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The acute abdomen 295
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• Leakage from the liver, the gallbladder or its ducts
after a biliary tract operation, for example
genic biliary injury during laparoscopic
cholecystectomy.
•
Perforation of an acutely inflamed gallbladder or
transudation of the bile through a gangrenous but
non-
perforated gallbladder.
Non- traumatic perforation of the bile duct where
•
the extrahepatic duct or intrahepatic duct is perforated spontaneously without traumatic or iatrogenic injury.
• Spontaneous perforation of the gallbladder, associated with infections, malignancies, stones,
thrombosis of intramural vessels, increased biliary
pressures, use of corticosteroids and systemic diseases such as diabetes mellitus and atherosclerotic heart disease.
•
Idiopathic is a rare but well- recognized condition
in which bile peritonitis occurs without obvious
cause, possibly a small perforation due to a calculus, which then becomes sealed.
Biliary peritonitis is associated with high risk of
morbidity and mortality, particularly in highelderly patients. The clinical signs and symptoms of
bile leakage may be nonrecognition and consequent increased risk of complications. The clinical picture is determined by the
amount and rate of bile leakage into the abdominal
cavity.
Imaging is crucial for establishing an early diagnosis and in guiding treatment.
CT and ultrasound can identify a collection of
•
peri- hepatic fluid.
• Magnetic resonance cholangiopancreatography
(MRCP) can detect active or contained bile leaks
and can help localize the site of leakage, which in
turn can help determine if endoscopic management is sufficient, or if surgical management is
warranted.
• ERCP may provide diagnostic confirmation of a
bile leak and also provides the opportunity of concurrent therapy, for example through common
bile duct stone removal, or elimination of the
transpapillary pressure gradient either by a
sphincterotomy, stent insertion or both.
It is important to drain the abdominal contamination caused by infected bilious peritoneal fluid,
which can be attempted through radiologically
guided drain insertion when nonment is pursued. The gallbladder itself may be
drained through a cholecystostomy (drain in the
specific resulting in delayed
surgical manage-
iatro-
risk
gallbladder). Surgery (with abdominal lavage) is an
effective and definitive treatment for biliary peritonitis and can deal with the underlying cause of bile
leak. For example, cholecystectomy is the definitive
treatment for biliary peritonitis due to gallbladder
perforation (see chapter34).
Mesenteric ischaemia
Pathophysiology
Bowel ischaemia is an important cause of an acute
abdomen. Splanchnic ischaemia is caused by a blood
supply which is inadequate for the metabolic and oxygen demands of the intraThe coeliac artery, the superior mesenteric artery
(SMA) and the inferior mesenteric artery (IMA) supply
the foregut (liver, spleen, stomach to second part of
duodenum), midgut (second part of duodenum to
splenic flexure of colon) and hindgut (splenic flexure of
colon to rectum), respectively. Mesenteric ischaemia is
caused by insufficient blood flow through the mesenteric blood vessels which potentially compromises the
small and large intestine. The overall prevalence of
acute mesenteric ischaemia is 0.1% of all hospital
admissions. Ischaemic colitis is caused by inadequate
blood supply specifically to the colon and is the most
common ischaemic injury of the gastrointestinal tract.
Ischaemia of the small or large bowel leads to
bowel wall spasm (causing vomiting or diarrhoea),
bowel wall oedema and mucosal sloughing with
bleeding into the gut wall, lumen and peritoneal cavity. Injury to the affected bowel may range from
reversible ischaemia to transmural infarction with
necrosis, gangrene and subsequent perforation.
During bowel ischaemia, the enteric mucosal barrier becomes disrupted, allowing the translocation of
bacteria, endotoxins and vasoactive substances into
the systemic circulation. A generalized proinflammatory state is produced with release of cytokines by
macrophages, with activation of the complement and
coagulation systems. This may lead to systemic
inflammatory response syndrome, septic shock and
multiorgan failure.
Aetiology
Mesenteric ischaemia may result from embolic (50%
of cases) or thrombotic (20% of cases) arterial occlusion,
thrombotic venous occlusion (10% of cases), or from
non- occlusive processes (20% of cases).
abdominal visceral organs.
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Acute mesenteric arterial
embolism
Emboli may arise from the left atrium in atrial fibrillation, or from a mural thrombus from a dilated ventricle secondary to myocardial infarction, vegetative
endocarditis, valvular disease, mycotic aneurysm, or
due to a ruptured atheromatous plaque of the aorta.
Rarely, it may be a paradoxical embolus originating in
the deep leg veins and crossing the septum of the
heart through a patent foramen ovale (see Figure
13.3). The SMA is the most susceptible visceral vessel
to emboli due to its size and angle at its origin from
the aorta. Embolism has a better overall prognosis
than thrombosis.
Acute mesenteric arterial
thrombosis
This represents progressive worsening of atherosclerotic vascular disease. It is associated with a history of chronic mesenteric ischaemia where patients
complain of ‘intestinal angina’, i.e., postprandial
abdominal pain in which severe abdominal pain
follows meals with a resultant fear of eating and
consequent weight loss. Minor degrees of occlusion
may be overcome by the development of a collateral
circulation, particularly if the occlusion develops
slowly. Patients may have a history of atherosclerotic disease at other sites (e.g. ischaemic heart
disease, cerebrovascular disease and peripheral
vascular disease). Thrombosis commonly occurs at
the origin of arteries resulting in extensive bowel
ischaemia, whereas embolism commonly occurs in
more distal arterial branches resulting in more
limited bowel ischaemia.
Mesenteric venous thrombosis
In mesenteric venous thrombosis, blood outflow is
restricted causing bowel wall oedema and increase in
vascular resistance, resulting in bowel ischaemia. Causes
of mesenteric venous thrombosis include portal hypertension, post- surgery (e.g. post- splenectomy, portacaval
surgery, pelvic surgery), pressure on the superior mesenteric vessels by a tumour, septic thrombophlebitis (e.g.
secondary to Crohn’s disease), trauma, pancreatitis or
intra- abdominal sepsis. It may affect younger patients
and may be associated with hypercoagulable states, e.g.
due to factor V Leiden deficiency, polycythaemia rubra
vera, protein C and S deficiency, antithrombin III defic ienc y,
thrombocytosis, dysfibrinogenaemia, sickle cell disease,
cancer, pregnancy and oral contraceptive use.
Low blood ow states
During states of shock or hypoperfusion, the mesenteric blood flow is preferentially reduced in order to
maintain blood supply to other vital organs and is one
of the last systems to recover blood flow when circulation improves. Nonmay occur in low blood flow states causing mesenteric
ischaemia, such as shock, hypovolaemia, dehydration,
sepsis, low cardiac output, congestive cardiac failure,
myocardial infarction, transient hypotension (e.g. perioperative) and cardiopulmonary bypass surgery.
occlusive ischaemia of the intestine
Other causes ofmesenteric
ischaemia
• Splanchnic vasoconstriction or vasospasm: caused
by reduced blood flow, vasopressors (e.g. vasopressin, α-
agonists), digoxin, drugs which produce
vasospasm (e.g. cocaine, amphetamines).
Intrinsic small vessel disease or vasculitis due to
•
rheumatoid arthritis, systemic lupus erythematosus, polyarteritis nodosa, dermatomyositis,
amyloidosis, diabetes mellitus.
Luminal bowel obstruction (e.g. due to strangulated
•
internal hernia, volvulus, tumour, intussusception).
•
Post- angiography complications: subintimal artery
dissection, thrombosis, arterial embolization.
Vascular surgery complications (e.g. aortic sur-
•
gery, renal allograft recipients).
•
Abdominal compartment syndrome.
• Tumour compression.
• Aortic dissection.
• Blunt or penetrating trauma.
primary
Clinical features
History
Initially, symptoms and signs are non- specific and are
most commonly found in advanced disease. A high
index of clinical suspicion should be maintained to
avoid delay in diagnosis and treatment. Patients
affected tend to be middle- aged or elderly patients
with risk factors for thromboembolism and atherosclerotic disease. They may have a history of intestinal
angina. There may be some pre- existing factor such as
heart valvular disease or liver disease. They may have
atrial fibrillation, either as a long- standing finding or of
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new onset. The classic triad of mesenteric ischaemia is:
Acute colicky abdominal pain.
•
•
Rectal bleeding.
•
Circulatory shock.
Commonly, the patient gives a history of vague, diffuse, colicky or constant abdominal pain, progressively getting worse. The abdominal pain may be
severe and disproportionate to physical examination
findings. The onset of the abdominal pain may be
sudden if the cause is an embolus, or of insidious
onset if thrombus is the cause. The patient may have
vomiting or diarrhoea due to bowel wall spasm and
rectal bleeding due to mucosal sloughing.
Examination
There may be no, or mild- to- moderate, abdominal
tenderness initially, until it progresses to perforation
or infarction causing peritonitis. The patient then
may become generally tender, and a vague, tender
mass may be felt, which is the infarcted bowel. Bowel
sounds range from hyperactive to absent. The abdomen may be distended, and rectal examination may
show blood mixed with stool. Examination may identify atrial fibrillation, heart murmurs or abdominal
murmurs (due to arterial stenosis). The patient may
have weak peripheral pulses (due to peripheral vascular disease or hypoperfusion) and signs of sepsis
(e.g. tachycardia, tachypnoea, pyrexia).
Investigations
• Blood tests: Laboratory findings are non- specific but
may include leucocytosis, haemoconcentration, el evated serum lactate and metabolic acidosis, elevated
liver enzymes (ALT, AST) due to hepatic ischaemia,
elevated amylase, elevated lactate dehydrogenase
(LDH) and elevated CRP. Dmarker for splanchnic ischaemia but is not specific.
Blood tests should include coagulation studies (PT,
APTT, INR) and screening for coagulopathies.
Plain radiographs: Erect chest and abdominal
•
X- rays often appear normal but may show signs of
perforated viscus, ileus, bowel obstruction, thickened bowel wall due to oedema, pneumatosis
intestinalis (i.e., submucosal air) and thumbprinting from submucosal oedema.
• Electrocardiogram (ECG) may show atrial fibrilla-
tion or myocardial infarction.
dimer is a sensitive
The acute abdomen 297
Echocardiography may identify the source of
•
embolization or demonstrate valvular pathology
(e.g. valvular vegetations).
•
Flexible sigmoidoscopy or colonoscopy can be per-
formed to confirm ischaemic colitis by demonstrating mucosal ulceration, haemorrhage, oedema
and fragility consistent with colonic ischaemia.
•
Computed tomography: A CT angiogram can iden-
tify bowel wall oedema, thumbprinting, pneumatosis intestinalis, pericolic stranding, portal venous
gas, pneumoperitoneum, lack of bowel wall
enhancement and ischaemia of other organs. It can
determine the extent of the disease, i.e., how much
bowel is affected and whether it is perforated. It
demonstrates arterial or venous occlusion and
excludes other differential diagnoses. It is noninvasive and readily available. In patients suspected
to have mesenteric vessel occlusion, the priority is
early diagnosis and treatment to improve chances
of survival, justifying the need for an urgent CT scan
with intravenous contrast despite the acknowledged risk of contrast- induced renal failure and
challenges in the presence of established renal
impairment. Renal support in these instances must
be discussed with the intensive care team.
• Diagnostic laparoscopy or laparotomy can be considered where other investigations have been
inconclusive.
Treatment
• Oxygen therapy. Consider invasive ventilation to
improve oxygenation.
Analgesia, with morphine if needed.
•
• Nasogastric tube for abdominal decompression.
• Optimization of volume status with intravenous
fluid resuscitation and optimization of cardiac
output. Monitor urine output, arterial pressure
and central venous pressure to guide rehydration.
• Use of inotropes if needed, but vasopressors (e.g.
adrenaline, noradrenaline, vasopressin, high dose
dopamine) may worsen ischaemia.
• Treat underlying conditions (e.g. atrial fibrillation,
cardiac failure, myocardial infarction).
• Broad- spectrum antibiotics covering grampositive, gram- negative and anaerobic bacteria.
• Anticoagulation with intravenous heparin in the
short- term, particularly if surgery is to be considered
as heparin is more reversible than the low molecular
weight heparin alternatives. Anticoagulation is the
main treatment for mesenteric venous thrombosis.
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In the long term, anticoagulation in the form of warfarin or novel oral anticoagulants (NOACs) should
be considered after embolic arterial occlusion or
after mesenteric venous occlusion. In addition, longterm therapy should address patient’s risk factors,
and antiplatelet agents and statins prescribed after
thrombotic arterial occlusion.
•
Endovascular therapy is an option which may be
available through interventional radiology.
Endovascular therapy options include intraarterial thrombolytic therapy (e.g. with tissue plasminogen activator) or intra- arterial vasodilators
(e.g. with papaverine). Other endovascular therapy options include aspiration embolectomy of
the SMA, or angioplasty and stenting for proximal
arterial thrombosis (e.g. origin of SMA).
Surgery
Surgery is the mainstay of treatment especially for
patients with signs of peritonitis due to perforation or
infarction, and where nonIntraoperatively, the extent and severity of intestinal
ischaemia is determined by assessing colour and peristalsis of the bowel and pulsations of the mesenteric
arteries. Ischaemic or necrotic bowel is resected.
Embolectomy, thrombo- endarterectomy or arterial
operative therapy fails.
reconstruction (e.g. mesenteric artery bypass) may be
required to re-
After bowel resection, the options are:
•
Primary anastomosis, provided the blood supply
to both proximal and distal bowel margins is adequate and the patient is not haemodynamically
compromised.
Stoma formation– double- barrelled stoma or end
•
stoma with separate mucous fistula. This is safer
and allows assessment of the bowel viability
postoperatively.
•
Staple off both bowel ends leaving anastomosis or
stoma formation for a second- look procedure.
Surgeons may rehours to reassess bowel viability. The abdomen may
be left open (laparostomy) to prevent abdominal
compartment syndrome.
For many patients where the entire small bowel is
found to be non- viable (due to thrombosis of the SMA
origin), resection should not be performed, and palliative treatment may be appropriate. However, in
selected cases, such as young patients without significant
comorbidities who have undergone extensive resection of the small bowel, longnutrition and potential intestinal transplantation may
be considered.
establish arterial blood supply.
explore the abdomen at 24 to 48
term total parenteral
Intestinal obstruction
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andparalytic ileus
Christopher Watson
Learning objectives
✓ To know the causes of mechanical obstruction in all age groups.
✓ To recognize the four common clinical features of mechanical
obstruction, the key points of clinical examination and the management
principles.
✓ To know the causes and management of paralytic ileus.
✓ To dierentiate mechanical obstruction from paralytic ileus.
•
The word ‘ileus’ comes from the Greek verb ‘to roll’,
from which it became applied to colic and hence to
obstruction. Obstructions are subdivided into
mechanical and paralytic, the latter produced by lack
of intestinal motility.
Mechanical obstruction
Classication
Intestinal obstruction (Box30.1) is a restriction to the
normal passage of intestinal contents. It may be
divided into two main groups: paralytic and mechanical. Paralytic (or adynamic) ileus is discussed later.
Mechanical intestinal obstruction is further classi-
fied according to the following:
Speed of onset: acute, chronic, acute on chronic.
•
• Site: high or low.
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
Nature: simple versus strangulating.
• Aetiology.
Speed ofonset
The speed of onset determines whether the obstruction is acute, chronic or acute on chronic.
Acute obstruction: the onset is rapid and the symp-
•
toms severe.
• Chronic obstruction: the symptoms are insidious
and slowly progressive, as, for example, in most
cases of carcinoma of the large bowel.
•
Acute on chronic obstruction: A chronic obstruc-
tion may develop acute symptoms as the
obstruction suddenly becomes complete, for
example when a narrowed lumen becomes totally
occluded by inspissated bowel contents.
Site
The site of the obstruction is generally classified
according to whether it originates in the small or large
intestine.
30
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Box 30.1 Intestinal obstruction
There are three important points to remember about
intestinal obstruction.
1 It is diagnosed by the presence of:
a Colicky abdominal pain.
b Distension.
c Absolute constipation.
d Vomiting.
2 Examination should always include a search for
hernias and abdominal scars, including laparoscopic port sites
3 Is it simple or strangulating? Features suggesting
strangulation are:
a Change in character of pain from colicky to
continuous.
b Tachycardia.
c Pyrexia.
d Peritonism.
e Bowel sounds absent or reduced.
f Leucocytosis.
g Raised C- reactive protein (CRP).
Nature
The nature of the obstruction is divided into simple or
strangulating.
•
Simple obstruction occurs when the intestine is
occluded without damage to its blood supply.
Strangulating obstruction is when the blood
•
supply of the involved segment of intestine is
compromised, as may occur, for example, in
strangulated hernia, volvulus, intussusception or
when a loop of intestine is occluded by a band.
Gangrene of the strangulated bowel is inevitable
if left untreated.
Aetiology
Whenever one considers obstruction of a tube anywhere in the body, the causes should be classified
into the following:
•
Causes in the lumen.
• Causes in the wall.
• Causes outside the wall.
This can be applied to intestinal obstruction.
• In the lumen: faecal impaction, food bolus, intussusception, gallstone ‘ileus’, parasites (e.g. ascaris
worms in small bowel).
In the wall: congenital atresia, Crohn’s disease,
•
tumours, diverticulitis of the colon, carcinoma of
the colon.
•
Outside the wall: strangulated hernia (external or
internal), volvulus and obstruction due to adhesions or bands.
It is also useful to think of the common intestinal
obstructions that may occur in each age group.
• Neonatal: congenital atresia and stenosis (e.g.
duodenal atresia), imperforate anus, volvulus
neonatorum, Hirschsprung’s disease and meconium ileus.
• Infants: intussusception, Hirschsprung’s disease,
strangulated hernia and obstruction due to
Meckel’s diverticulum.
•
Young adults and middle age: strangulated hernia,
adhesions and bands, Crohn’s disease.
•
The elderly: strangulated hernia, carcinoma of the
colon, colonic diverticulitis causing stricture,
impacted faeces.
A strangulated hernia is an important cause of intestinal obstruction from infancy to old age. The hernial
orifices must, therefore, be carefully examined in
every case.
Pathology
When the bowel is obstructed by a simple occlusion,
the intestine distal to the obstruction rapidly empties
and becomes collapsed. The bowel above the obstruction becomes dilated, partly with gas (most of which
is swallowed air) and partly with fluid poured out by
the intestinal wall together with the gastric, biliary
and pancreatic secretions. There is increased
peristalsis in an attempt to overcome the obstruction,
which results in intestinal colic. As the bowel distends,
the blood supply to the tensely distended intestinal
wall becomes impaired and, in extreme cases, there
may be mucosal ulceration and eventually perforation. Perforation may also occur from the pressure of
a band or the edge of the hernia neck on the bowel
wall, producing local ischaemic necrosis, or from
pressure from within the gut lumen, for example, by a
faecal mass (stercoral perforation).
In strangulating obstruction, the integrity of the
mucosal barrier is lost as ischaemia progresses, so
bacteria and their toxins can no longer be contained
within the lumen. Transudation of organisms into the
peritoneal cavity rapidly takes place, with secondary
Intestinal obstruction andparalytic ileus 301
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peritonitis. Unrelieved strangulation is followed by
gangrene of the ischaemic bowel with perforation.
The lethal effects of intestinal obstruction result
from fluid and electrolyte depletion owing to the
copious vomiting and loss into the bowel lumen, protein loss into the gut and toxaemia due to migration of
toxins and intestinal bacteria into the peritoneal cavity, either through the intact but ischaemic bowel wall
or through a perforation.
Clinical features
The four cardinal symptoms of intestinal obstruction
are:
Colicky abdominal pain.
1
Distension.
2
3 Absolute constipation.
4 Vomiting.
It is important to note that not all of these four features need necessarily be present in a case of intestinal obstruction. The sequence of onset of symptoms
will help localize the obstruction to the upper or
lower intestine.
Pain
This is usually the first symptom of intestinal obstruction and is colicky in nature. In small bowel obstruction, it is periumbilical, reflecting the midgut
derivation of this bowel; in distal colonic obstruction,
it may be more suprapubic in location. In postoperative obstruction, the colic may be disguised by the
general discomfort of the operation and by opiates
that the patient may be receiving.
Distension
This is particularly marked in chronic large bowel
obstruction and also in volvulus of the sigmoid colon.
In proximal small bowel obstruction, there may only
be a short segment of bowel proximal to the obstruction, and distension will not usually be marked.
Absolute constipation
Absolute constipation is the failure to pass either flatus
or faeces. Although it is a usual feature of acute obstruction, a partial or chronic obstruction may be accompanied by the passage of small amounts of flatus. Absolute
constipation is an early feature of large bowel obstruction but a late feature of small bowel obstruction as,
even when the obstruction is complete, the patient
may pass one or two normal stools as the lower bowel
empties after the onset of the obstruction.
Vomiting
This usually occurs early in proximal small bowel
obstruction, but is often late or even entirely absent in
large bowel obstruction. In the late stages of intestinal
obstruction, the vomiting becomes faeculent but not
faecal.
Faeculent vomiting is due to bacterial decomposition of the stagnant contents of the obstructed small
intestine and of the altered blood that may transude
into the bowel lumen.
True vomiting of faeces only occurs in patients with
gastrocolic fistula (e.g. because of a carcinoma of the
stomach, carcinoma of the colon or ulceration of a
stomal ulcer into the colon), or in coprophagia.
Clinical examination
The patient may be obviously dehydrated if vomiting
has been copious. The patient is in pain and may be
rolling about with colic. The pulse is usually elevated,
but the temperature is frequently normal. A raised
temperature and a tachycardia suggest strangulation.
The abdomen is distended and visible peristalsis may
be present. Visible peristalsis itself is not diagnostic of
intestinal obstruction, as it may be seen in the normal
subject if the abdominal wall is very thin.
During inspection, it is important to look carefully
for two features: (1) the presence of a strangulated
external hernia, which may require a careful search in
the case of a small strangulated femoral hernia in a
very obese and distended patient, and (2) the presence of an abdominal scar. Intestinal obstruction in
the presence of this evidence of a previous operation
immediately suggests adhesions as the cause.
Palpation reveals generalized abdominal tenderness. A mass may be present (e.g. in intussusception
or carcinoma of the bowel).
Bowel sounds are usually accentuated and tinkling.
Rectal examination may reveal an obstructing mass in
the pouch of Douglas, the apex of an intussusception
or faecal impaction.
Simple obstruction versus
strangulating obstruction
Clinically, it is extremely difficult to distinguish with
any certainty between simple obstruction and
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strangulation. The distinction is important, as strangulating obstruction with ensuing peritonitis has a high
mortality. Features suggesting strangulation include:
Toxic appearance, with a rapid pulse and some
•
elevation of temperature.
Colicky pain, becoming continuous as peritonitis
•
develops.
•
Tenderness and abdominal rigidity more marked.
Bowel sounds becoming reduced or absent,
•
reflecting peritonism.
•
Raised white cell count, mostly neutrophils, which
is usual with infarcted bowel.
Special investigations
• Computed tomography (CT) scan, combined with
oral water- soluble contrast (e.g. Gastrografin), is
the investigation of choice; it can localize the site
of obstruction, detect obstructing lesions and
colonic tumours and may diagnose unusual hernias (e.g. obturator hernias). The addition of intravenous contrast allows an assessment of bowel
wall perfusion, which is very helpful when assessing for strangulating obstruction.
• Water- soluble contrast study. An emergency con-
trast enema may detect a suspected large bowel
obstruction due to carcinoma or diverticular disease. Unlike a normal barium enema, no preexamination laxative is given because of the risk of
exacerbating the obstruction, and causing perforation if a closed loop exists. This has been largely
superseded by CT scan with rectal contrast.
• Abdominal X- rays (erect and supine) were widely
used prior to the widespread availability of CT. A
loop or loops of distended bowel are usually seen,
together with fluid levels on an erect film.
– Small bowel obstruction is suggested by a lad-
der pattern of dilated loops, their central position and by striations that pass completely
across the width of the distended loop produced by the circular mucosal folds (known as
valvulae conniventes).
– Distended large bowel tends to lie peripherally
and to show the haustrations of the taenia coli,
which do not extend across the whole width of
the bowel. A small percentage, perhaps 5%, of
patients with intestinal obstruction show no
abnormality on plain X- rays because the bowel
is completely distended with fluid in a closed
loop and without the fluid levels produced by
co- existent gas.
Treatment
Although the treatment of specific causes of intestinal
obstruction is considered under the appropriate
headings, certain general principles can be enunciated here.
Chronic large bowel obstruction, slowly progressive and incomplete, can be investigated with less
urgency (including sigmoidoscopy or colonoscopy
and CT scan) and treated electively.
Acute obstruction, of sudden onset, complete and
with risk of strangulation, is invariably an urgent
problem requiring emergency surgical intervention.
Preoperative preparation inacute
obstruction
1 Gastric aspiration by means of nasogastric tube.
This helps to decompress the bowel and lessen the
risk of inhalation of gastric contents during induction of anaesthesia.
2 Intravenous fluid replacement. The large amount
of fluid sequestered into the gut, together with
losses due to vomiting, means that a lot of fluid
may be required. Hartmann’s solution or normal
saline is given, with potassium if this is low and
renal function satisfactory.
3
Antibiotic therapy is commenced if intestinal
strangulation is likely (or is found at operation).
Operative treatment
The affected bowel is carefully inspected to determine its viability, either at the site of the obstruction
(e.g. where a band or the margins of a hernial orifice
have pressed against the bowel) or the whole segment
of bowel involved in a closed loop obstruction. Loss of
viability is determined by four signs:
1
Loss of peristalsis.
2 Loss of normal sheen.
3 Colour (greenish or black bowel is non- viable;
purple bowel may still recover).
4 Loss of arterial pulsation in the supplying
mesentery.
Doubtful bowel may recover after relief of the obstruction. It should be reassessed after it has been left for a
few minutes wrapped up in a warm wet pack. If extensive areas of bowel are of doubtful viability, it may be
worthwhile planning a second48 hours to reassess the necessity for an extensive
bowel resection.
look laparotomy in
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The general principle is that small bowel in intestinal obstruction can be resected and primary anastomosis performed because of its excellent blood
supply. Large bowel obstruction is treated by resection of the obstructing lesion, with a primary ileocolic
anastomosis in the case of obstructing lesions proximal to the splenic flexure. Leftaged by excision of the affected segment and either a
primary anastomosis with temporary covering stoma
or exteriorizing the proximal colon as a temporary
end colostomy and either exteriorizing the distal end
as a mucous fistula (see Chapter28), or more commonly, closing the distal large bowel (often the rectum) and leaving it inside the abdomen (Hartmann’s
procedure
colonic obstruction reflects the intraluminal bacterial
flora and poorer blood supply of the large bowel; a
colohigher risk of anastomotic leak in the presence of
obstruction. Where a primary large bowel anastomosis is performed, a defunctioning loop ileostomy
should be considered in order to mitigate the effects
of an anastomotic leak. The role of an endoscopically
placed colonic stent in the management of acute
malignant large bowel obstruction is discussed in
Chapter27.
1
). This difference in management of
colonic or colorectal primary anastomosis has a
sided lesions are man-
Conservative treatment
Conservative treatment of obstruction by means of
intravenous fluid and nasogastric aspiration (‘drip
and suck’) is indicated only under the following
conditions.
•
When distinction from postoperative paralytic
ileus is uncertain and when a period of careful
observation is indicated.
•
When the obstruction is one of repeated episodes
due to extensive intradering surgery hazardous, and when, once again,
a short period of observation with conservative
treatment is indicated. Gastrografin is given via
the NG tube; if it fails to pass through the
obstructed bowel, surgery is indicated. It is also
indicated if distension is increasing, pain is worsening or there is an increase in abdominal tenderness or a rising pulse.
abdominal adhesions, ren-
• When chronic obstruction of the large bowel has
occurred. Here, it is reasonable to attempt to
remove the obturating faeces by enema, prepare
the bowel and carry out further investigation and a
subsequent elective operation.
Closed loop obstruction
This is a specific form of mechanical obstruction. It is
characterized by increasing distension of a loop of
bowel due to a combination of complete obstruction
distally and a valveing the bowel to fill but preventing reflux back. It is
most commonly seen with a leftobstruction, in the presence of a competent ileocaecal valve. The caecum, the most distensible part of the
large bowel, blows up like a balloon, and perforation
of the caecum, with faecal peritonitis, may occur if the
obstruction is not rapidly relieved. Diagnosis is most
commonly made on CT scan showing characteristic
dilation of the caecum and dilated colon down to the
site of stricture/obstruction. Other examples of closed
loop obstruction include volvulus (gastric, caecal,
sigmoid) and stomal obstruction of the afferent loop
following Pólya
like mechanism proximally allow-
sided colonic
2
partial gastrectomy.
Adhesive obstruction
Intra- abdominal adhesions are an almost invariable
consequence of abdominal or pelvic surgery, although
they are less common after minimal access (laparoscopic and robotic) surgery than after open surgery. In
most cases, these are asymptomatic, but a small number of patients develop small bowel obstruction as a
consequence. This may occur at any time from the
immediate postoperative period to many years later.
Because abdominal surgery is now so common, adhesions account for about threesmall bowel obstruction (large bowel obstruction from
this cause is extremely rare). Treatment is initially conservative, with nasogastric suction and intravenous
fluid replacement. Clinical features of strangulation,
peritonitis or failure to respond to the conservative
regimen are indications for urgent surgery.
quarters of all cases of
1
Henri Hartmann (1860–1952), Professor of Surgery, Hôtel
Dieu, Paris, France.
2
Eugen Alexander Pólya (1876–1944), Surgeon, St Stephen’s
Hospital, Budapest, Hungary.
304 Intestinal obstruction andparalytic ileus
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Volvulus
Denition
A twisting of a loop of bowel around its mesenteric
axis, which results in a combination of obstruction
together with occlusion of the main vessels at the
base of the involved mesentery. Most commonly, it
affects the sigmoid colon, caecum and small intestine, but volvulus of the gallbladder and stomach may
also occur.
Aetiology
Precipitating factors include:
•
An abnormally mobile loop of intestine, for exam-
ple congenital failure of rotation of the small intestine, or a particularly long sigmoid loop.
•
An abnormally loaded loop – as in the sigmoid
colon of chronic constipation.
•
A loop fixed at its apex by adhesions, around
which it rotates.
A loop of bowel with a narrow mesenteric
•
attachment.
Sigmoid volvulus
This occurs usually in elderly, constipated patients.
Itis four times more common in men than in women.
It is relatively rare in the UK (about 2% of intestinal
obstructions) but is much more common in Russia,
Scandinavia and central Africa. The loop of sigmoid
colon usually twists anticlockwise, from one- half to
three turns.
Clinical features
There is a sudden onset of colicky pain with characteristic gross and rapid dilation of the sigmoid
loop.
A plain X- ray (or CT scan) of the abdomen shows
an enormously dilated oval gas shadow on the left
side, which may be looped on itself to give the typical
appearance various described as the ‘coffee bean’
sign or ‘bent inner- tube’ sign. If left untreated, the
strangulated bowel undergoes gangrene, resulting in
death from peritonitis. The caecum is usually visible
and dilated in the right lower quadrant, distinguishing it radiologically from caecal volvulus.
Treatment
An urgent flexible sigmoidoscopy should be performed. This often untwists an early volvulus and
isaccompanied by the passage of vast amounts of flatus and liquid faeces. If this method fails, the volvulus
is untwisted at surgery (open or laparoscopic) and the
bowel is decompressed via a rectal tube threaded
upwards from the anus. If gangrene has occurred, the
affected segment is excised, the proximal end being
brought out as an end colostomy while the distal end
is stapled closed (a Hartmann’s procedure).
Recurrent sigmoid volvulus is an indication for
elective resection of the redundant sigmoid loop, or
for percutaneous endoscopic colostomy (PEC) in
those who are unfit for major surgery.
Caecal volvulus
Caecal volvulus is usually associated with a congenital malrotation where, in contrast to the incomplete
rotation which causes volvulus neonatorum (see later
in this chapter), the caecum and proximal ascending
colon rotate beyond the right iliac fossa (RIF) during
development so that, instead of being fixed in the RIF,
it has a persistent mesentery.
Clinically, there is an acute onset of pain in the RIF
with rapid abdominal distension. Plain radiograph or
CT of the abdomen shows a grossly dilated caecum,
which is often ectopically placed and is frequently
located in the left upper quadrant of the abdomen.
Treatment
At surgery, the volvulus is untwisted. Right hemicolectomy is necessary, especially if the caecum is
infarcted; it is also the most reliable way to prevent
recurrence.
Small intestine volvulus inadults
This may occur when a loop of the small intestine is
fixed at its apex by adhesions or by a fibrous remnant
of the vitelloMeckel’s diverticulum). Occasionally, the apex of the
volvulus bears a tumour.
In Africa, primary volvulus of the small bowel is
relatively common, and may be due to the loading of
a loop of gut with large quantities of vegetable foodstuffs. The clinical picture is one of acute intestinal
obstruction.
intestinal duct (often associated with a
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