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The small intestine
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Justin Davies
Learning objectives
✓ To know the varying presentations of a Meckel’s diverticulum.
✓ To have knowledge of Crohn’s disease of the small intestine, in
particular its varying presentations and treatment.
✓ To know the rare possibility of small bowel tumours, and how they may
present.
• Intussusception (ileoileal), often gangrenous by
Meckel’s diverticulum
Meckel’s diverticulum1 is the remnant of the vitellointestinal duct of the embryo. It lies on the antimesenteric border of the ileum and, as an approximation,
occurs in 2% of the population, arises approximately
60cm (2 feet) from the caecum, and averages 5 cm
(2inches) in length.
Clinical features
Meckel’s diverticulum may present in numerous
ways.
A symptomless finding at operation or autopsy.
•
•
Acute inflammation, clinically similar to acute
appendicitis.
• Perforation by a foreign body, presenting as
peritonitis.
1
Johann Frederick Meckel (1781–1833), Professor of
Anatomy and Surgery, Halle, Germany. His grandfather and
father were both Professors of Anatomy.
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
the time the patient comes to operation.
•
Peptic ulceration due to heterotopic gastric epithe-
lium in the diverticulum, which bears HClsecreting parietal cells. This particularly occurs in
children and characteristically is the cause of melaena at about the age of 10 years. Rarely, the peptic
ulceration perforates or gives rise to pain after eating. The diverticulum may also contain ectopic
pancreatic tissue.
•
Patent vitellointestinal duct, presenting as
an umbilical fistula that discharges intestinal
contents.
• Raspberry tumour at the umbilicus due to a persistent
umbilical extremity of the duct.
• Vitellointestinal band stretching from the tip of the
diverticulum to the umbilicus, which may obstruct
a loop of small intestine or act as the apex of a
small bowel volvulus.
Special investigations
Most diverticula are incidental findings. However, the
following investigations may be indicated.
Computed tomography (CT) scan may demon-
•
strate the diverticulum, and given the increased
access to CT scans in emergency presentations,
the diagnosis may be increasingly made prior to
surgery.
25
246 The small intestine
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• Technetium scan. Radiolabelled technetium
99m
(
Tc) is taken up by gastric mucosa, and scintigraphy will outline the stomach and, in addition,
the Meckel’s diverticulum, usually near the right
iliac fossa (RIF).
Barium follow- through or small bowel enema may
•
show the diverticulum arising from the antimesenteric border of the ileum, but these investigations are much less commonly performed
nowadays.
Treatment involves surgical resection of the diver-
ticulum if it is symptomatic.
Crohn’s disease
Crohn’s disease2 is a non- specific inflammatory disease of the gastrointestinal tract, with diseased
segments sandwiched between normal segments
(i.e. it is discontinuous). Crohn and colleagues first
described its occurrence in the ileum and termed it
‘regional ileitis’. However, this description is inaccurate, as the disease may affect any part of the alimentary tract from the mouth to the anus. Crohn’s disease
may also affect the large bowel alone (see Chapter27).
Aetiology
The aetiology of Crohn’s disease likely has environmental (e.g. a triggering infection yet to be identified,
smoking) and genetic (20% of patients have an affected
relative) components. These aetiological factors
remain poorly understood, and other factors such as
stress and diet are more likely to trigger flares of the disease than be the initial cause. Recent work has pointed
to a genetic mutation in the NOD gene family, among
others. These genes are involved in the innate immune
response to bacterial antigens within the gut. This
observation may explain the success of dietary manipulation, such as the elemental diet (see later in this
chapter). The presence of granulomas on histology
previously led to suggestion of infection by a mycobacterium species, possibly Mycobacterium avium ssp.
paratuberculosis. However, the success of immunosuppression in the control of Crohn’s disease points to
an autoimmune cause, although an initial infectious
2
Burrill Bernard Crohn (1884–1983), Gastroenterologist,
Mount Sinai Hospital, NewYork, NY, USA. e disease was
rst described by Morgagni (1682–1771).
trigger (by an as- yet- unidentified causative organism)
may turn out to be important. Acute ileitis can also be
caused by bacteria such as Yersinia enterocolitica.
Pathology
Distribution
The small bowel is affected in two- thirds of cases,
with the terminal ileum being the most common site,
although the disease may affect any part of the gastrointestinal tract from the mouth to the anus. Oneof patients with ileal disease also have large bowel
manifestations.
third
Macroscopic appearance
In the acute stage, the bowel is bright red and swollen;
mucosal ulceration and intervening oedema result in
a ‘cobblestone’ appearance of the mucosa. The wall of
the intestine is greatly thickened, as is the adjacent
mesentery, and the regional lymph nodes are
enlarged. Mesenteric fat advances over the serosal
surface in affected segments, known as ‘fat wrapping’
or ‘creeping fat’. There may be skip areas of normal
intestine between involved segments. Fistulas may
occur into adjacent viscera, for example other loops
of bowel, the bladder, uterus or vagina.
Microscopic appearance
There is fibrosis, lymphoedema and a chronic inflammatory infiltrate through the whole thickness of the
bowel with noncells. Ulceration is present, with characteristic fissuring ulcers extending deeply through the mucosa.
These may extend through the bowel wall to form
abscesses, or fistulas into adjacent viscera.
caseating foci of epithelioid and giant
Clinical features
Crohn’s disease occurs at any age, but is particularly
common in young adults with a peak age of onset
between 20 and 40 years of age. There is no sex difference. The typical clinical picture is a young adult with
abdominal pain and diarrhoea, often with a palpable
mass in the RIF. However, Crohn’s disease may manifest clinically in several ways.
•
Acute Crohn’s disease. Crohn’s disease may pre-
sent like appendicitis with acute abdominal pain,
usually in the RIF, and vomiting. Rarely, there is
perforation of the bowel or acute haemorrhage.
The small intestine 247
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Unlike appendicitis, the history is usually of
several days or weeks, and investigation may
reveal anaemia, or other features of Crohn’s disease may be present. The typical features of
Crohn’s disease in the terminal ileum may be evident on CT scan, thus differentiating from appendicitis at presentation.
•
Intestinal obstruction. Following inflammatory
exacerbations, fibrosis of the intestinal wall
occurs, leaving stenosed segments (strictures)
that may result in intestinal obstruction.
Obstruction may also follow an intraperitoneal
abscess if this causes external compression of the
bowel.
•
Fistula formation. Fistulas may develop, penetrat-
ing adjacent loops of gut or the pelvic organs such
as bladder, uterus or vagina or they may be perianal. External faecal fistulas may follow operative
intervention.
• Malabsorption. Extensive involvement of the
small bowel produces malabsorption with steatorrhoea and multiple vitamin deficiencies. It is exacerbated when bowel resections have already
occurred.
• Diarrhoea. Diarrhoea may be due to inflammation and mucosal ulceration, colonic or rectal
involvement, bacterial overgrowth in obstructed
segments and malabsorption secondary to either
disease or short bowel following previous surgery.
Mucosal ulceration causes diarrhoea, with raised
faecal calprotectin levels and often anaemia.
•
Perianal disease. Ten per cent of patients with
small bowel Crohn’s disease also have perianal
disease, including anal skin tags, fissures, fistulas
and stenosis (see Chapter28).
Special investigations
Crohn’s disease is associated with anaemia, raised
faecal calprotectin and occasionally steatorrhoea.
Serum albumin is low, and inflammatory markers
such as Cdisease activity. Additional investigations include the
following.
• CT or magnetic resonance enteroclysis will demon-
reactive protein (CRP) are a helpful index of
strate areas of active Crohn’s disease, as well as
areas of stricture and any pre- stenotic dilatation. It
is also possible to demonstrate fistulas and to
assess for any extraluminal disease. MRI has the
advantage of no radiation exposure, but access to
MRI scans is more limited and some individuals
find the experience claustrophobic.
•
Small bowel enema, or enteroclysis, in which con-
trast is instilled into the duodenum via a nasogastric tube and followed fluoroscopically as it passes
through the bowel, is much less commonly
employed now with advances in CT and MRI, but
contrast injected via a likely fistula site on the
abdominal wall (a fistulogram) can often help to
delineate anatomy prior to surgery.
• Technetium- labelled leucocyte (white cell) scan is a
sensitive way to show the extent of disease activity.
Leucocytes are taken up in the inflamed segments,
and also localize to abscesses. These are less commonly performed now due to increased access to
CT and MRI scans.
Complications outside
thegastrointestinal tract
In addition to those already mentioned, the following
are associated with the disease.
•
Primary sclerosing cholangitis, arthritis, sacroilii-
tis, pyoderma gangrenosum, erythema nodosum,
and uveitis may occur, but are more common
when the colon is also involved.
• Renal calculi: usually oxalate stones secondary to
hyperoxaluria, which occurs as a consequence of
steatorrhoea.
•
Gallstones are more common in patients with ileal
Crohn’s disease, and in whom the ileum has been
resected. This is due to the interruption of the
enterohepatic bile salt circulation.
Treatment
Treatment is often medical initially, although surgery
is appropriate in the management of complications
and chronic disease. Surgery should always be carefully considered and planned because of the malabsorption that may follow extensive or multiple
resections of the bowel or the production of blind
loops of intestine.
Medical management
Initial management is often non- operative.
Nutritional support may be required, and an elemental diet may be useful. Acute episodes are
treated with steroids and immunosuppressants
248 The small intestine
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such as azathioprine; parenteral nutrition may be
required.
Mild symptoms are treated with 5drugs such as mesalazine, and steroids may be
required. Antibiotics, such as metronidazole, may
also help.
Acute exacerbations and fistulating disease may be
effectively treated with Infliximab and adalimumab,
monoclonal antibodies to tumour necrosis factor
alpha (TNF-
Increasing evidence now supports use of second
and third line immunosuppressants/biologics but it is
very important that decisions to escalate medical biologic therapy are made in a joint inflammatory bowel
disease clinic setting that involves the patient, a gastroenterologist and a colorectal surgeon. These
advanced agents include:
•
Ustekinumab: a monoclonal antibody against the
p40 protein subunit of interleukins IL- 12 and
IL- 23.
• Vedolizumab: a monoclonal antibody against the
α4
gut- homing T lymphocytes.
α).
β7 integrin preferentially expressed on
aminosalicylate
Surgical management
If found at surgery in the acute stage, the condition
should be left undisturbed since in a high proportion
the acute phase may subside completely with medical
therapy.
In the chronic stage of the disease, surgery is indicated for:
•
Severe or recurrent obstructive symptoms.
• Symptomatic fistulas.
• When medical treatment either leads to complica-
tions or is not sufficient to allow the patient an
adequate quality of life.
Recognizing that the disease is recurrent and that
further resections may be required, surgery should be
as conservative as possible. Either resection of the
affected segment or a strictureplasty (widening of the
narrowed segment, rather than removal) is performed;
laparoscopic (‘keyhole’) surgery is increasingly used.
order to reduce the risk of recurrence. Stopping smoking is essential to lower this risk.
Tumours ofthe small
intestine
One of the many mysteries of tumour formation is their
rarity from beyond the pylorus to the ileocaecal valve.
Classication
Benign
• Adenoma.
• Gastrointestinal stromal tumour (see
Chapter23).
Lipoma.
•
•
Hamartoma (e.g. Peutz–Jeghers syndrome,
ated with circumoral pigmentation and multiple
intestinal polyps).
Malignant
1 Primary:
a Neuroendocrine tumour (previously known as
‘carcinoid’).
Adenocarcinoma.
b
c
Lymphoma.
d Gastrointestinal stromal tumour (see
Chapter23) .
Secondary invasion (e.g. from stomach, colon or
2
bladder, or from a lymphoma).
Clinical features
Tumours of the small intestine may present with:
Intestinal bleeding.
•
Obstruction.
•
• Intussusception.
• Volvulus.
• Anaemia.
3
associ-
Prognosis
Recurrence of the disease after resection occurs in
some 50% of cases within 10 years, and repeated
operations may be required over time. Patients will
often require ongoing medication after surgery in
3
Johannes Peutz (1886–1957), Physician, the Hague, the
Netherlands. Harold Jeghers (1940–1990), Professor of
Medicine, Georgetown University School of Medicine,
Washington, DC, and Tufts University Medical School,
Boston, MA, USA.
Neuroendocrine tumours
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Neuroendocrine tumours (previously known as
carcinoid tumours) are amine precursor uptake and
decarboxylation (APUD) tumours, and share this
property with cells of neural crest origin with which
they were once confused. They belong to a group of
neuroendocrine tumours called gastroenteropancreatic tumours; the other tumours in this group are
pancreatic endocrine tumours such as gastrinomas
and insulinomas. In 10% of cases, there is an association with the multiple endocrine neoplasia type 1
(MEN1) syndrome (see Chapter38). Neuroendocrine
tumours are most commonly found in the appendix, but may be found anywhere in the gastrointestinal tract and occasionally in the lung (10%). They
commonly secrete 5- hydroxytryptamine (5- HT, also
called serotonin), in addition to other hormones,
but are rarely symptomatic until they have metastasized to the liver and are thus able to secrete their
hormone directly into the systemic circulation,
since the liver normally inactivates these hormones.
This can lead to the symptoms of sonoid syndrome’ (see later in this chapter).
Pathology
called ‘carci-
The small intestine 249
the appendix lumen, but most will be found incidentally when the removed appendix is examined under
the microscope for histological diagnosis. Those
arising in the ileum and large bowel may spread to the
regional lymph nodes and the liver.
Clinical features
Neuroendocrine tumours present with local features related to the primary tumour or due to metastatic spread, including the sosyndrome’ due to liver metastases and their endocrine products:
•
Flushing (90%) with attacks of cyanosis and a
chronic redby stress or ingestion of food or alcohol.
Diarrhoea (70%), often profuse, with noisy
•
borborygmi.
•
Bronchospasm (15%).
• Abdominal pain (40%) owing to mesenteric fibrosis resulting in partial obstruction.
Abnormalities in the heart (pulmonary and tricuspid
stenosis) are late manifestations; lung neuroendocrine tumours may cause stenosis of the left heart
valves (mitral and aortic). Hepatomegaly and a palpable abdominal mass produced by the tumour and its
secondaries may occasionally be present.
faced appearance, often precipitated
called ‘carcinoid
Macroscopic appearance
The tumour appears as a yellowish submucosal nodule. The overlying mucosa is at first intact but later
ulcerates. Extension to the serosa leads to fibrosis and
obstruction. Often, the tumour encircles the bowel at
the time of diagnosis, and has infiltrated the mesenteric lymph nodes.
Microscopic appearance
The tumour is made up of Kulchitsky cells,4 which
take up silver stains and arise in the crypts of the
intestinal mucosa.
The tumour is very slow growing, and usually presents after the fourth decade. Up to one- quarter are
multiple. Neuroendocrine tumours of the appendix
are relatively benign but 4% eventually metastasize.
They may present early as appendicitis by obstructing
4
Nikolai Kulchitsky (1865–1925), Professor of Histology,
Kharkov, Russia. After the Russian Revolution he became
Lecturer in Anatomy at University College, London, UK.
Special investigations
• 5- Hydroxyindole acetic acid (5- HIAA) urinary
concentration. 5- HT is broken down to 5- HIAA,
which is excreted in the urine. A 24 h urine
collection contains raised levels of 5- HIAA.
• Chromogranin A serum concentration is raised in
patients with neuroendocrine tumours.
• CT or ultrasound of the liver to seek metastases.
The primary tumour is often elusive, but CT may
show mesenteric infiltration.
• Radiolabelled octreotide scintigraphy is a useful
screening test for tumour and for detection of
metastases; the octreotide binds to somatostatin receptors that are often expressed on the
tumour.
Treatment
Resection of the tumour in early and symptomatic
cases is the optimal treatment. Local metastases in
the liver are also occasionally resectable. Palliation of
250 The small intestine
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more extensive tumour deposits can be achieved by
embolizing the hepatic arterial supply via a catheter
passed through the femoral artery. Cytotoxic therapy
may induce worthwhile remission, but is not commonly used.
Symptoms may be controlled with octreotide,
a somatostatin analogue that inhibits 5release. Targeted radiotherapy, using radiolabelled octreotide, may have a place in treatment.
Even if widespread deposits are present, the
HT
tumour is slow growing and the patient may
survive for many years.
Additional resources
Case 62: An unusual case of severe rectal bleeding
in a child
Case 63: An abdominal mass in a young man
Case 64: A striking facial appearance
The appendix
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Ioanna G. Panagiotopoulou
Learning objective
✓ To learn the anatomical and histological features of the appendix.
✓ To appreciate the clinical presentation of acute appendicitis and its
management.
✓ To be aware of rare appendiceal tumours.
26
The appendix (also known as the vermiform
appendix) is considered a remnant in the human evolution process. Inflammation of the appendix is the
most common abdominal surgical emergency. Acute
appendicitis may present with a multitude of symptoms and signs, and has a wide differential diagnosis.
Although the diagnosis of acute appendicitis is made
largely on clinical grounds, relevant blood tests and
imaging are important adjuncts of clinical practice.
Finally, one needs to be aware of rare appendiceal
tumours that may require referral and treatment,
sometimes within specialist centres.
Embryology andanatomy
The appendix is a blind- ended, tubular, vermiform
(worm- like) structure that arises from the posteromedial aspect of the caecal wall, and as such derives
from midgut. During week 6 of gestation, the caecal
diverticulum develops as the precursor of the appendix and the caecum. The caecum and appendix
undergo medial rotation along with the midgut and
descend in the right lower abdomen. The continued
growth of the caecum even during childhood most
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
commonly rotates the appendix into a retrocaecal
position (74% of cases). The appendix may assume
several other different positions within the right lower
abdominal cavity such as paracaecal/paracolic, subcaecal, pelvic and prea position over the right upper abdomen in malrotation cases (Figure26.1). The varying position of the
appendix explains its varying presentations.
The appendix varies between 5 and 10 cm in
length, with its base at the confluence of the three
taenia coli of the caecum, which fuse to create the
outer longitudinal muscular layer of the appendix.
The mesentery of the appendix (mesoappendix) is
triangular in shape and arises from the terminal ileal
mesentery. It contains the appendiceal artery that
originates from the ileocolic artery and passes posterior to the terminal ileum before it enters the mesoappendix. The appendicular artery is an end artery
distal to the midpoint of the mesoappendix
(Figure26.2). Inflammation results in thrombosis of
this end artery and this disruption of the blood supply leads to gangrene, and perforation.
/post- ileal, or may even adopt
Histology
Microscopically, the appendix consists of four layers:
mucosa, submucosa, muscularis propria and serosa.
The muscularis propria includes an outer longitudinal and an inner circular muscular layer. The submucosa contains blood vessels, nerves and lymphoid
252 The appendix
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Retrocolic and
retrocaecal 75%
Retro-ileal an
pre-ileal 5%
Subcaecal and
pelvic 20%
lleocolic artery
Appendicular artery
Appendix mesentery
d
Figure26.1 The positions in which the
appendix may lie, together with their
approximate incidence.
tissue. The lymphoid follicles seen within the appendix are not present at birth; they develop over the first
10 years of life and subsequently disappear. The
mucosa of the appendix is similar to the colon. It contains tall columnar epithelial cells, mucin- secreting
goblet cells and enteroendocrine or enterochromaffin cells that lie in the base of crypts.
Acute appendicitis
Acute appendicitis is the most common abdominal
surgical emergency affecting around 10% of the population. Although it can occur at any age, it is uncommon in the very young, where the appendix has a
wide mouth, and in the elderly where its lumen is
obliterated; the peak incidence is in the third decade
of life with a second peak in the seventh decade.
Figure26.2 The blood supply of the
appendix.
Aetiology andpathology
Various theories have been put forward to explain its
occurrence.
a) Mechanical obstruction
Obstruction of the appendix lumen by faecoliths, or
from enlargement of lymphoid aggregates or from
tumours of the appendix or the caecum results in
inflammation. Faecoliths, which are largely composed of fats (coprosterols), epithelial debris, calcium
phosphates and vegetable fibres, form when there is
slower stool transit time usually reflecting a low fibre
intake. The mechanical hypothesis is thought to
explain why there is a lower incidence of appendicitis
in populations with a high fibre diet such as in
Southern Africa.
Once obstruction of the appendix lumen occurs,
the intraluminal pressure increases due to the
ongoing inflammatory exudate production and
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mucus secretion. Lymphatic and venous drainage
become impaired with the increased appendiceal
intraluminal pressure resulting in oedema and
mucosal ulceration. Bacterial translocation then sets
on the already oedematous appendiceal wall leading
to acute appendicitis. Inflammation of the appendix
causes thrombosis of the appendicular artery, resulting in gangrenous appendicitis which then results in
perforation and bacterial contamination of the peritoneal cavity.
b) Infection hypothesis
This is based on the finding of microbes in
appendiceal specimens. Viruses (e.g. dengue, influenza, Epstein- Barr), bacteria (e.g. campylobacter, salmonella) and parasites (e.g. enterobius vermicularis)
may proliferate in the appendix and invade the lamina propria leading to oedema of the appendix wall
and luminal obstruction.
c) Hygiene
The hygiene hypothesis relates to improved hygiene
and a change in childhood gastrointestinal infection and gut immune system interaction. This
hypothesis has been considered due to the increase
in the incidence of appendicitis in developing
countries.
Clinical features
History
The clinical presentation of acute appendicitis varies
widely among individuals.
•
Pain. The classical presentation involves central
peri-
umbilical colicky pain that migrates to the
right iliac fossa over 4–24 hours. The initial appendicular dilatation and inflammation result in
poorly localized midgut pain experienced centrally around the umbilicus. Localization of the
pain to the right iliac fossa (RIF) occurs when parietal peritoneal structures are involved in the
inflammation, stimulating somatic nociceptors.
Coughing and/or movement exacerbate the
localized RIF pain.
•
Nausea and vomiting, usually follow the onset of
pain.
The appendix 253
•
Anorexia is almost universal.
•
Fever and occasional diarrhoea or constipation.
Examination
• Low- grade pyrexia, around 37.5 °C, and flushed
facies.
Foetor oris, and coated tongue are usually
•
present.
Motionless: the patient lies still as movement exac-
•
erbates the pain.
•
Localized tenderness in the RIF, with guarding and
rebound tenderness.
Rebound tenderness may be elicited with gentle
•
percussion over the site of maximum tenderness
or by asking the patient to cough. The finding of
generalized peritonitis with the abdomen being
diffusely tender and rigid would be a sign of
uncontained appendiceal perforation.
•
Rectal examination may reveal tenderness when
the appendix is in the pelvic position with pus
present in the rectovesical pouch or pouch of
Douglas.
Further eponymous signs that could be consistent
with the diagnosis of acute appendicitis are shown in
Box26.1.
Atypical presentation
The typical migratory RIF pain and associated tenderness probably occurs in 50% of patients presenting
with acute appendicitis.
Retrocaecal appendix: inflammation may result in
•
right loin pain rather than RIF pain. Tenderness
and guarding in the RIF are unlikely due to the
caecum being present between the inflamed
appendix and the anterior abdominal wall. The
psoas sign may be present.
Pelvic appendix: inflammation may result in
•
suprapubic tenderness without RIF tenderness.
Irritation of the rectum may result in diarrhoea,
irritation of the bladder may cause frequency of
micturition due to irritation of the bladder and
spasm of the obturator internus muscle (obturator
sign). Rectal examination may be painful as the
inflamed pelvic peritoneum is irritated by the
examining finger.
• Obese patients may not manifest guarding
since the presence of an increased depth of
254 The appendix
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Box 26.1 Eponymous signs inacute appendicitis
Rovsing’s sign1Deep palpation over the left iliac fossa causing pain in the right iliac fossa, as the peritoneal
Psoas sign
Obturator sign Pain on flexion and internal rotation of the right hip joint, which stretches obturator internus
subcutaneous fat may hamper efforts to elicit
abdominal signs.
Pregnant women with acute appendicitis in the
•
second or third trimester of pregnancy are likely to
show right upper quadrant tenderness rather than
RIF tenderness in view of the appendix having
been displaced cranially to the right upper quadrant by the gravid uterus.
•
Appendicitis in the elderly or in children may not
present with the typical localizing symptoms and
signs in the RIF due to the poorly developed or
atrophic omentum at those extremes of age. The
surgeon should have a low threshold of clinical
suspicion for atypical presentations of acute
appendicitis in such cases.
Special investigations
Investigations are particularly useful in helping the
surgeon diagnose or exclude acute appendicitis in
patients presenting with RIF pain, since there is a
wide differential diagnosis (see below).
•
Full blood count: a neutrophilia is common. A
microcytic anaemia would raise suspicion of a
coincidental caecal cancer.
•
C- reactive protein (CRP) is usually raised. Both
CRP and WCC have good diagnostic accuracy for
acute appendicitis but cannot exclude or confirm
appendicitis. The diagnostic accuracy of WCC
and CRP combined is higher for cases of perforated appendicitis, but 5% of cases have normal
indices.
1
Niels orkild Rovsing (1862–1927), Professor of Operative
Surgery, University of Copenhagen, Denmark.
2
e psoas sign is also known as Cope’s sign, after Sir
Vincent Zachary Cope (1881–1974), Surgeon, StMary’s
Hospital, London.
contents are displaced irritating the inflamed parietal peritoneum on the right.
2
The patient lying with the right hip flexed due to spasm in the iliopsoas hip flexors against which
the inflamed retrocaecal appendix lies. Pain may also be elicited by passive extension of the hip.
against which the inflamed appendix lies.
Urinalysis looking for evidence of infection
•
(pyelonephritis may mimic a retrocaecal appendix).
• Pregnancy test (β- human chorionic gonadotrophin [βHCG]) to rule out an ectopic pregnancy.
Ultrasound scan may diagnose appendicitis, but
•
its main role is in excluding gynaecological causes
of pain.
•
CT scans are accurate in diagnosing appendici-
tis, and in evaluating atypical presentations.
They can also diagnose an appendix mass or
abscess. Radiation exposure means it is less
suited to the assessment of young adults or during pregnancy.
MR imaging (MRI): valuable in the assessment of
•
a pregnant patient where ultrasound is inconclusive and CT contraindicated. Appendicectomy
during pregnancy is high risk for mother and
foetus, as is untreated appendicitis, so an accurate
preoperative diagnosis is essential.
•
Diagnostic laparoscopy is an option for young
females where there are more potential differential diagnoses in circumstances where appropriate
imaging is not available, but carries a risk of bowel
injury, infection and potential removal of a
appendix. A detailed discussion is crucial to help
the patient appreciate the available diagnostic
modalities and their associated potential risks for
shared decision- making.
Differential diagnosis ofRIF pain
Nothing can be so easy, nor anything so difficult, as
the diagnosis of acute appendicitis. The differential
diagnosis of appendicitis includes most of the causes
of acute abdominal pain. They should be considered
systematically under the following headings:
• Other gastrointestinal causes of acute pain.
• The urogenital tract.
normal
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