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.
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
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