluble contrast in the colon on X-ray within 24 hours from administration predicts resolution. In the absence of signs of strangulation or peritonitis non-operative treatment can be prolonged up to 72 hours (Bologna Guidelines for Diagnosis and Management of Adhesive Small Bowel Obstruction – 2010).
6
The particular circumstances of any given patient determine the need for surgical intervention, but some of the commonest features in decision-making are listed in
Box 9.2
.
Box 9.2
Small-bowel obstruction: indications for surgery
Absolute indication (surgery as soon as patient resuscitated)
Generalised peritonitis
Visceral perforation
Irreducible hernia
Localised peritonitis
Relative indication (surgery within 24 hours)
Palpable mass lesion
‘Virgin’ abdomen
Failure to improve (continuing pain, high nasogastric aspirates)
Trial of initial conservative treatment (with further investigations)
Incomplete obstruction
Previous surgery
Advanced malignancy
Diagnostic doubt (possible ileus)
Once a decision to operate has been made, patients should be fully resuscitated, treatment of comorbidity optimised and the stomach emptied with a nasogastric tube. The wide range of possible surgical procedures should be explained to the patient. Prophylactic antibiotics and antithromboembolic prophylaxis (if not already started) should be administered.
Generally, a midline incision is the most flexible when the diagnosis is unknown. If the patient has a previous midline incision, this should be excised and extended cranially or caudally so that the peritoneal cavity can be entered through a ‘virgin’ area. Loops of small bowel may be densely adherent to the back of the old scar and attempts to enter the peritoneal cavity through this area can result in an inadvertent enterotomy. This is clearly best avoided, particularly if the bowel wall is grossly distended, friable and diseased.
Having entered the abdominal cavity, the first step is to identify the point at which the dilated bowel proximal to the obstruction changes to collapsed distal bowel. It is important to demonstrate that such a change is present as this confirms the diagnosis of mechanical obstruction and identifies the obstructing point. The presence of uniformly dilated small bowel, or no definite point of change in diameter of the bowel, suggests that the clinical diagnosis of mechanical obstruction may be incorrect. Dilated bowel can be decompressed, usually by milking the contents proximally and aspirating via a large-bore nasogastric tube. If the small-bowel contents will not easily pass to the stomach or the bowel is so friable that retrograde decompression might produce a tear, then a suction catheter may be inserted through a small enterotomy. Where possible this should be carried out through non-diseased bowel. Decompression is particularly useful in distal obstruction when a large number of dilated loops can be difficult to handle and make subsequent abdominal closure difficult. The fluid within the bowel makes it heavy and if it is removed from the abdominal cavity, it should be handled with care so that the mesentery is not damaged. The large surface area of dilated loops results in considerable insensible fluid loss and if it is anticipated that the viscera will lie outside the abdominal cavity for a significant length of time, it should be placed in a waterproof ‘bowel’ bag or wrapped in moist swabs.
Having identified the point of obstruction, the cause is dealt with. If it is due to adhesions, they should be divided as completely as possible. Although it is not necessary or helpful to divide every last adhesion within the abdomen (as these will inevitably re-form), enough should be divided to confirm that there remains no possible site of obstruction between the duodenojejunal (DJ) flexure and the caecum. It is essential to recognise the patient in whom the clinical diagnosis of mechanical small-bowel obstruction is incorrect, as the presence of adhesions does not in itself confirm the diagnosis.
The small bowel should be resected if it is clearly ischaemic or there is disease or narrowing in the bowel at the point of obstruction, and an anastomosis may be carried out if both ends of the bowel are healthy. If the viability of a segment of bowel is unclear then it should be wrapped in warm moist swabs for several minutes and re-examined. Where viability remains in doubt it should be resected. Even after removing the obstruction, exteriorisation of the bowel may be indicated if there is generalised disease of the bowel and when an anastomotic dehiscence might be more likely. An ileostomy may be indicated in patients with Crohn's disease as part of their long-term management, and the possibility of such a step should be recognised, considered and discussed with the patient before undertaking the laparotomy. When the viability of large sections of bowel is unclear or the patient is unstable a reasonable option is to resect clearly ischaemic bowel and return the stapled ends to within the abdomen. A planned re-look laparotomy is then performed at 24–36 hours, when either an anastomosis or exteriorisation of bowel ends can be performed, depending on the patient's condition.
There has been considerable research aimed at reducing the development of further adhesions after surgery. There is some evidence that the intraperitoneal administration of icodextrin 4% solution (ADEPT®) at the end of surgery reduces intra-abdominal adhesion formation and the risk of re-obstruction. In a randomised trial the small-bowel obstruction recurrence rate was 2% (2/91) in the icodextrin groups versus 11% (10/90) in the control group after a mean follow-up period of 41.4 months (
P
< 0.05). However, no difference was found in the need for laparotomy.
7
Abdominal closure should be carried out using a mass closure technique. There are some patients with gross obstruction or repeated procedures in whom, even after relief of obstruction, the oedematous bowel makes closure impossible. In these patients the use of a vacuum-assisted closure dressing or prosthetic mesh to allow temporary closure, with subsequent removal and formal closure a few days later, should be considered. If at subsequent surgery it is still not possible to approximate the fascial edges, alternative techniques can be used: the mesh can be left in situ and the wound edges mobilised and closed over the top; a component separation technique can be used to allow fascial closure; or vacuum-assisted closure dressings can be continued and the abdomen managed as a laparostomy. Further discussions on abdominal sepsis and dehiscence are covered in
Chapter 18
.