29 Large Bowel Obstruction
Abstract
Acute large bowel obstruction is a common surgical emergency associated with high morbidity and mortality. Symptoms include abdominal distension and constipation. Survival is maximized by appreciation of the etiology and pathophysiology of large bowel obstruction along with the risks of various treatment options.
29.1 Introduction
Acute large bowel obstruction is a common surgical emergency associated with high morbidity and mortality rates unless treatment is expedient. Large bowel obstruction can be defined as an impediment to the passage of intraluminal contents in the colon and/or rectum resulting in abdominal distension and constipation. Patients are often elderly and unwell. The chances of survival will be maximized if one appreciates the etiology and pathophysiology of large bowel obstruction along with the risks of various treatment options.
The most common cause of large bowel obstruction in adults (78%) is adenocarcinoma of the colon and rectum. 1 It is followed by benign conditions, including diverticulitis, colonic volvulus, metastatic cancer, and inflammatory bowel disease. 1 Of note, the etiology of large bowel obstruction varies worldwide, as does the patient population affected. In Africa and India, the primary cause of large bowel obstruction is volvulus (60%) affecting patients who are young and fit. 2
29.2 Mechanical Large Bowel Obstruction
29.2.1 Etiology and Pathophysiology
Large bowel obstruction can be divided into mechanical and nonmechanical causes (pseudo-obstruction). In this section, we will focus on mechanical causes and the pathophysiology; pseudo-obstruction will be discussed later.
Mechanical large bowel obstruction causes changes in intestinal motility, the intraluminal colonic milieu, and colonic blood flow. Proximal to the site of obstruction, the bowel becomes dilated and fluid is sequestered due to disturbed reabsorption. Up to 10 L of fluid can be sequestered into the bowel over a 24-hour period and major fluid loss can occur. This is made worse by limited oral intake and vomiting. There is decreased intravascular volume and electrolyte disturbance, which causes hypovolemic shock.
Initially, peristaltic activity may be increased in an attempt to overcome the obstruction, with the patient experiencing colicky abdominal pain. With time, the intestinal smooth muscle becomes enervated and peristalsis stops. The bowel empties distal to the obstruction (the patient can present with diarrhea initially), before becoming collapsed. In cases where adynamic obstruction occurs, abdominal discomfort is secondary to the distension due to the reduced or absent peristaltic activity.
Systemic inflammatory response syndrome (SIRS) supervenes as the intraluminal pressure increases, causing microvascular changes with loss of mucosal integrity and translocation of bacteria into the bloodstream.
With worsening distension of the bowel wall, venous return becomes disrupted and leads to progressive congestion, loss of fluid into bowel lumen, and third space (due to the leakage of serosal fluid into the abdomen causing ascites). Intestinal ischemic occurs with worsening venous engorgement that jeopardizes the arterial inflow into the capillary bed. Eventually, the bowel wall becomes necrotic and perforation occurs.
In “closed-loop” obstruction, two limbs of the bowel are involved and obstructed. This can occur when a loop of bowel is trapped by a band adhesion or an internal hernia. In this situation, increase in distension and intraluminal pressure will be swift with sudden vascular occlusion.
The most common cause of mechanical large bowel obstruction is primary colonic carcinoma. Buechter et al 1 reported 127 patients presenting with large bowel obstruction with 90% being due to colonic carcinoma. ▶ Table 29.1 lists the causes of mechanical large bowel obstruction including rare causes such as diverticular disease, hernia, inflammatory bowel disease, foreign body, colonic intussusception, and deep penetrating endometriosis.
Causes of mechanical large bowel obstruction |
Primary colonic carcinoma (60–80%) |
Volvulus (11–15%) |
Diverticulitis (4–10%) |
Hernia |
Inflammatory bowel disease |
Intraluminal foreign body |
Extrinsic compression from masses (benign or malignant) and abscesses |
Colonic intussusception |
Diaphragmatic disease of the colon |
Deep penetrating endometriosis |
Iatrogenic causes |
Postoperative adhesions |
Radiation stricture |
Anastomotic stricture |
Carcinoma
Large bowel obstruction due to carcinoma is not common. In a series of 908 cases, Serpell et al 3 reported that 16% of patients presented with complete obstruction and 31% had partial obstruction. Of 4,583 patients in the Large Bowel Cancer Project in the United Kingdom, obstruction was noted in 16%. 4 In this series, the splenic flexure was the site of obstruction in 49% of cases, followed by the left colon (23%), the right colon (23%), and the rectum and rectosigmoid colon (6%). In the series by Buechter et al, 1 the sigmoid colon was the most common site of obstruction, accounting for 38%, followed by the descending colon, splenic flexure, transverse colon, rectum, cecum, ascending colon, and hepatic flexure. The sigmoid colon was also noted by Kyllönen 5 as the predominant site of obstruction. Due to the fact that the lumen of the sigmoid and descending colon is smaller and the stool more solid in this region, obstruction in the left colon manifests earlier than that caused by obstruction in the right colon.
Volvulus
Approximately 10 to 15% of large bowel obstruction is due to acute colonic volvulus. 6 Volvulus is an axial rotation of a segment of bowel about its mesentery. It is improbable for the volvulus to settle without intervention if the twist is greater than 360 degrees. Narrowing at the site of torsion produces signs and symptoms of obstruction. The torsion of the mesentery causes vascular compromise at the site of volvulus, which leads to ischemia, necrosis, and perforation.
Sigmoid volvulus is three to four times more prevalent than cecal volvulus (60–75 vs. 25–33%, respectively). It is rare to acquire a volvulus at the transverse colon or splenic flexure (< 1%). 7 , 8 A very mobile redundant colon on a mesentery and a fixed point about which the colon can twist are usually the main precipitating factors leading to a colonic volvulus. Sigmoid volvulus commonly occurs in the elderly, who tend to have poor mobility and a history of constipation, as well as a chronically dilated and elongated sigmoid colon. Volvulus is associated with certain comorbidities such as Parkinson’s disease, Alzheimer’s disease, and multiple sclerosis. Electrolyte disturbance, particularly hypokalemia, should be excluded. Studies have also shown that a high dietary fiber intake is associated with sigmoid volvulus and this might explain why volvulus is the most common cause of bowel obstruction in Africa and India. 9 Factors that provoke a dilatation of the right colon, such as pregnancy and colonoscopy, can increase the risk of cecal volvulus (Chapter 28). 10
Diverticular Disease
Some degree of colonic obstruction occurs in approximately two-thirds of the patients with acute diverticulitis. This partial obstruction is usually caused by inflammation with spasm and edema together with an element of adynamic ileus. Complete obstruction occurs in approximately 10% of cases and is the second most frequent cause of acute colonic obstruction. Complete obstruction usually implies abscess formation with encroachment of the lumen or repeated episodes of diverticulitis with fibrosis and stenosis.
Large bowel obstruction caused by diverticulitis can occur at any location, but the most common location is the sigmoid colon (▶ Fig. 29.1). In Asian countries, however, it is not uncommon for obstruction to occur in the right colon. 11 In patients presenting with a first attack of diverticulitis, it is recommended that they undergo visualization of the colon, usually by colonoscopy, to exclude a coexisting carcinoma that may then present as obstruction (Chapter 25). 12
Hernias
Hernias tend to be associated with small bowel obstruction and less commonly are a cause of large bowel obstruction. However, large bowel obstruction can occur secondary to inguinal, femoral, umbilical, Spigelian, incisional, lumbar, and diaphragmatic hernias. 8 The most common internal hernia to produce large bowel obstruction involves the foramen of Win-slow hernia, a condition in which small bowel, and in one-third of cases the right colon, herniate through the normal communication between the greater and lesser peritoneal cavities, between the free edge of the lesser omentum and the hepatoduodenal ligament. 13
Crohn’s Disease
Colonic involvement with Crohn’s disease occurs in about 20 to 50% of patients. 14 , 15 Colonic obstruction in patients with Crohn’s disease is usually due to strictures formed after repeated attacks of transmural inflammation of the colon causing fibrosis and scarring. Symptoms of progressive bowel obstruction become apparent as the bowel becomes strictured and the lumen narrows. Patients with Crohn’s disease have a two to three times higher risk of developing colon carcinoma compared with age-matched standard population. 16 It is therefore important to exclude malignancy in such patients.
Intraluminal Contents
The rectum (70%) and sigmoid colon (20%) are the most common sites of colonic obstruction due to intraluminal contents such as bezoars (▶ Fig. 29.2). 7 , 8 The most likely causes include gallstones, enteroliths, intentionally inserted foreign body, medications, and illegal drugs. Fecal impaction is seen the most frequently in the elderly, the chronically debilitated patients, and among patients taking constipating medications, such as opiates. 6 , 17
External Compression
External compression of the bowel, usually from adjacent masses, can cause large bowel obstruction. The possible underlying causes are extensive and include endometriosis, lymphadenopathy, pancreatitis, intra-abdominal abscess, peritoneal carcinomatosis, and direct invasion from gynecologic or prostatic malignancies. 6
Intussusception
Intussusception is the invagination (telescope or accordion) of a proximal segment of the bowel (intussusceptum) into an adjacent distal segment (intussuscipiens). 18 As the intussusceptum enters the intussuscipiens, the mesentery is carried with it and becomes trapped between the overlapping layers of the bowel. This causes vascular compression with eventual ischemic necrosis unless timely intervention is undertaken. The classic CT appearance of intussusception (▶ Fig. 29.3) includes the following:
Target appearance (intraluminal soft tissue mass and eccentric fat density).
Reniform pattern (bilobed density with peripheral high-density attenuation and low attenuation centrally).
Sausage pattern (alternating areas of low and high attenuation related to the bowel wall, mesenteric fat and fluid, intraluminal fluid, contrast material or air). 19
Adult intussusception is rare. In 30 years at Massachusetts General Hospital in Boston, there were 58 cases of surgically proven adult intussusception. 20 Adult intussusception accounts for 1 to 5% of all intestinal obstruction and 5% of all intussusceptions; the other 95% of intussusceptions occur in children. 20 , 21 In adults, approximately 90% of the cases are secondary to a definable lesion, while in children the opposite is true. 20 , 21 In adults, primary colon carcinoma is the most common cause, 22 followed by a number of benign pathologies, including lipomas and adenomatous polyps. 23 Various other lesions have been described as a cause for colonic intussusception, including gastrointestinal stromal tumors and a variety of appendiceal lesions, such as an inverted appendiceal stump, endometriosis involving the appendix and mucocele of the appendix 24 , 25 . Other reported causes of colonic intussusception include eosinophilic colitis, pseudomembranous colitis, and epiploic appendagitis. 22 , 26 , 27 , 28
Adult intussusception can occur at any age, with a mean of 47 to 54 years. 20 , 21 Of the 58 cases reported by Azar and Berger, 20 44 were small bowel and 14 colonic; 48% of the small bowel lesions were malignant, compared with 43% of the colonic lesions. Intussusception may present as acute or chronic.
Diaphragmatic Disease of the Colon
Debenham was the first to describe nonsteroidal anti-inflammatory drug (NSAID) induced enteropathy. 29 Lang et al reported evidence of ulceration and stricture formation in the small bowel in long-term users of NSAIDs 30 and it was subsequently referred to as “diaphragm disease.” The condition is thought to occur due to NSAID-induced inhibition of prostaglandins in the bowel mucosa. 31 Newer preparations of NSAIDs, such as the “slow release” or “modified release” agents, have some protective effect against the upper gastrointestinal side effects of NSAIDs. As a result, there is an increasing incidence of colonic enteropathy, although this is still rare.
Diaphragmatic disease of the colon is more prevalent in women and is commonly seen in patients in their seventh decade of life. Patients usually present chronically rather than acutely. Symptoms tend to relate to loss of blood and protein from these ulcers. Stricturing can occasionally cause large bowel obstruction.
Histological analysis of the diaphragms typically shows areas of ulceration and granulation, supporting the reactive theory of “healing by fibrosis.” 32 , 33 , 34 Several studies have shown that colonic enteropathic ulceration can progress to diaphragm disease on serial follow-up. 35 The presence of a circumferential “rim ulcer” seen at the edge of the diaphragms suggests that the luminal contents containing active NSAID products come into contact with the diaphragmatic orifice. 36 To differentiate diaphragms from a prominent plica fold, it is essential to identify the histological hallmark of submucosal fibrosis with intact muscularis propria. Collagen fibers are often predominant and concentrate toward the apex of the strictures.
The main treatment for this condition is to discontinue the usage of NSAIDs with resolution of inflammation as soon as the medication is withdrawn. 37 , 38 , 39 Other described therapies are aimed at reducing inflammation, such as steroids 40 , 41 and 5-aminosalicylic acid. 36 However, the fibrotic process that led to the formation of diaphragms is permanent and cannot always be reversed. In this event, mechanical dilation of the diaphragms is necessary using endoscopy techniques 42 and failing this surgical resection may be necessary.
Deep Penetrating Endometriosis
Intestinal involvement occurs in approximately 12 to 37% of women with endometriosis. Most cases are asymptomatic or subclinical. 43 , 44 The most common site of involvement is at the rectosigmoid colon (70%). The rest occur in the small bowel (7%), cecum (3.6%), and appendix (3%). 43 , 45
Extraintestinal involvement can also involve other organs, such as the bladder, kidneys, and peritoneum. 43 Endometriosis is commonly seen in women of reproductive age, with a median of 34 to 40 years, although it can occur in postmenopausal women. 45 There are three main theories to explain the etiology of endometriosis. The first theory advocates that retrograde menstruation causes endometrial tissue to implant into the peritoneum. The second theory claims that endometriosis is a result of metaplastic peritoneal tissue. Finally, it has been proposed that endometrial tissues can be transplanted hematogenously or lymphatically, which may explain some cases of distant involvement. 45
Symptoms indicating intestinal involvement can be vague and may include abdominal pain, nausea, vomiting, tenesmus, and change in bowel habit. 43 , 44 , 45 , 46 , 47 Symptoms typically fluctuate with the menstrual cycle, being worse at times of menstruation. Endometrial tissue in the bowel tends to involve either the serosa or subserosa. It is rare for endometrial tissue to involve the mucosa and if it does the patient will present with rectal bleeding.
Only 0.1 to 0.7% of cases of endometriosis present with bowel obstruction. 44 , 45 , 46 It has been hypothesized that the endometrial tissue implanted on the bowel is sensitive to ovarian hormones. The cyclical nature of hormonal changes causes repeated attacks of inflammation, fibrosis, and resultant hypertrophy of the bowel smooth muscle. 45 These changes lead to narrowing of the bowel lumen causing obstruction.
Differentiating large bowel endometriosis from other pathologies can be difficult because the symptoms are often nonspecific. Most patients are misdiagnosed as irritable bowel syndrome, inflammatory bowel disease, ischemic colitis, or even malignancy. Imaging and endoscopic evaluation have a limited role in diagnosing colonic endometriosis. Colonoscopy may reveal a site of narrowing; however, the mucosal biopsy is often normal as the stricture is due to the pressure effect from the muscular and serosal involvement (▶ Fig. 29.4). Barium enema or CT will only reveal external compression. The definitive diagnosis can often only be made at the time of surgery and confirmed on histopathology. 48
Treatment for endometriosis is generally conservative using medication such as NSAIDS, oral contraceptive pills, and gonadotropin-releasing hormone (GnRH) agonists. However, surgical intervention is warranted if a patient presents with symptoms of bowel obstruction.
Adhesions
Adhesions are a very rare cause of large bowel obstruction. Studies have reported adhesive bands causing large bowel obstruction in the right, transverse, and sigmoid colon. 8 , 49 , 50
Sarcoidosis
Hilzenrat et al 51 reported a case of colonic obstruction secondary to sarcoidosis. Two areas of narrowing were observed in the rectum and at the splenic flexure, through which a colonoscopy could not pass, but biopsies demonstrated sarcoidosis. Despite the abdominal and proximal bowel distension, treatment with oral prednisolone resulted in symptomatic improvement in 3 days. Follow-up colonoscopy 1 month later was essentially normal and the patient avoided operation.
29.2.2 Clinical Manifestations
A patient with large bowel obstruction usually presents with abdominal pain, distension, and constipation. Vomiting in a patient with large bowel obstruction is a late manifestation unless there is an associated small bowel obstruction. Abdominal tenderness associated with peritoneal irritation is caused by distension of the colon and the small bowel and perhaps by edema of the mesentery. Marked abdominal pain, peritoneal irritation out of proportion, and a white blood count greater than 20,000/mL suggest ischemia or gangrene of the bowel.
Colonic distension produces pain, usually colicky, in the lower abdomen. The pain may be associated with reflexive nausea. Somatic pain occurs when an inflammatory process such as sigmoid diverticulitis reaches the peritoneum and is sensed by afferent fibers there. 52
The clinical picture of large bowel obstruction is often dictated by whether the ileocecal valve is competent, with 75% of patients having a competent ileocecal valve. In this scenario, closed-loop large bowel obstruction will occur as the obstruction cannot decompress into the small bowel. 7 Cecal distension increases the bowel wall tension and, without intervention, will progress to ischemia and necrosis. The size of the cecum at risk of perforation ranges from 9 to 12 cm. 8
An important cause of colonic dilatation and perforation, which should not be confused with an underlying obstructing etiology, is toxic megacolon. Toxic megacolon is usually a consequence of failed treatment of inflammatory bowel disease (ulcerative colitis) or an acute infective etiology, with the associated inflammation leading to weakening of the bowel wall. If perforation occurs, mortality ranges from 19 to 41%. 53 Toxic megacolon may be diagnosed according to a well-defined set of clinical parameters, including pyrexia, tachycardia, raised white cell count, and anemia. 54
29.2.3 Diagnosis and Clinical Evaluation
Surgical assessment should include any recent change of bowel function or habit, weight loss over the preceding few months, signs of lethargy, patient or family history of colorectal cancer or other malignancies, and finally the results of any recent diagnostic tests. At initial presentation, the patient may show signs of dehydration, which may include a dry, furred tongue, sunken dull eyes, a characteristic fetor or decreased tissue turgor. All these signs advocate loss of extracellular fluid. At a later stage, the patient could develop hypovolemic shock with signs of tachycardia, hypotension, and cold peripheries. On physical examination, the surgeon should actively seek for signs of peritonitis, scars indicating previous abdominal surgery, and evidence of any hernias. A digital rectal examination should always be performed. The rectum is often empty when there is large bowel obstruction. It is possible to feel a palpable tumor within the cul-de-sac on rectal examination. 55
Blood and urine test should be taken to look for signs of anemia, electrolyte disturbances, coagulation abnormalities, dehydration, ischemia, and perforation. Arterial or venous blood gas will show a raised lactate or a negative base excess. These findings will suggest dehydration and/or ischemia. Before any intervention, a large-bore intravenous line should be obtained with fluid and electrolyte replacement started. Any clinically significant anemia should be corrected with blood transfusion. A chest radiograph and electrocardiogram should be obtained if surgical intervention is being considered. 55
A plain film of the abdomen is the simplest test for diagnosing obstruction of the large bowel, although it does not provide reliable information about the site of the obstruction (▶ Fig. 29.5). 56 Initially, the large bowel is distended. If there is a cutoff between the distended colon and the collapsed colon, the diagnosis of large bowel obstruction can be entertained, although the specific cause cannot be established. In the presence of an incompetent ileocecal valve, air will fill the small bowel and a picture of small bowel obstruction may supervene.
Distension of the right and transverse colon associated with minimal gas in the left colon suggests acute pseudo-obstruction. Water-soluble or contrast enema distinguishes between a mechanical cause and pseudo-obstruction, and in the former, may identify the site of obstruction and the underlying pathology (▶ Fig. 29.6). Previously, a single contrast enema was recommended as the preferred means of diagnosing large bowel obstruction. 57 The sensitivity of a contrast enema in the diagnosis of large bowel obstruction is 80%, with specificity of 100%. 57 , 58 , 59 More recently, the CT scan has become the preferred imaging modality (▶ Fig. 29.7). Multidetector CT is a well-tolerated, quick examination that allows the images to be obtained in one breath hold without the need of rectal contrast agent or air insufflation. CT can reveal the cause of large bowel obstruction and whether it is intraluminal, mural, or extramural. 60 CT has been reported to have a sensitivity and specificity of 96 and 93%, respectively. 59 , 61
Flexible sigmoidoscopy allows a direct visualization of the distal colon and the obstructing lesion and can exclude other causes of obstruction. One of its disadvantages is that it is not readily available at all hours for emergencies, but it has the advantages that it allows direct inspection of the obstructing lesion and biopsy. In some cases, endoscopic decompression may be achievable, for example, by insertion of an endoluminal stent through an obstructing cancer or untwisting of a colonic volvulus.
29.2.4 Management
There are some fundamental principles that must be followed in managing patients with large bowel obstruction regardless of the underlying cause. The principle of “drip and suck” is the foundation of conservative management. Fluid and electrolyte losses should be replaced and urine output closely monitored. The patient should also be given adequate analgesia (usually intravenous opiates) as well as anti-emetics.
Aims of Surgery
One of the major aims of surgery is to avoid fatal outcomes due to cardiovascular collapse or perforation secondary to bowel distension. It is also essential to consider the oncological principles if the obstruction is due to a malignancy. For patients who are high risk or suffer from disseminated disease, it may be prudent to offer a temporary solution to relieve the obstruction that will allow an extended period of optimization and neoadjuvant therapy with subsequent elective surgery at a later date.
Preoperative Preparation
It is important that patients receive adequate fluid resuscitation and electrolyte replacement. Blood results of urea and electrolytes (U&Es) and arterial blood gas (ABGs) should guide the rate of fluid replacement. Patients should have a urinary catheter so that hourly measurement of urine output (> 0.5 mL/kg) can be assessed. In addition, critical care should be consulted early, especially in patients with preexisting cardiac or renal disease, as they may benefit from more invasive monitoring. Patients should be kept “nil by mouth,” but can be allowed sips of clear fluids for comfort. Placement of a nasogastric tube is advisable to relieve nausea and/or vomiting and minimize the risk of aspiration, especially when there is evidence of small bowel distension. The nasogastric tube may be either left on free drainage or aspirated regularly. The total measurement of the gastric losses can aid fluid replacement therapy. 62
Operative Management
There is good evidence that elective surgery has superior outcomes to emergency surgery and hence, elective surgery should be chosen wherever possible. The preoperative mortality for emergency surgery and elective surgery for colorectal cancer is 50 and 5%, respectively, and the morbidity is double in a patient undergoing emergency surgery as compared to elective surgery. 63 , 64 , 65 Predictive factors for postoperative mortality in large bowel obstruction include age of 70 years or above, America Society of Anesthesiologists (ASA) score III–IV, presence of proximal colon damage, and preoperative renal failure. 66 During the past 20 years, endoluminal therapies have been pursued as they have several advantages, including temporary relief of obstruction and as a bridge to elective surgery.
Obstruction of the Right or Transverse Colon
Obstruction involving the cecum to the splenic flexure can be treated by (extended) right hemicolectomy with immediate ileocolic anastomosis. As long as complete oncologic resection can be achieved, this should be the standard treatment for obstructing colon cancers, with the benefit of immediate restoration of intestinal continuity. 58 Anastomotic leak rates of 2.8 to 4.6% have been published when primary ileocolic anastomosis is undertaken in the emergency setting. 58 However, if the patient presents with hemodynamic instability and/or fecal peritonitis at the time of surgery, a right hemicolectomy with an end ileostomy should be advocated instead as the initial management to avoid the risk of anastomotic leak in an unfit patient.
Left Colon Obstruction
The surgical treatment of distal colonic obstruction has evolved in the past 60 years from a three-stage procedure (proximal colostomy, second-stage resection, and third-stage stoma closure) to management as a one-stage procedure. Previous studies have shown that staged resection does not improve survival and is instead associated with high morbidity and mortality rates. 57 , 58 , 67 , 68 , 69 Recent technological advances, which include the development of endoluminal stents, have led to many changes in the management strategies for left colonic obstruction. 57 , 58 , 64 , 68 , 69 , 70 This has led to diversity in the management of distal malignant colonic obstruction, which includes the following procedures.
Single or Staged Procedure
Traditionally, the three-stage procedure (proximal stoma, tumor resection, and stoma reversal) was proposed as a safe method to decrease mortality in acute obstruction. However, a Cochrane review in 2004 71 and a randomized trial studied by Kronborg 72 did not confirm any true advantage from a stoma compared with those receiving a primary resection.
Kronborg 72 reported on 121 patients who either had a three-stage or a two-stage procedure, of whom most had cancer as the cause of obstruction. Mortality was similar in the two groups (13 and 12%). However, only 6% of patients who had the three-stage procedure ended up with a permanent stoma compared to 28% of patients who had Hartmann’s procedure as their initial operation. None of the patients underwent a single-stage operation. Other studies have shown comparable mortality with low anastomotic leak rates after primary resection, 73 , 74 , 75 , 76 but with a high proportion of patients ending up with a permanent stoma after staged procedures. 77 , 78 It should be noted that staged procedures cause further morbidity and mortality during the second/third procedures. In addition, the overall hospital stay is longer compared to patients receiving a primary anastomosis.
Although the data on single versus multistage procedures might suggest an advantage for the single-stage approach, the published studies all suffer from potential biases. Surgeons will tend to perform a primary resection and anastomosis in younger and healthier patients and, unsurprisingly, the outcomes for staged procedures will appear worse. The Cochrane review from 2004 comparing primary with staged resection for large bowel obstruction could not find any studies worthy of inclusion. Results were inconclusive and there was no evidence to recommend either primary or staged resection. It was concluded that it is unlikely that a large enough trial could be performed to address the question. 75
In emergency surgery where there is obstruction or perforation due to a left colonic lesion, Hartmann’s procedure is the most frequent approach. 57 , 66 , 72 , 79 Hartmann’s procedure is a less complex procedure to perform in the emergency setting because it avoids the morbidity associated with an anastomosis and requires less colorectal surgical expertise. It is also recommended in patients who are of high risk. 70 , 75
Currently, staged management (proximal stoma and resection later) tends to be reserved for mid or low rectal cancers causing obstruction, so that neoadjuvant treatment can be administered if tumor downstaging is required, followed by elective resection. Formation of a defunctioning proximal stoma is also used if the tumor is unresectable or if the patient is unfit for a major resection in the absence of colonic perforation. In cases of uncomplicated malignant left-sided large bowel obstruction, primary resection with anastomosis is the preferred option because it carries a low mortality and morbidity rate and is safe under favorable circumstances. 57 However, if there is fecal peritonitis, shock, severe sepsis, ASA IV patient, or widespread peritoneal malignancy, Hartmann’s procedure is preferred as it removes the additional risks associated with a primary anastomosis.
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