Acute appendicitis
While there are isolated reports of
perityphlitis (fatal inflammation of the caecal region) from the late 1500s,
recognition of acute appendicitis as a clinical entity is attributed to
Acute
appendicitis is relatively rare in infants, and becomes increasingly common in
childhood and early adult life, reaching a peak incidence in the teens and early
20s. After middle age the risk of developing appendicitis in the future is quite
small. The incidence of appendicitis is equal amongst males and females before
puberty. In teenagers and young adults the male:female ratio increases to 3:2 at
the age of 25 years, thereafter the greater incidence in males declines.
Aetiology
There is no unifying hypothesis regarding the
aetiology of acute appendicitis. While appendicitis is clearly associated with
bacterial proliferation within the appendix, no single organism is responsible,
indeed a mixed growth of aerobic and anaerobic organisms is usual. The
initiating event causing bacterial proliferation is controversial. Obstruction
of the appendix lumen has been widely held to be important, and indeed some form
of luminal obstruction by either a faecolith or stricture is found in the
majority of cases.
A
faecolith is composed of inspissated faecal material, calcium phosphates,
bacteria and epithelial debris. Rarely a foreign body is incorporated into the
mass. The incidental finding of a faecolith is a relative indication for
prophylactic appendicectomy (Fig. 59.5).
A
fibrotic stricture of the appendix usually indicates previous appendicitis which
resolved without surgical intervention (Fig. 59.6). Obstruction of the appendiceal orifice by tumour,
particularly carcinoma of the caecum, is an occasional cause of acute
appendicitis in middle age and the elderly. Intestinal parasites, particularly Oxyuris
vermicularis (syn. pinworm), can proliferate in the appendix and occlude the
lumen.
Pathology
Obstruction
of the appendiceal lumen seems to be essential for development of appendiceal
gangrene and perforation. Yet, in many cases of early appendicitis the
appendix lumen is patent despite the presence of mucosal inflammation and
lymphoid hyperplasia. Occasional clustering of cases amongst children and young
adults suggests an infective agent, possibly viral, which initiates an
inflammatory response, which within the narrow lumen of the appendix leads to
luminal obstruction. Once obstruction occurs, continued mucus secretion and
inflammatory exudation increase intraluminal pressure, obstructing lymphatic
drainage. Oedema and mucosal ulceration develop with bacterial translocation to
the submucosa. Resolution may occur at this point either spontaneously or in
response to antibiotic therapy. Where the condition progresses, further
distension of the appendix may cause venous obstruction and ischaemia of the
appendix wall. With ischaemia, bacterial invasion occurs through the muscularis
propria and submucosa producing acute appendicitis (Fig.
59.7). Finally,
ischaemic necrosis of the appendix wall produces gangrenous appendicitis, with
free bacterial contamination of the peritoneal cavity. Alternatively, the
greater omentum and loops of small bowel become adherent to the
inflamed appendix, walling off the spread of peritoneal contamination resulting
in a phlegmonous mass or paracaecal abscess (Fig.
It
is the potential for peritonitis that is the great threat of acute appendicitis.
Peritonitis occurs as a result of free migration of bacteria through an
ischaemic appendicular wall, through frank perforation of a gangrenous appendix
or delayed perforation of an appendix abscess. Factors which promote this
process include extremes of age, immunosuppression, diabetes mellitus,
faecolith obstruction of the appendix lumen, a free-lying pelvic appendix and
previous abdominal surgery which limits the ability of the greater omentum to
wall off the spread of peritoneal contamination (Table
59.1). In these
situations a rapidly deteriorating clinical course is accompanied by signs of
diffuse peritonitis and systemic sepsis syndrome.
Clinical
diagnosis —
history
The classical features of acute appendicitis
begin with poorly localised colicky abdominal pain (Table
59.2). This is due to
midgut visceral discomfort in response to appendiceal inflammation and
obstruction. The pain is frequently first noticed in the periumbilical region
and is similar to, but less intense than, the colic of small bowel obstruction.
Central abdominal pain is associated with anorexia, nausea and usually one or
two episodes of vomiting which follow the onset of pain (Murphy). Anorexia is a
useful and constant clinical feature, particularly in children. The patient
often gives a history of similar discomfort which settled spontaneously.
With
progressive inflammation of the appendix, the parietal peritoneum in the right
iliac fossa becomes irritated producing more intense, constant and localised
somatic pain which begins to predominate. This is often reported by the patient
as an abdominal pain which has shifted and changed in character. Typically,
coughing or sudden movement exacerbates the right iliac fossa pain.
The
classical visceral—somatic sequence of pain is present in only about half
those patients subsequently proven to have acute appendicitis. Atypical
presentations include pain which is predominantly somatic or visceral and poorly
localised. Atypical pain is more common in the elderly in whom localisation to
the right iliac fossa is unusual. An inflamed appendix in the pelvis may never
produce somatic pain involving the anterior abdominal wall, but may instead
cause suprapubic discomfort and tenesmus. In this circumstance, tenderness may
only be elicited on rectal examination and is the basis for the recommendation
that a rectal examination should be performed on every case of lower abdominal
pain.
During
the first 6 hours there is rarely any alteration in temperature or pulse rate.
After that time, slight pyrexia
Typically,
two clinical syndromes of acute appendicitis can be discerned, acute catarrhal (nonobstructive) appendicitis and acute obstructive appendicitis. The latter is characterised by a
much more acute course. The onset of symptoms is abrupt and there may be
generalised abdominal pain from the start. The temperature may be normal and
vomiting is common, so that the clinical picture may mimic acute intestinal
obstruction. Once recognised, urgent surgical intervention is required because
of the more rapid progression to perforation.
Clinical
diagnosis —
signs (Tables 59.3 and
59.4)
The diagnosis of appendicitis rests more on
thorough clinical examination of the abdomen than on any aspect of the history
or laboratory investigation. The cardinal features are those of an unwell
patient with low grade pyrexia, localised abdominal tenderness, muscle guarding
and rebound tenderness. Inspection of the abdomen may show limitation of
respiratory movement in the lower abdomen. The patient is then asked to point to
where the pain began and to where it moved (the pointing sign). Gentle superficial palpation of the abdomen,
beginning in the left iliac fossa moving anticlockwise to the right iliac fossa,
will detect muscle guarding over the point of maximum tenderness, classically McBurney
point. Asking the patient to cough or gentle percussion over the
site of maximum tenderness will elicit rebound tenderness.
Deep
palpation of the left iliac fossa may cause pain in the right iliac fossa (Rovsing’s
sign), which is helpful in supporting a clinical diagnosis of appendicitis.
Occasionally
Special
features, according to position of the appendix
Retrocaecal
Rigidity is often absent and even on deep
pressure tenderness may he lacking (silent appendix), the reason being that the
caecum, distended with gas, prevents the pressure exerted by the hand from
reaching the inflamed structure. However, deep tenderness is often present in
the loin, and rigidity of the quadratus lumborum may he in evidence. Psoas
spasm, due to the inflamed appendix being in contact with that muscle, may he
sufficient to cause flexion of the hip joint. Hyperextension of the hip joint
may induce abdominal pain when the degree of psoas spasm is insufficient to
cause flexion of the hip.
Pelvic
Occasionally early diarrhoea results from an
inflamed appendix being in contact with the rectum. When the appendix lies
entirely within the pelvis there is usually complete absence of abdominal
rigidity, and often tenderness over McBurney’s point is lacking as well. In
some instances deep tenderness can he made out just above and to the right of
the symphysis pubis. In either event, a rectal examination reveals tenderness in
the rectovesical pouch or the pouch of Douglas, especially on the right side.
Spasm of the psoas and obturator internus muscles may he present when the
appendix is in this position. An inflamed appendix in contact with the bladder
may cause frequency of micturition.
Post
ileal
Although this is rare, it accounts for some of
the cases of missed appendix’. Here the inflamed appendix lies behind the
terminal ileum. It presents the greatest difficulty in diagnosis because the
pain may not shift, diarrhoea is a feature and marked retching may occur.
Tenderness, if any, is ill-defined, although it may he present immediately to
the right of the umbilicus.
Special
features, according to age
Infants
Appendicitis is relatively rare in infants
under 36 months of age and for obvious
reasons the patient is unable to give a history. Because of this, diagnosis is
often delayed and thus the incidence of perforation and postoperative morbidity
is considerably higher than in older children. Diffuse peritonitis can develop
rapidly due to the underdeveloped greater omentum, which is unable to give
much assistance in localising the infection.
Children
It is rare to find a child with appendicitis
who has not vomited. Children with appendicitis usually have complete aversion
to food. In addition, they do not sleep during the attack and very often bowel
sounds are completely absent in the early stages.
The elderly
Gangrene and perforation occur much more
frequently in elderly patients. Elderly patients with lax abdominal walls or
obesity may harbour a gangrenous appendix with little evidence of it, and the
clinical picture may simulate subacute intestinal obstruction. These features
coupled with coincident medical conditions produce a much higher mortality for
acute appendicitis in the elderly.
The obese
Obesity can obscure and diminish all the local
signs of acute appendicitis. Delay in diagnosis coupled with the technical
difficulty of operating in the obese make it wiser to consider operating through
a midline abdominal incision
Pregnancy
Appendicitis is the most common extra uterine acute abdominal condition in pregnancy with a frequency of from one in 1500 to
one in 2000 pregnancies. Diagnosis is complicated by delay in presentation;
early nonspecific symptoms are often attributed to the pregnancy, and the
changing location of the appendix during pregnancy. As pregnancy develops during
the second and third trimesters, the caecum and appendix are progressively
pushed to the right upper quadrant of the abdomen. This displacement can result
in flank or back pain, and may be confused with pyelonephritis, while lower
abdominal pain may be confused with torsion of an ovarian cyst. Foetal loss
occurs in 3—5 per cent of cases, increasing to 20 per cent if perforation is
found at operation.