Treatment of acute intestinal obstruction

There 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 treatment

The 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 obstruction

This 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 bands

In 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 adhesions

Several 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 obstruction

Differentiation 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 obstruction

Internal hernia

Internal 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 strictures

Small 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 obstruction

Bolus 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 intussusception

This 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 95 per 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 few minutes, 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 5 per 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 5 per cent of idiopathic cases. Anchorage of the last part of the terminal ileum to the ascending colon has been advocated where repeat surgery is required.