58  Intestinal obstruction  MARC CHRISTOPHER WINSLET

Introduction Intestinal obstruction may be classified into two types. • Dynamic — where peristalsis is working against a mechanical obstruction. The obstructing lesion may be:—intraluminal, for example impacted faeces, foreign bodies,bezoar, gallstones;— intramural, for example malignant or inflammatory strictures;—extramural, for example intraperitoneal bands and adhesions, hernias, volvulus or intussusception.• Adynamic — this may occur in two forms. Peristalsis may be absent (e.g. paralytic ileus) or it may be present in a non-propulsive form (e.g. mesenteric vascular occlusion or   pseudo-obstruction). In both types a mechanical element is absent. Dynamic obstructionThe diagnosis of intestinal obstruction is based on the classic quartet of pain, distension, vomiting and absolute constipation.Obstruction may be classified clinically into two types:• small bowel obstruction — high or low;• large bowel obstruction.In high small bowel obstruction vomiting occurs early and is profuse with rapid dehydration. Distension is minimal with little evidence of fluid levels on abdominal radiography.In low small bowel obstruction pain is predominant with central distension. Vomiting is delayed. Multiple central fluid levels are seen on radiography.In large-bowel obstruction distension is early and pronounced. Pain is mild and vomiting and dehydration are late. The proximal colon and caecum are distended on an abdominal radiograph.The nature of presentation will also be influenced by whether the presentation is:•acute;   • chronic;   • acute on chronic;   • subacute.  Acute obstruction usually occurs in small bowel obstruction with sudden onsets of severe colicky central abdominal pain, distension, with early vomiting and constipation.Chronic obstruction is usually seen in large bowel obstruction with lower abdominal colic and absolute constipation, followed by distension.In acute on chronic obstruction there is a short history of distention and vomiting against a background of pain and constipation.Subacute obstruction implies an incomplete obstruction. Presentation will be further influenced by whether the obstruction is:• simple — where the blood supply is intact;  •strangulating/strangulated — where there is direct interference to blood flow, usually by hernial rings or intraperitoneal adhesions/bands.

The common causes of intestinal obstruction in Western countries and their relative frequency are shown in Fig. 58.1. The underlying mechanisms are shown in Table 58.1.PathophysiologyIrrespective of aetiology or acuteness of onset, the proximal bowel dilates and develops an altered motility. Below the obstruction, the bowel exhibits normal peristalsis and absorption until it becomes empty, when it contracts and becomes immobile. Initially, proximal peristalsis is increased to overcome the obstruction, with the length of time it remains vigorous being proportional to the distance of the obstruction. If the obstruction is not relieved the bowel begins to dilate causing a reduction in peristaltic strength, ultimately resulting in flaccidity and paralysis. This is a protective phenomenon to prevent vascular damage secondary to increased intraluminal pressure.The distension proximal to an obstruction is produced by two factors:• Gas — regardless of the level of obstruction, there is a significant overgrowth of both aerobic and anaerobic organisms resulting in considerable gas production. Following the reabsorption of oxygen and carbon dioxide, the majority is made up of nitrogen (90 per cent) and hydrogen sulphide.• Fluid — this is made up of the various digestive juices (Table 58.2). Following obstruction, fluid accumulates within thebowel wall and any excess is secreted into the lumen,whilst absorption from the gut is retarded. Dehydrationand electrolyte loss are therefore due to:—      reduced oral intake;—      defective intestinal absorption;—     losses due to vomiting;—     sequestration in the bowel lumen.StrangulationWhen strangulation occurs the viability of the bowel is threatened secondary to a compromised blood supply. This may be due to:• external compression (hernial orifices/adhesions/bands);• interruption of mesenteric flow (volvulus, a twist of bowel loop on its mesenteric pedicle or intussusception where a segment of bowel invaginates into an adjacent segment);• rising intraluminal pressure (closed-loop obstruction);• primary obstruction of intestinal circulation (mesenteric infarction).The venous return is compromised before the arterial supply unless primary obstruction is present. The resultant increase in capillary pressure leads to local mural distension with loss of intravascular fluid and red blood cells intramurally and intra-and extraluminally. Once the arterial supply is impaired, haemorrhagic infarction occurs. As the viability of the bowel wall is compromised there is marked translocation and systemic exposure to aerobic and anaerobic organisms with their associated toxins. The associated danger is far greater for intraperitoneal strangulation than that of an external hernia where there is a smaller absorptive surface.The morbidity and mortality associated with strangulation are dependent on age and extent. In strangulated external hernias the segment involved is short and the resultant blood and fluid loss is small. When bowel involvement is extensive the loss of blood and circulatory volume will cause peripheral circulatory failure.Closed-loop obstructionThis occurs when the bowel is obstructed at both the proximal and distal point (Fig. 58.2). It is present in many cases of intestinal strangulation. Unlike cases of

nonstrangulating obstruction, there is no early distension of the proximal intestine. When gangrene of the strangulated segment is imminent, retrograde thrombosis of the mesenteric veins results in distension on both sides of the strangulated segment.A classic form of closed-loop obstruction is seen in the presence of a tight carcinomatous stricture of the colon with a competent ileocaecal valve (present in up to a third of individuals). The inability of the distended colon to decompress itself into the small bowel results in an increase in luminal pressure, greatest at the caecum, with subsequent impairment of blood supply. Unrelieved, this results in necrosis and perforation (Fig. 58.3).Acute intestinal obstructionClinical featuresThere are four cardinal features:• pain;•vomiting;•distension;•constipation. These features vary according to:•the location of the obstruction;•the age of the obstruction;•the underlying pathology;•the presence or absence of intestinal ischaemia. Late manifestations which may be encountered include dehydration, oliguria, hypovolaemic shock, pyrexia, septicaemia, respiratory embarrassment and peritonism. In all cases of suspected intestinal obstruction, all hernial orifices must be examined.PainPain is the first symptom, it occurs suddenly and is usually severe. It is colicky in nature and is usually centred around the umbilicus (small bowel) or lower abdomen (large bowel). The pain coincides with increased peristaltic activity. With increasing distension, the colicky pain is replace by a mild constant diffuse pain. The development of severe pain is indicative of the presence of strangulation. Pain may not be a significant feature in postoperative simple mechanical obstruction and does not occur in paralytic ileus.VomitingThe more distal the obstruction, the longer the interval between the onset of symptoms and the appearance of nausea and vomiting. As obstruction progresses the character of the vomitus alters from digested food to faeculent material due to the presence of enteric bacterial overgrowth.DistensionIn the small bowel the degree of distension is dependent on the site of the obstruction and is greater the more distal the lesion. Visible peristalsis may be present (Fig. 58.4). It is delayed in colonic obstruction and may be minimal or absent in the presence of mesenteric vascular occlusion.ConstipationThis may be classified as absolute (i.e. neither faeces nor flatus is passed) or relative (where flatus only is passed). Absolute constipation is a cardinal feature of complete intestinal obstruction. Some patients may pass flatus or faeces after the onset of obstruction owing to the evacuation of distal bowel contents.The rule that constipation is present in intestinal obstruction does not apply in:

• Richter’s hernia;• gallstone obturation;• mesenteric vascular occlusion;•obstruction associated with a pelvic abscess;• partial obstruction (faecal impaction/colonic neoplasm) where diarrhoea may often occur.Other manifestationsDehydrationThis is seen most commonly in small bowel obstruction due to repeated vomiting and fluid sequestration. This results in dry skin and tongue, poor venous filling and sunken eyes with oliguria. The blood urea level and haematocrit rise giving a secondary polycythaemia.HypokalaemiaThis is not a common feature in simple mechanical obstruction. An increase in serum potassium, amylase or lactate dehydrogenase may be associated with the presence of strangulation, as may leucocytosis or leucopenia.Pyrexia in the presence of obstruction may indicate:• the onset of ischaemia;• intestinal perforation;•inflammation associated with the obstructing disease. Hypothermia indicates septicaemic shock.Abdominal tendernessLocalized tenderness indicates pending or established ischaemia. The development of peritonism or peritonitis indicates overt infarction and/or perforation.Clinical features of strangulationIt is vital to distinguish strangulating from nonstrangulating intestinal obstruction, as the former is a surgical emergency. The diagnosis is entirely clinical. In addition to the features outlined above, the following should be noted:• the presence of shock indicates underlying ischaemia;• in impending strangulation, pain is never completely absent;•symptoms usually commence suddenly and recur regularly;•the presence and character of any local tenderness are of great significance and, however mild, tenderness requires frequent reassessment.In nonstrangulated obstruction there may be an area of localized tenderness at the site of the obstruction; in strangulation there is always localized tenderness associated with rigidity/rebound tenderness.•Generalized tenderness and the presence of rigidity are indicative of the need for early laparotomy.•In cases of intestinal obstruction where pain persists despite conservative management, even in the absence of the above signs, strangulation should be diagnosed.•When strangulation occurs in an external hernia the lump is tense, tender, irreducible, there is no expansile cough impulse and it has recently increased in size.Radiological diagnosisErect abdominal films are no longer routinely provided and the radiological diagnosis is based on a supine abdominal film (Fig. 58.5).When distended with gas the jejunum, ileum, caecum and remaining colon have a characteristic appearance that allows them to be distinguished radiologically. The diameter of the distended viscus is not diagnostic.

•The obstructed small bowel is characterized by straight segments that are generally central and lie transversely. No gas is seen in the colon.•The jejunum is characterized by its valvulae conniventes that completely pass across the width of the bowel and are regularly spaced giving a ‘concertina’ or ladder effect.• Ileum — the distal ileum has been piquantly described by Wangensteen as featureless.• Caecum — a distended caecum is shown by a rounded gas shadow in the right iliac fossa.• Large bowel — except for the caecum shows haustral folds which, unlike valvulae conniventes, are spaced irregularly and the indentations are not placed opposite one another.Volvulus of the sigmoid colon has a characteristic radiological appearance with a grossly dilated loop of colon, with or without visible haustrae which arises from the pelvis and extends obliquely across the spine to the upper abdomen.In intestinal obstruction fluid levels appear later than gas shadows as it takes time for gas and fluid to separate (Fig. 58.6). In infants less than 2 years of age, a few fluid levels in the small bowel may be physiological. In adults, two inconstant fluid levels may be regarded as normal — one at the duodenal cap and the other in the terminal ileum.During the obstructive process, fluid levels become more conspicuous and more numerous when paralysis has occurred. When fluid levels are pronounced the obstruction is advanced. In the small bowel, the number of fluid levels is directly proportional to the degree of obstruction and to its site; the number increasing the more distal the lesion.In contrast, low colonic obstruction does not commonly give rise to small bowel fluid levels unless advanced, whilst high colonic obstruction may do in the presence of an incompetent ileocaecal valve. Colonic obstruction is usually associated with a large amount of gas in the caecum. A limited water-soluble enema may be undertaken to differentiate large bowel obstruction from pseudo-obstruction. A barium follow-through is contraindicated in the presence of acute obstruction and may be life threatening.Impacted foreign bodies may be seen on abdominal radiographs. In gallstone ileus, gas may be seen in the biliary tree with the stone visible, usually in the right iliac fossa, in 25 per cent of cases.It is noteworthy that gas-filled loops and fluid levels in the small and large bowel can also be seen in established paralytic ileus and pseudo-obstruction. The former can, however, normally be distinguished on clinical grounds whilst the latter can be confirmed radiologically. Fluid levels may also be seen in non obstructing conditions such as inflammatory bowel disease, acute pancreatitis and intra-abdominal sepsis.  Treatment of acute intestinal obstructionThere are three main measures:•  gastrointestinal drainage;• fluid and electrolytic replacement;• relief of obstruction, usually surgical.The first two steps are always necessary prior to the surgical relief of obstruction and are the mainstay of postoperative management. In a proportion of cases, particularly adhesive obstruction, they may be used exclusively.

Surgical treatment is necessary for most cases of intestinal obstruction, but should be delayed until resuscitation is complete, provided there is no: • sign of strangulation;• evidence of closed-loop obstruction. There are three principles of surgical intervention (Table 58.3).Supportive management•  Nasogastric decompression is achieved by the passage of a nonvented (Ryle) or vented (Salem) tube. The tubes are normally placed on free drainage, with 4-hourly aspiration, but may be placed on continuous or intermittent suction. As well as facilitating decompression proximal to the obstruction, they also reduce the risk of subsequent aspiration during induction of anaesthesia and postextubation.• The basic biochemical abnormality is sodium and water loss, and therefore the appropriate replacement is Hartmann’s solution or normal saline. The volume required varies and should be determined by clinical haematological and biochemical criteria.•  Antibiotics — whilst not mandatory, many clinicians initiate broad-spectrum antibiotic early in therapy because of bacterial overgrowth. Antibiotic therapy is mandatory for all patients undergoing small or large bowel resection.Surgical treatmentThe timing of surgical intervention is dependent on the clinical picture with the indications of early operation being: •  obstructed or strangulated external herniae;•  internal intestinal strangulation;•  acute obstruction.The classic clinical advice that ‘the sun should not both rise and set’ on a case of unrelieved intestinal obstruction is sound and should be followed unless there are positive reasons for delay. Such cases may include obstruction secondary to adhesions where there is no pain or tenderness, despite continued radiological evidence of obstruction. Under these circumstances, conservative management may be continued for up to 72 hours in the hope of spontaneous resolution.If the site of obstruction is unknown, adequate exposure is best achieved by a midline incision. Operative assessment is directed to: •  the site of obstruction;•  the nature of the obstruction;•  the viability of the gut.Identification and assessment of the caecum is the best initial manoeuvre. If it is collapsed, the lesion is in the small bowel and may be identified by careful retrograde assessment. A dilated caecum indicates large bowel obstruction. To display the cause of obstruction, distended loops of small bowel should be displaced with care and covered with warm moist abdominal packs. Operative decompression may be required if dilatation of bowel loops prevents exposure, the viability of the bowel wall is compromised or subsequent closure will be compromised. Its benefits should be balanced against potential risk of septic complications from spillage. Decompression may be performed using Savage’s decompressor within a seromuscular purse-string suture (Fig. 58.7). Alternatively, with a large-bore nasogastric tube in place the small bowel contents may be gently

milked in a retrograde manner to the stomach for aspiration. All volumes of fluid removed should be accurately measured and appropriately replaced.The type of surgical procedure required will depend upon the nature of the cause — division of adhesions (enterolysis), excision, bypass or proximal decompression.                                                         Following relief of obstruction, the viability of the involved bowel should be carefully assessed (see Table 58.4). Whilst frankly infarcted bowel is obvious, the viability status in many cases may be difficult to discern. If in doubt, the bowel should be wrapped in hot packs for 10 minutes with increased oxygenation and reassessed. The state of the mesenteric vessels and pulsation in adjacent arcades should be sought. Nevertheless, nonocclusive vascular insufficiency may occur despite adequate pulsation. In doubtful cases, following resection, both ends of the bowel should be raised as stomas. This is not only safe but also allows regular assessment of the bowel. Where no resection has been undertaken or there are multiple ischaemic areas (mesenteric vascular occlusion) a second look laparotomy at 24—48 hours may be required.Special attention should always be paid to the sites of constriction at each end of an obstructed segment. If of doubtful viability they should be infolded by the use of a seromuscular suture and covered with omentum.The surgical management of massive infarction in the form of superior mesenteric artery occlusion is dependent on the patient’s overall prognostic criteria. In the elderly, infarction of the small bowel from the duodenojejunal flexure and the right colon may be considered incurable, whilst in the young, with potential for long-term intravenous alimentation and small bowel transplantation, a less conservative policy may be justified. Whenever small bowel is resected, the exact site of resection, the length of the resected segment and that of the residual bowel should be recorded.Large bowel obstructionThis is usually due to underlying carcinoma or occasionally diverticular disease, and presents in an acute or chronic form. The condition of pseudo-obstruction should always be considered and excluded by a limited contrast study or air computerised tomography (CT) scan to confirm organic obstruction.After full resuscitation the abdomen should be opened through a midline incision. Distension of the caecum will confirm large bowel involvement. Identification of a collapsed distal segment of the large bowel and its sequential proximal assessment will readily lead to identification of the cause. When a removable lesion is found in the caecum, ascending colon, hepatic flexure or proximal transverse colon an emergency right hemicolectomy should be performed. If the lesion is irremovable, a proximal stoma (colostomy or ileosotomy if the ileocaecal valve is incompetent) or ileotransverse bypass should be considered. Obstructing lesions at the splenic flexure should be treated by an extended right hemicolectomy with ileodescending colonic anastomosis.For obstructing lesions of the left colon or rectosigmoid junction, immediate resection should be considered unless there are clear contraindications such as:• inexperienced surgeon;   •  moribund patient;   • advanced disease.In rate instances, or where caecal perforation is imminent, time to improve the patient’s clinical condition can be bought by performing an emergency caecostomy (or ileosotomy in the presence of an incompetent ileocaecal valve).

In the absence of senior clinical staff, it is safest to bring the proximal colon to the surface as a colostomy. Where possible the distal bowel should be brought out at the same time (Paul—Mikulicz procedure) to facilitate subsequent extraperitoneal closure. In the majority of cases the distal bowel will not reach and is closed and returned to the abdomen (Hartmann’s procedure). A second-stage colorectal anastomosis can be planned when the patient is fit.If an anastomosis is to be considered using proximal colon, in the presence of obstruction, it must be decompressed and cleaned by an on-table colonic lavage. Nevertheless, the subsequent anastomosis should still be protected with a covering stoma.Obstruction by adhesions and bandsIn Western countries where abdominal operations are common, adhesions and bands are the commonest cause of intestinal obstruction. Furthermore, in the early postoperative period, the onset of such a mechanical obstruction may be difficult to differentiate from paralytic ileus.The causes of intraperitoneal adhesions are shown in Table 58.5.Any source of peritoneal irritation results in local fibrin production which produces adhesions between opposed surfaces. Early fibrinous adhesions may disappear when the cause is removed or they may become vascularised and replaced by mature fibrous tissue.Prevention. The following factors may limit adhesion formation:•  good surgical technique;•  washing of the peritoneal cavity with saline to remove clots, etc.;•  minimize contact with gauze;•  cover anastomosis and raw peritoneal surfaces.Numerous substances have been instilled in the peritoneal cavity to prevent adhesion formation, including hyaluronidase, hydrocortisone, silicone, dextran, polyvinylpropylene (PVP), chondroitin and streptomycin, anticoagulants, antihistamines, nonsteroidal anti-inflammatory drugs and streptokinase. Currently no single agent has been shown to be safe and effective, and their use is not recommended.Adhesions may he classified into various types by virtue of whether they are early (fibrinous) or late (fibrous) or by the underlying aetiology. From a practical perspective, there are only two types — ‘easy’ flimsy ones and ‘difficult’ dense ones.Postoperative adhesions giving rise to intestinal obstruction usually involve the lower small bowel. Operations for appendicitis and gynaecological procedures ate the most common precursors and are an indication for early intervention. Usually only one band is culpable. This may be: •  congenital, for example obliterated vitellointestinal duct;•  a string band following previous bacterial peritonitis;•  a portion of greater omentum usually adherent to the parietes.Treatment. Initial management is based on intravenous rehydration and nasogastric decompression. Occasionally it is curative. Whilst an initial conservative regime is considered appropriate, regular assessment is mandatory to ensure that strangulation does not occur. Conservative treatment should not be prolonged beyond 72 hours.When, as is usual, laparotomy is required, although multiple adhesions may be found, only one may be causative. This should be divided and the remaining adhesions left in situ unless severe angulation is present. Division of these adhesions will only cause further adhesion formation.

When obstruction is caused by an area of multiple adhesions, they should be freed by sharp dissection. To prevent recurrence the bate area should be covered with omental grafts.Following release of band obstruction, the constriction sites that have suffered direct compression should be carefully assessed and if they show residual colour changes, invaginated.Treatment of recurrent intestinal obstruction due to adhesionsSeveral procedures may be considered in the presence of recurrent obstruction, including:• repeat adhesiolysis (enterolysis) alone;• Noble’s plication operation;• Charles—Phillips transmesenteric plication;• intestinal intubation.Their relative efficacy remains unclear.In Noble’s intestinal plication (Fig. 58.8) all involved intestine is freed. Adjacent coils (average length 15—20 cm) are sutured with serosal sutures to form gentle curves. If only a proportion of the small bowel is plicated, the mesentery must be united to prevent internal hernias. This procedure is time-consuming, and associated with a high morbidity and recurrent symptoms.In the Charles—Phillips operation (Fig. 58.9), following adhesiolysis, the bowel is placed in an orderly fashion and three long synthetic sutures ate passed through the mesentery of the plicated bowel, each doubled hack upon itself and tied loosely. The stitch should pass a few centimetres from the bowel wall and not be adjacent to it. The resultant bowel should look like a packet of sausages. Results from this procedure are relatively good.Intraluminal tube insertion (Baker), via a Witzel jejunostomy or gastrostomy, may facilitate the formation of gentle curves. Most tubes have an inflatable balloon near the tip to facilitate placement within the caecum. This procedure is associated with a long postoperative ileus, and reports of outcome are conflicting (Figs 58.10 and 58.11).Postoperative intestinal obstructionDifferentiation between persistent paralytic ileus and early mechanical obstruction may be difficult in the early postoperative period. In practice, the latter is probably more common. Early evidence of obstruction (days 1—5) is usually due to nonstrangulating causes such as fibrinous adhesions and oedema. Obstruction is usually incomplete and the majority settles with continued conservative management. Late postoperative obstruction (greater than 7 days) is usually more significant in nature and timely surgical intervention is usually required.Special types of mechanical intestinal obstructionInternal herniaInternal herniation occurs where a portion of the small intestine becomes entrapped in one of the retroperitoneal fossae or into a congenital mesenteric defect.The following are potential sites of internal herniation: •the foramen of Winslow;•a hole in the mesentery;•a hole in the transverse mesocolon;•defects in the broad ligament;•congenital or acquired diaphragmatic hernia;•duodenal retroperitoneal fossae — left paraduodenal and right duodenojejunal;

•caecal/appendiceal retroperitoneal fossae — superior,             inferior and retrocaecal;•intersigmoid fossa.Internal herniation in the absence of adhesions is uncommon and a preoperative diagnosis is unusual. The standard treatment for a hernia is to release the constricting agent by division. This should not be undertaken in cases of herniation involving the foramen of Winslow, mesenteric defects and the paraduodenal/duodenojejunal fossae as major blood vessels run in the edge of the constriction ring. The distended loop in such circumstances must first be decompressed with minimal contamination and then reduced.Obstruction from enteric stricturesSmall bowel strictures usually occur secondary to tuberculosis or Crohn’s disease. Malignant strictures associated with lymphoma are common, whilst carcinoma and sarcoma are rare. Presentation is usually subacute or chronic. Standard surgical management consists of resection and anastomosis. In Crohn’s disease strictureplasty may be considered in the presence of short multiple strictures without active sepsis.Bolus obstructionBolus obstruction in the small bowel may be caused by food, gallstones, trichobezoar, phytobezoar, stercoliths and worms.Gallstones. These tend to occur in the elderly secondary to erosion of a large gallstone through the gall bladder into the duodenum. Classically, there is impaction about 60 cm proximal to the ileocaecal valve. The patient may have recurrent attacks as the obstruction is frequently incomplete or relapsing due to a ball-valve effect. A radiograph will show evidence of small bowel obstruction with a diagnostic air—fluid level in the biliary tree. The stone may or may not be visible. At laparotomy it may be possible to crush the stone within the bowel lumen if it is soft, after milking it proximally. If not, the intestine is opened and the gallstone disimpacted, milked back and removed. If the gallstone is faceted a careful check for other enteric stones should be made. The region of the gall bladder should not be explored.Food. Bolus obstruction may occur after partial or total gastrectomy when unchewed articles can pass directly into small bowel. Apple, coconut, brussels sprouts, dried fruit and orange pips are particularly liable to cause obstruction. The management is similar to a gallstone with intraluminal crushing usually being successful.Trichobezoars and phytobezoar. These are firm masses of undigested hair balls and fruit/vegetable fibre, respectively. The former is due to persistent hair chewing and sucking, and may he associated with an underlying psychiatric abnormality. Phytobezoars are predisposed to by high fibre intake, inadequate chewing, previous gastric surgery, hypochlorhydria and loss of gastric pump mechanism. Where possible, the lesion may be kneaded into the caecum, otherwise open removal is required.Stercoliths. Usually found in the small bowel in association with a jejunal diverticulum or ileal stricture. Presentation and management are identical to gallstones.Worms. Ascaris lumbricoides may cause low small bowel obstruction particularly in children, the institutionalized and those near the tropics (Fig. 58.12). An attack frequently follows initiation of antihelminthic therapy. Debility is frequently out of proportion to that produced by the obstruction. If worms are not seen in stool or vomitus, the diagnosis may be indicated by eosinophilia or the sight of worms within gas-filled small bowel loops on a plain radiograph (Naik). At laparotomy it may be possible to knead the tangled mass into the caecum; if not it should be removed.

Occasionally worms may cause a perforation and peritonitis, especially if the enteric wall is already weakened by such conditions as ameobiasis.Acute intussusceptionThis occurs when one portion of the gut becomes invaginated within an immediately adjacent segment; invariably it is the proximal into distal bowel.Aetiology. The condition is encountered most commonly in children, where it occurs in an idiopathic form with a peak incidence at 3—9 months. Seventy to 95per cent of cases are classed as idiopathic, and an associated illness such as gastroenteritis or urinary tract infection is found in 30 per cent. It is believed that hyperplasia of Peyer’s patches in the terminal ileum may be the initiating event. This may occur secondary to weaning. In light of the seasonal variation with peak incidence in spring and summer, it may be related to upper respiratory tract infection pathogens such as adenovirus or rotavirus.Children with intussusception associated with a lead point— such as Meckel’s diverticulum, polyp, duplication, Henoch— Schonlein purpura or appendix — are usually older than the idiopathic cases. Adult cases are invariably associated with a lead point which is usually a polyp (e.g. Peutz—Jegher syndrome), a submucosal lipoma or tumour, the exception being after periods of long fasting (Moro). The colocolic variety is common in adults.Pathology. An intussusception is composed of three parts (Fig. 58.13):• the entering or inner tube;• the returning or middle tube;• the sheath or outer tube (intussuscipiens).The part which advances is the apex; the mass is the intussusception and the neck is the junction of the entering layer with the mass.An intussusception is an example of strangulating obstruction as the blood supply of the inner layer is usually impaired. The degree of ischaemia is dependent on the tightness of the invagination, which is usually greatest as it passes through the ileocaecal valve.Intussusception may be anatomically defined as ileo-ileal, ileo-caecal and ileo-colic depending on the site and extent of invagination (Table 58.6).Clinical features. The presentation of intussusception in a child is classical. An otherwise fit and well male child of 6 months develops sudden onset of screaming associated with drawing up of the legs. The attacks last for a fewminutes, recur every 15 minutes and become progressively severe. During attacks the child has facial pallor whilst between episodes he is listless and drawn.Vomiting may or may not occur at the outset but becomes conspicuous with time. Initially the passage of stool may be normal, whilst later blood and mucus are evacuated — the ‘redcurrent’ jelly stool.Examination should be undertaken, wherever possible, between episodes without disturbing the child. Classically, the abdomen is not distended, a lump may be felt which hardens on palpation but this is present in only 50—60 per cent of cases (Fig. 58.14). There may be an associated feeling of emptiness in the right iliac fossa (the sign of Dance). On rectal examination blood-stained mucus may be found on the finger. Occasionally, in extensive ileocolic or colocolic intussusception, the apex may be palpable or even protrude from the anus.Unrelieved, the pain will become continuous with abdominal distension and profound vomiting. Ultimately death occurs from small bowel obstruction or peritonitis secondary to gangrene. Rarely, natural cure may occur due to sloughing of the intussusceptium.

Radiography. A plain abdominal film usually reveals evidence of small or large bowel obstruction with an absent caecal gas shadow in ileo-ileal or ileo-colic cases. A barium enema may be used to diagnose the presence of an ileo-colic or colocolic form (the claw sign) (Fig. 58.15) but would be negative for the ileo-ileal variant in the presence of a competent ileocaecal valve. Equivocal cases of ileo-ileal intussusception may be further evaluated by CT scan which should reveal the presence of a small bowel mass.Barium enema may also be used therapeutically in selected cases to reduce an infant intussusception. Hydrostatic reduction is contraindicated in the presence of obstruction, peritonism or a prolonged history (greater than 48 hours) and is unlikely to succeed where a lead point is likely. It is successful in 50 per cent of cases with a recurrence rate in the order of 5per cent. Complete reduction must be confirmed by the visualization of contrast entering the terminal ileum. In cases where complete reduction is not possible, the intussusception may be so reduced in size and near its origin that only a grid-iron incision is required for surgical management.Unfortunately, in many cases the clinical scenario is not clear-cut enough for an early diagnosis to be made and the bowel is already ischaemic by the time treatment in hospital is instituted.Differential diagnosis.•  Acute enterocolitis — whilst abdominal pain and vomiting are common with occasional blood and mucus in the stool, diarrhoea is a leading symptom and faecal matter or bile is always present in the stool.•  Henoch—Schönlein purpura (HSP) — HSP is associated with a characteristic rash and abdominal pain but intussusception may also occur. Laparotomy should be considered in equivocal cases.• Rectal prolapse — this may be easily differentiated by the fact that the projecting mucosa can be felt in continuity with the perianal skin whereas in intussusception the finger may pass indefinitely into the depths of a sulcus.Operative management. This is required where hydrostatic reduction has failed or is contraindicated.A midline incision is used after complete preoperative resuscitation with nasogastric decompression and intravenous rehydration. Reduction is achieved by squeezing the most distal part of the mass in a cephalad direction (Fig. 58.16). Do not pull. The last part of the reduction is the most difficult and the majority of cases is achieved by squeezing the apex. After reduction, the terminal part of the small bowel and the appendix will be seen to he reddened and stiffened with oedema. The viability of all bowel should he checked carefully.In difficult cases the little finger may he gently inserted into the neck of the intussusception to try and separate adhesions (Cope’s method). Subsequently, the thumb and forefinger are placed in such a way as to de-invaginate the apex. Gentle pressure is applied and gradually increased to reduce the oedema around the ileocaecal valve (Fig. 58.17). After reduction the underlying cause requires appropriate treatment.In the presence of an irreducible or gangrenous intussusception the mass should be excised in situ and an anastomosis or temporary end stoma created.Postoperative care. In the uncomplicated cases, gastric aspiration and intravenous rehydration should be continued for 24 hours. Oral fluids or breast feeding may he restarted on day 2 or when postoperative ileus shows signs of resolving.

Recurrent intussusception. This rare complication may occur in 5percent of idiopathic cases. Anchorage of the last part of the terminal ileum to the ascending colon has been advocated where repeat surgery is required.  VolvulusA volulus is a twisting or axial rotation of a portion of bowel about its mesentery. When complete it forms a closed loop of obstruction with resultant ischaemia secondary to vascular occlusion.Volvuli may be primary or secondary. The primary form occurs secondary to congenital malrotation of the gut, abnormal mesenteric attachments or congenital bands. Examples include volvulus neonatorum, caecal and sigmoid volvulus. A secondary volvulus, which is the more common variety, is due to actual rotation of a piece of bowel around an acquired adhesion or stoma.Volvulus neonatorum is predisposed to by arrested gut rotation with a resultant narrow mesentery of the small bowel and caecum. The symptoms are similar to arrested rotation (vide in Ira) with repeated vomiting, hut the onset is more catastrophic with abdominal distention and rapid dehydration. Abdominal radiography reveals evidence of duodenal obstruction. Laparotomy reveals a distended stomach and coils of small bowel (Fig. 58.19). The whole midgut should he delivered to the wound and wrapped in warm, moist towels, in order to demonstrate the volvulus which usually occurs in a clockwise direction. The operation consists of reduction by untwisting and division of any secondary obstructive lesions — such as the transduodenal band of Ladd.Volvulus of the small intestineThis may be primary or secondary and usually occurs in the lower ileum. It may occur spontaneously in Africans, particularly following consumption of a large volume of vegetable matter, whilst in the West it is usually secondary to adhesions passing to the parietes or female pelvic organs. Treatment consists of reduction of the twist and is then directed to any underlying cause.Caecal volvulusThis may occur as part of volvulus neonatorum or de novo and is usually a clockwise twist. It is more common in females and usually presents acutely with the classic features of obstruction. At first the obstruction may be partial with the passage of flatus and faeces. In 25 per cent of cases, examination may reveal a palpable tympanic swelling in the midline or left side of the abdomen. Plain radiograph may reveal a gas-filled ileum and occasionally a distended caecum. A barium enema may be used to confirm the diagnosis with an absence of barium in the caecum and a bird beak deformity.At operation the volvulus should be reduced. Sometimes this can only be achieved after decompression of the caecum by a needle. Further management consists of either fixation of the caecum to the right iliac fossa (caecopexy) and/or a caecostomy. If the caecum is ischaemic or gangrenous a right hemicolectomy should be performed.Sigmoid volvulusThis is rare in Europe and the USA but more common in Eastern Europe and Africa; indeed it is the commonest cause of large bowel obstruction in indigenous black Africans (Loefler). The predisposing cause is summarised in Fig. 58.18. Rotation nearly always occurs in an anticlockwise direction. Predisposing factors include high residue diet and chronic constipation. Thesymptoms are of large bowel obstruction which may initially be intermittent, followed by the passage of large quantities of

flatus and faeces. Presentation varies in severity and acuteness, with younger patients appearing to develop the more acute form. Abdominal distension is an early and progressive sign which may be associated with hiccough and wretching; vomiting occurs late. Constipation is absolute. In the elderly a more chronic form may be seen. A plain radiograph shows massive colonic distension. The classic appearance is of a dilated loop of bowel running diagonally across the abdomen from right to left with two fluid levels seen, one within each loop of bowel.Treatment Flexible sigmoidoscopy or rigid sigmoidoscopy and insertion of a flatus tube should be carried out to allow deflation of the gut. Success, as long as ischaemic bowel is excluded, will provide temporary respite allowing resuscitation and an elective procedure. Failure results in an early laparotomy, with untwisting of the loop and per-anal decompression (Fig. 58.19).When the bowel is viable, fixation of the sigmoid colon to the posterior abdominal wall may be a safer manoeuvre in inexperienced hands. Resection is preferable if it can be achieved safely. A Paul—Mikulicz procedure is a useful procedure particularly if there is suspicion of impending gangrene (Fig. 58.20).An alternative is a sigmoid colectomy and, where anastomosis is considered unwise, a Hartmann’s procedure with subsequent reanastomosis.Compound volvulusThis is a rare condition also known as ileo-sigmoid knotting. The long pelvic mesocolon allows the ileum to twist around the sigmoid colon resulting in gangrene of either or both segments of bowel. The patient presents with acute intestinal obstruction, but distension is comparatively mild. Plain radiography reveals distended ileal loops in a distended sigmoid colon. At operation decompression, resection and anastomosis are required.Acute intestinal obstruction of the newbornNeonatal intestinal obstruction has an approximate incidence of 1:2000 live births. Congenital atresia and stenosis are the commonest causes. Volvulus neonatorum, meconium ileus and Hirschsprung's disease may also be responsible.Congenital atresiaThe incidence of atresia varies with anatomical site:•duodenum — 35 per cent;•jejunum — 15 per cent;•ileum — 25 per cent;•ascending colon — 10 per cent;• multiple sites — 15 per cent.The high incidence of multiple sites makes peroperative assessment of the whole small and large bowel mandatory. Except in the case of duodenal atresia there are frequently associated abnormalities of the heart and great vessels.Atresia/stenosis of the duodenumAtresia and stenosis occur with equal frequency. In most cases, except for the oesophagus, duodenum and rectum, the atresia is a result of an intrauterine vascular accident occurring late in pregnancy such as volvulus, intussusception or strangulation at the umbilical ring. As the foetus is germ-free the ischaemic portion is absorbed and disappears. In the presence of complete obstruction, persistent vomiting occurs from birth. The presence or absence of bile is dependent on the relationship of the septum to the duodenal papilla. Bile-stained vomiting is nearly always organic in origin. Distension is often absent but visible peristalsis may be seen in the left upper quadrant. Atresia of the duodenum occurs at the level of the ampulla of Vater. Thirty per cent of babies have associated Down’s syndrome. Radiography reveals a classic

so-called double stomach due to gross distention of the stomach and upper part of the duodenum with two air—fluid levels (Fig. 58.21).In cases of partial obstruction the location of the lesion may be confirmed by installation, via a nasogastric tube, of a small volume of gastrograffin. Once the lesion is confirmed the medium must be aspirated. Suprapapillary duodenal atresia may be distinguished from oesophageal atresia by the absence of dribbling saliva, and from infantile pyloric stenosis by the absence of a lump.Duodenal obstruction in infancy may also be due to midgut volvulus, a band obstruction or an annular pancreas.TreatmentSurgery is required as soon as resuscitation is complete. Duodenojejunostomy is the operation of choice. A silastic catheter is introduced through a stab incision in the antrum and guided through the anastomosis. A Witzel gastrostomy is constructed around the proximal tube which is brought out through a stab incision. Early enteral feeding through this tube is recommended.Atresia/stenosis of the jejunum/ileumThere are four main types:•type 1 — diaphragm with continuity of the bowel wall;•type 2 — gap between the two ends (may be connected by fibrous cord) plus a mesenteric defect;•type 3 — multiple atresias;•type 4 — apple peel atresia with loss of dorsal mesentery.The vital importance of a diagnosis lies in the fact that proximal distention of the bowel may be so great that the vascular integrity of the bowel wall is compromised leading to gangrene and perforation (Fig. 58.22).In ileal atresia the child is born with abdominal distension or it presents within 24 hours of birth. In jejunal atresia early distention is lacking but vomiting occurs early. In both conditions the vomit contains bile and some meconium is likely to be evacuated.RadiographyPlain radiographs are only diagnostic when air—fluid levels are seen. When they are present the obstruction is usually well advanced.SurgeryIf the stenosis is ileal and the discrepancy in bowel diameter above and below the obstruction is marked the two limbs may he brought out in a manner similar to the Paul—Mikulicz procedure. The proximal limb will need to he proud of the abdominal wall (usually by eversion) in order to prevent skin excoriation. Secondary closure by circumstomal mobilization and anastomosis, rather than use of crushing clamps, is recommended. When the stenosis is jejunal, the impact of the high jejunostomy output can make subsequent management difficult and wherever possible an end-to-end anastomosis is recommended.Arrested rotationUp to 10 weeks of gestation the gut lies outside the abdominal cavity. The orderly return may he arrested at any stage resulting in four major types of arrest.The whole bowel may remain free as a narrow-based mesentery. The caecum may he displaced with transduodenal bands. The intestine may return in a clockwise direction producing a reversed intestinal rotation or a failure of rotation altogether, with the small bowel on the right and the large bowel on the left.The most common anomaly is where the caecum remains in the left hypochondrium and a peritoneal band is found running from the caecum to the right side of the

abdomen and then across the second part of the duodenum — the transduodenal hand of Ladd. The symptoms of repeated vomiting, due to pressure on the duodenum, and the radiographic appearances are identical to those of duodenal stenosis. Treatment consists of early laparotomy after appropriate resuscitation. The band is divided near its attachment to the parietal peritoneum. Often there is a second band which must also be divided, extending from the midline to the commencement of the caecum. The caecum and the colon are centred on the left of the abdominal cavity with the small bowel on the right (Nixon).Meconium ileusThis is the neonatal manifestation of cystic fibrosis. Meconium is normally kept fluid by the action of pancreatic enzymes. The terminal ileum becomes filled with meconium and viscid mucus resulting in progressive inspissation in utero and neonatal obstruction. Inspissated meconium may be palpated as a rubbery swelling. Abdominal radiography may reveal a distended small intestine, with mottling. Fluid levels are generally not seen. Unlike ileal atresia there is no abrupt termination of the gas-filled intestine. As the condition is due to an autosomal recessive genetic defect a family history may he present. Further assessment includes absence of trypsin from stool or bile and a concentration of sodium chloride in sweat greater than 80 mmol/litre, or a negative immunoreactive blood trypsin estimation.Forty per cent of cases are associated with complications such as volvulus neonatorum, atresia or meconium peritonitis (Dickson). Any evidence to suggest an acute intra-abdominal process due to twisting of the grossly distended proximal bowel indicates the need for urgent laparotomy. When this is not so, a gastrografin or mypaque enema may be given to confirm the diagnosis. The radio-opaque fluid will pass easily to the ileum where it may disperse the obstructing meconium and relieve the condition owing to its high osmolarity and detergent action. As the instilled solution is markedly hypertonic, the rapid loss of fluid into the bowel lumen must be corrected by replacement. If conservative management fails, laporotomy is indicated. The only condition with which meconium ileus may be confused is Hirschsprung’s disease affecting the whole colon. The standard treatment is resection of the most dilated segment with an end-to-side anastomosis of the colon to the ileum. The distal ileal opening is formed into an ileostomy, through which the meconium may he irrigated postoperatively (the Bishop—Koop operation). The ilesotomy becomes a mucus flstula which usually requires subsequent closure (Fig. 58.23).Necrotising enterocolitisThis is a common phenomenon amongst sick premature neonates. The risk is inversely proportional to birth weight and may be associated with hypoxia, hypothermia, hypotension and umbilical artery cannulation. The ileum, caecum, distal colon and total colon are affected with a complete spectrum from mucosal to transmural necrosis.The usual presentation is bilious vomiting, abdominal distension, colour change and lethargy in a high-risk neonate. The abdomen is usually soft. Abdominal radiographs may show pneumatosis intestinalis or free intraperitoneal air. Management consists of aggressive resuscitation with intravenous feeding. The optimal time for surgery is not in the acute phase as the baby can withstand the pressure of necrosis better than an adult but not the stress of laparotomy. At laparotomy excision of all necrotic bowel with primary anastomosis is usual. The overall mortality is 25 per cent with 10—30 per cent of neonates developing a colonic stricture.  

Chronic intestinal obstructionThe symptoms of chronic intestinal obstruction may arise from two sources — the cause and the subsequent obstruction.The causes of obstruction may be organic:•intramural — faecal impaction;•mural — colorectal cancer, diverticulitis, strictures (Crohn’s disease, ischaemia), anastomotic stenosis;•extramural — adhesion (small bowel only), metastatic deposits, endometriosis;or•functional — Hirschsprung’s disease, idiopathic megacolon, pseudo-obstruction.The symptoms of chronic obstruction differ in their predominance, timing and degree from acute obstruction. Constipation appears first. It is initially relative and then absolute, associated with distension. In the presence of large bowel disease, the point of greatest distension is in the caecum and this is heralded by the onset of pain. Vomiting is a late feature and therefore dehydration is exceptional. Examination is unremarkable, save for confirmation of distension and the onset of peritonism in late cases. Rectal examination may confirm the presence of faecal impaction or a tumour.InvestigationPlain abdominal radiography may confirm the presence of large bowel obstruction. All such cases should be confirmed by a subsequent single contrast water-soluble enema study to rule out functional disease. Organic disease requires a laparotomy, whilst functional disease requires colonoscopic decompression and conservative management.In the presence of organic obstruction, after resuscitation surgical management depends on the underlying cause and the relevant chapters in this book should be consulted.Hirschsprung’s diseaseThis is due to failure of complete migration of the ganglion cells of the large bowel to the anus. This results in an aganglionic segment producing physiological obstruction. Eighty per cent present in the neonatal period with acute large bowel obstruction, whilst 20 per cent present with failure to thrive or severe constipation.Barium enema reveals a characteristic narrow segment, whilst a full-thickness rectal strip biopsy will show absence of ganglion cells. The rectoanal inhibitory reflex is absent on physiological testing.Treatment consists of an initial loop colostomy followed by a definitive pull-through procedure.  Further readingBizer, L.S., Liebling, R.W, Delaney, H.M. and Gliedman, M.L. (1981) Small bowel obstruction: the role of non-operative treatment in simple intestinal obstruction and predictive criteria for strangulation obstruction. Surgery,89, 407—13.Dudley, H.A.F., Radcliffe, A.G. and McGeehan, D. (1980) Intra-operative irrigation of the colon to permit primary anastomosis. British Journal of Surgery, 67, 80—8 1.Ellis, H, (1971) The causes and prevention of postoperative sntraperitoneal adhesions. Surgery, Gynaecology and Obstetrics, 133, 497—511.Fielding, L.P. (1993) Colonic surgery for acute conditions:obstruction. In Rob & Smith’s Operative Surgery, 5th edn (eds L.P. Fielding and S.M. Goldberg), ButterworthHeinemann, Oxford, pp. 397—415.Omas, S. and Shirazi, S.S. (1984) Colonic pseudo-obstruction. American Journal of Gastroenterology, 79, 525—32.

Jones, P.F. (1993) Stomas. In Rob & Smith’s Operative Surgery, 5th edn (eds L.P. Fielding and S.M. Goldberg), Butterworth-Heinemann, Oxford, pp. 240—301.