Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice (51 page)
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Authors: Simon Paterson-Brown MBBS MPhil MS FRCS
Neutropenic enterocolitis, also known as typhlitis, is a potentially life-threatening condition characterised by an inflammatory process that usually involves the caecum and ascending colon. It occurs most often as a complication of chemotherapy and can progress to necrosis and perforation. Although it can affect any part of the small and large intestine, the cause of its predisposition for the right colon is unclear.
Clinical features include nausea, vomiting, abdominal pain, distension and diarrhoea, which can be bloody. Right iliac fossa tenderness and pyrexia are quite common and in later stages peritonitis may be present. CT is the diagnostic modality of choice and may reveal right-sided colon wall thickening, mesenteric stranding, pneumatosis and ascites (
Fig. 10.11
).
Figure 10.11
CT scan showing large retroperitoneal collection (indicated by arrows) secondary to acute necrotising enterocolitis with a delayed perforation of the posterior wall of the caecum and ascending colon.
Management demands careful evaluation of the patient, with each case treated individually. An initial conservative approach includes fluid and electrolyte replacement, broad-spectrum antibiotics, correction of any attendant coagulopathy and complete bowel rest with parenteral nutrition. The use of recombinant granulocyte colony-stimulating factor to correct chemotherapy-induced neutropenia should be considered. Colonic perforation and generalised peritonitis are clear indications for surgery. The operative procedure of choice is a right hemicolectomy, with either exteriorisation of the bowel ends or a primary anastomosis, depending on the extent of sepsis and peritoneal soiling. In general, most patients can be managed non-operatively.
Toxic colitis is a potentially fatal complication of inflammatory bowel disease, particularly if accompanied by megacolon. While several schemes exist to accurately identify toxic colitis, one reasonably simple system employs a definition that includes a disease flare-up accompanied by two of the following criteria: hypoalbuminaemia (< 3.0 g/dL), leucocytosis (> 10.5 × 10
9
cells/L), tachycardia (> 100 beats/minute), temperature elevation (> 38.6 °C).
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Use of this relatively objective definition may aid in the diagnosis and care of these patients, whose severe condition can be under-appreciated because of high dosages of steroids, immunomodulators or biological agents.
The initial management is directed at reversing physiological deficits with intravenous hydration, correction of electrolyte imbalances, and blood product transfusions. Free perforation, increasing colonic dilatation, massive haemorrhage, peritonitis and septic shock are indications for emergency operation after the patient has been adequately resuscitated. In the absence of these features, medical therapy is initiated with high dosages of intravenous corticosteroids, immunomodulators and/or biological agents. Broad-spectrum antibiotics directed against intestinal flora are prescribed to minimise the risk of sepsis secondary to transmural inflammation or microperforation. Anticholinergics, antidiarrhoeals and narcotics are avoided as they may worsen already impaired colonic motility or conceal ominous symptoms. Hyperalimentation may be started and the patient is closely observed with serial examinations and abdominal roentgenograms. Any worsening of the clinical course over the ensuing 24–72 hours mandates urgent laparotomy. If the patient improves minimally after 5–7 days of conventional therapy, the medical therapy should be altered or surgery should be advised. Experience with ciclosporin or infliximab in this setting is anecdotal, and should be weighed against operative therapy while understanding that surgery in this setting often relegates the patient to an ileostomy.
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The principal operative options in patients with toxic colitis are subtotal colectomy with end ileostomy or loop ileostomy with decompressive blowhole colostomy. The most difficult aspect of a subtotal colectomy is managing the distal bowel stump. The distal limb may be closed with sutures or staples and then delivered to the anterior abdominal wall, where it can lie without tension in the subcutaneous fat of the lower midline wound. If the bowel end is placed above the fascia, dehiscence of the rectal closure during the postoperative period results in a mucous fistula. If the closed stump is left within the peritoneal cavity, staple line dehiscence will produce a pelvic abscess. If the bowel wall is too friable to hold sutures or staples, creation of a mucous fistula is preferred. If there is inadequate residual bowel length to create a mucous fistula, many surgeons will place a catheter through the anus (e.g. Mallencott or Foley) to decompress the rectum and reduce the chance of a stump blowout.
The patient typically improves over the ensuing few days and can be discharged within a week of the operation. An appropriate elective procedure can be considered several months after the patient recovers.
Proctocolectomy with end ileostomy is rarely performed in the severely ill patient with toxic colitis because of the excessive rates of morbidity and mortality.
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Proctectomy increases the difficulty of the procedure and risks pelvic bleeding as well as autonomic nerve damage. In rare instances of rectal perforation or profuse colorectal haemorrhage, proctocolectomy may be an option. The surgeon must be cautioned, however, that the macroscopic and microscopic differentiation of ulcerative colitis from Crohn's proctocolitis is especially difficult in severe colitis, and primary proctocolectomy would nullify the future option of a restorative procedure in a patient with ulcerative colitis.
The need for loop ileostomy combined with decompression blowhole colostomy has virtually disappeared with improved medical recognition and more sophisticated management of toxic colitis. The operation is still useful in extremely ill patients or those in whom colectomy would be especially hazardous (e.g. contained perforation, high-lying splenic flexure and pregnancy). Contraindications to the procedure include colorectal haemorrhage, free perforation and intra-abdominal abscess. The operation is considered only a temporising procedure, and a definitive operation is commonly performed approximately 6 months later.
Stercoral perforation
The word
stercus
means dung or faeces. Perforation of the bowel caused by pressure necrosis from a faecal mass is a rare entity, first reported by Berry at the Pathological Society of London in 1894. Fewer than 100 cases have been reported in the literature, although this may reflect the poor outcome (with mortality rates approaching 50%), an increasing reluctance to publish case reports and ill-defined diagnostic criteria. There appears to be an equal incidence in men and women and the median age for these patients is said to be 60 years.
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Reported predisposing factors have included chronic constipation, megacolon, scleroderma, hypercalcaemia, renal failure and renal transplantation. Medications associated with stercoral perforation include narcotics, postoperative analgesia, antacids, calcium channel blockers and antidepressants. Only 11% of cases are accurately diagnosed prior to operation,
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with investigations frequently non-contributory. Perforations usually occur on the antimesenteric border, with the majority occurring in the sigmoid colon and rectosigmoid region. Multiple perforations are found in about one-fifth of patients, with the remaining patients usually having ulceration extending away from the perforation.
The suggested clinicopathological diagnostic criteria are:
A round or ovoid colonic perforation exceeding 1 cm in diameter.
Faecolomas present within the colon.
Microscopic evidence of pressure necrosis or ulcer and chronic inflammatory reaction around the perforation site.
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This study, which constitutes one of the largest single-institution reports on stercoral perforation of the colon, defined strict clinical and pathological criteria for its diagnosis. Using these criteria stercoral perforation of the colon would appear to occur more frequently than previously reported in the literature.
Management of these patients is surgical, with the resection margins sufficiently wide to encompass all areas of perforation or impending perforations. The bowel is universally loaded with stool and the tendency towards constipation is not removed by a limited resection. The operation should involve resection of the affected segment and exteriorisation of the bowel for left-sided perforations, with resection and primary anastomosis being reserved for those patients with a right-sided perforation. The risk of recurrent perforation in the proximal colon presents a further problem for those with a left-sided perforation. Milking the stool in an antegrade direction into the resected segment and orthograde colonic irrigation may combine to avoid early re-perforation. However, the fear of recurrent perforation from persistent constipation has led some surgeons to suggest a subtotal colectomy.
Breakdown of an anastomosis is one of the most significant complications after large-bowel surgery. The presentation can be insidious but more commonly the patient becomes acutely ill, particularly if there is generalised peritonitis. If the diagnosis is not made and appropriate treatment undertaken, death is likely to follow. There is no doubt that the presence of anastomotic leakage significantly increases mortality and one study noted a mortality rate of 22% in 191 patients who had leakage after large-bowel anastomosis compared with only 7.2% in 1275 patients without a leak.
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In the patients who survive this serious complication, morbidity and hospital stay are greatly increased.
A variety of general and local causative factors of anastomotic dehiscence have been described. General factors listed usually include poor nutritional state, anaemia, uraemia, diabetes, steroid administration and old age, while suggested local factors involved tension, ischaemia or infection of the anastomosis. The risk of anastomotic leakage in low colorectal anastomosis is several times higher than in either ileocolic or colocolic anastomosis. In one report a clinical leak rate for ileocolic and colocolic anastomosis was 0.4%, whereas the leak rate after low colorectal anastomosis was 4.7%.
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In a review of 477 large-bowel anastomoses, which included 215 colorectal anastomoses, there were eight colorectal and one ileocolic leaks. All nine patients required laparotomy, and seven were salvaged with no mortality. Three colorectal leaks (small posterior defects in stapled anastomoses) were closed with interrupted endoanal sutures and a proximal loop stoma fashioned in two patients who did not already have one. The other two leaks (defect in suture line attributable to a single suture cutting through) were managed by creating a controlled external fistula. None of these patients had further complications and all the stomas were subsequently closed. It is therefore possible to salvage anastomotic leaks with a good outcome in selected patients with appropriate operative treatment.
Another important factor in dehiscence is the oxygen tension at the bowel ends used for the anastomosis. In an elegant study reported in 1987, it was shown that if tissue oxygen tension in the ends of bowel to be anastomosed fell to less than 20 mmHg (2.66 kPa), there was a high likelihood of anastomotic breakdown.
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However, a significant factor in anastomotic failure is poor surgical technique, irrespective as to whether sutures or staples are used.
In general, the clinical features of anastomotic dehiscence will depend on whether the leak is localised or more extensive, causing generalised peritonitis. At one end of the spectrum, when sepsis associated with the leak is localised, the patient may have minimal symptoms and only a few physical signs. There may be ‘flu-like’ symptoms of feeling vaguely unwell with shivering and nausea. If the anastomosis lies low in the pelvis, there may be some lower abdominal pain and tenderness and on rectal examination a defect can often be felt in the anastomosis. Tachycardia is a common general feature and is often associated with pyrexia. If a drain is still in situ, faecal material or pus may be seen.
At the other end of the spectrum the scenario is associated with a major leak, when faecal material or pus has leaked into the general peritoneal cavity. The effect on the patient is usually profound. Abdominal pain is difficult to control and tachycardia and tachypnoea are common. The temperature is raised and hypotension is often a feature. The patient is distressed and sweaty and on abdominal examination the abdomen is tender with abdominal guarding. Sometimes the features of even an extensive leak can be more insidious, with the patient not making progress as rapidly as expected and suffering abdominal pain that is vague rather than dramatic.
Delay in diagnosis of large-bowel anastomotic leakage is still a major problem and leads to increased morbidity and mortality. It is crucial that surgeons are vigilant about deterioration of any patient who has a large-bowel anastomosis and maintain a low threshold for ordering investigations to identify a leak. It should be remembered that the anastomosis may leak any time during the first 2–3 weeks after operation.
Usually the white blood count is elevated, except in patients who have overwhelming sepsis, when it may be either normal or even low. However, the earliest derangement in the white blood count is an increase in the less mature polymorphic neutrophils (e.g. left shift). Erect chest radiograph or abdominal films will sometimes show gas under the diaphragm, but this sign is of debatable significance in the first few days after the original operation because of the presence of intra-abdominal air introduced at the time of operation. The absence of pneumoperitoneum should not discourage the clinician from pursuing investigations to check the integrity of the anastomosis.
Ultrasound examination can be helpful in the patient with a suspected collection of pus related to anastomotic leakage, but the value of this investigation is often impaired by the presence of dilated gas-filled loops of bowel, with dressings and drains on the abdomen further increasing technical difficulties. CT or contrast studies are the investigation of choice.
Water-soluble contrast enema is a simple investigation for assessing anastomotic leakage, particularly on the left side of the large bowel. Another option is a pelvic CT scan with rectal contrast. In addition to demonstrating whether a leak has occurred, assessment of the extent of leakage is of value in deciding the overall management. It is important to be aware of two caveats, however. Occasionally, when the contrast study shows no leak, a later investigation will show one. The corollary of this is also sometimes true. The enema or scan may show a leak that is of no clinical consequence (radiological leak). It is therefore important to look at the overall clinical picture and attempt to assess all the clinical and radiological evidence before coming to a final conclusion about the presence of a clinically significant leak.
Although the literature on colonic anastomotic leak rates is extensive, there is a paucity of information on how to treat the leakage. It is best to consider the management of localised leakage separately from those who present with generalised peritonitis. Most patients with
localised leakage
can be treated non-operatively with bowel rest and antibiotic therapy. If there is a large collection of pus around the anastomosis, it is usual to drain this percutaneously under ultrasound or CT guidance. Patients with
generalised peritonitis
from a large-bowel anastomotic leak are usually dramatically ill and require resuscitation. Assuming that investigations have been performed and the diagnosis confirmed, the next step is to improve the patient's condition before surgical intervention.
Haemodynamic status needs to be assessed and treatment given to improve cardiac and respiratory function. Parenteral antibiotic administration is a priority and inotropic support may be necessary. Adequate pain control is important and these patients are best managed in a high-dependency unit or intensive therapy unit. Anaesthesia is alerted and only when the patient's condition is stabilised is operation undertaken.
The patient is usually placed in the lithotomy/Trendelenburg position. The previous midline incision is reopened and great care is taken not to damage adherent loops of small intestine. Bowel loops are dissected free and the area of anastomosis exposed. Faecal material and pus are removed from the peritoneal cavity and pelvis. Occlusion clamps are gently placed on bowel above and below the leaking anastomosis to limit further contamination. Extensive lavage of the peritoneal cavity is performed with saline or antibiotic solution.
The next steps depend on the size and location of the anastomotic defect. In the majority of cases, the anastomosis is taken apart and the proximal end of bowel is brought out as an end stoma and the distal end as a mucous fistula. If the distal stump is not long enough to be brought out on the abdominal wall, it should be closed carefully using a series of interrupted seromuscular sutures. Some surgeons will place a transanal drain to decompress the bowel. Surgeons must be aware that the more distal the leak, the lower the chances of bowel continuity being restored at a later date.
In selected patients (usually those with a small defect in a low colorectal anastomosis), the anastomosis may be salvaged. A defunctioning ileostomy can be constructed for diversion and the area of the leak can be drained. However, the faecal loading in the colon can lead to continued soiling unless it is removed with transanal irrigation. However, in a patient who has already had an anastomotic leak it is poor practice to risk a further leak and the patient's safety should be the prime objective.
The perforation rate at colonoscopy is now generally agreed to be about 1 in 500, varying with the level of intervention employed.
There are three proposed mechanisms for colonoscopic perforation:
mechanical perforation directly from the colonoscope or biopsy forceps;
barotrauma from overzealous air insufflation;
perforations occurring as a result of therapeutic procedures (use of energy sources).
Measurement of forces exerted during colonoscopy has only been reported in one paper from the Royal London Hospital,
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where an electronic device was used in a research setting. The caecum and right colon are most susceptible to barotrauma, although diverticula can also be directly inflated. The use of carbon dioxide for insufflation may decrease perforation rates and increase levels of patient comfort. Therapeutic interventions such as polyp removal with a hot biopsy or snare and balloon dilatation of strictures are, not surprisingly, associated with a higher risk of perforation.
The most common site of perforation is the sigmoid colon. Signs and symptoms of a perforation are not always obvious at the time of colonsocopy. In retrospective studies, the diagnosis of a perforation is delayed in about 50% of patients.
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If the endoscopist is worried after an examination has been completed, an erect chest radiograph should be ordered as a screening test and the patient observed until symptoms have settled. In cases where there is a high index of suspicion, a water-soluble enema or CT scan with contrast can be used to confirm the diagnosis.
Non-operative treatment with close observation, intravenous fluids and antibiotics may be possible in selected patients.
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The authors' approach is presented in
Fig. 10.12
. A large defect or symptoms of peritoneal contamination will usually require operative treatment. If the injury is operated upon early, a direct repair of the defect or small resection and a primary anastomosis is possible. It may also be possible to effect the repair laparoscopically. With delayed diagnosis or clinical deterioration during observation, patients will usually require a temporary defunctioning stoma.
Figure 10.12
Algorithm for the management of colonoscopic perforation.