Acute appendicitis in adults: Clinical manifestations and differential diagnosis

Author
Ronald F Martin, MD
Section Editor
Martin Weiser, MD
Deputy Editor
Wenliang Chen, MD, PhD
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Dec 2015. | This topic last updated: Jul 09, 2014.
INTRODUCTION Appendicitis, an inflammation of the vestigial vermiform appendix, is one
of the most common causes of the acute abdomen and one of the most frequent indications
for an emergent abdominal surgical procedure worldwide [1,2].
The clinical manifestations and diagnosis of appendicitis in adults will be reviewed here. The
management of appendicitis in adults and appendicitis in pregnancy and children are
discussed separately. (See "Management of acute appendicitis in adults" and "Acute
appendicitis in pregnancy" and "Acute appendicitis in children: Clinical manifestations and
diagnosis".)
ANATOMY The vermiform appendix is located at the base of the cecum, near the ileocecal
valve where the taenia coli converge on the cecum (figure 1) [3,4]. The appendix is a true
diverticulum of the cecum. In contrast to acquired diverticular disease, which consists of a
protuberance of a subset of the enteric wall layers, the appendiceal wall contains all of the
layers of the colonic wall: mucosa, submucosa, muscularis (longitudinal and circular), and the
serosal covering [5].
The appendiceal orifice opens into the cecum. Its blood supply, the appendiceal artery, is a
terminal branch of the ileocolic artery, which traverses the length of the mesoappendix and
terminates at the tip of the organ (figure 2) [4].
The attachment of the appendix to the base of the cecum is constant. However, the tip may
migrate to the retrocecal, subcecal, preileal, postileal, and pelvic positions. These normal
anatomic variations can complicate the diagnosis as the site of pain and findings on the clinical
examination will reflect the anatomic position of the appendix.
The presence of B and T lymphoid cells in the mucosa and submucosa of the lamina propria
make the appendix histologically distinct from the cecum [5]. These cells create a lymphoid
pulp that aids immunologic function by increasing lymphoid products such as IgA and
operating as part of the gut-associated lymphoid tissue system [3]. Lymphoid hyperplasia can

cause obstruction of the appendix and lead to appendicitis. The lymphoid tissue undergoes
atrophy with age [6].
EPIDEMIOLOGY Appendicitis occurs most frequently in the second and third decades of life.
The incidence is approximately 233/100,000population and is highest in the 10 to 19 year-old
age group [7]. It is also higher among men (male to female ratio of 1.4:1), who have a lifetime
incidence of 8.6 percent compared with 6.7 percent for women [7].
PATHOGENESIS The natural history of appendicitis is similar to that of other inflammatory
processes involving hollow visceral organs. Initial inflammation of the appendiceal wall is
followed by localized ischemia, perforation, and the development of a contained abscess or
generalized peritonitis.
Appendiceal obstruction has been proposed as the primary cause of appendicitis [3,8-11].
Obstruction is frequently implicated but not always identified. A study of patients with
appendicitis showed that there was elevated intraluminal pressure in only one-third of the
patients with nonperforated appendicitis [12].
Appendiceal obstruction may be caused by fecaliths (hard fecal masses), calculi, lymphoid
hyperplasia, infectious processes, and benign or malignant tumors. However, some patients
with a fecalith have a histologically normal appendix and the majority of patients with
appendicitis do not have a fecalith [13,14].
When obstruction of the appendix is the cause of appendicitis, the obstruction leads to an
increase in luminal and intramural pressure, resulting in thrombosis and occlusion of the small
vessels in the appendiceal wall, and stasis of lymphatic flow. As the appendix becomes
engorged, the visceral afferent nerve fibers entering the spinal cord at T8-T10 are stimulated,
leading to vague central or periumbilical abdominal pain [8]. Well-localized pain occurs later in
the course when inflammation involves the adjacent parietal peritoneum.
The mechanism of luminal obstruction varies depending upon the patient's age. In the young,
lymphoid follicular hyperplasia due to infection is thought to be the main cause. In older
patients, luminal obstruction is more likely to be caused by fibrosis, fecaliths, or neoplasia
(carcinoid, adenocarcinoma, or mucocele). In endemic areas, parasites can cause obstruction
in any age group. (See "Cancer of the appendix and pseudomyxoma peritonei".)
Once obstructed, the lumen becomes filled with mucus and distends, increasing luminal and
intramural pressure. This results in thrombosis and occlusion of the small vessels, and stasis of
lymphatic flow. As lymphatic and vascular compromise progress, the wall of the appendix
becomes ischemic and then necrotic.

Bacterial overgrowth occurs within the diseased appendix. Aerobic organisms predominate
early in the course, while mixed infection is more common in late appendicitis [15]. Common
organisms involved in gangrenous and perforated appendicitis include Escherichia coli,
Peptostreptococcus, Bacteroides fragilis, and Pseudomonas species [16]. Intraluminal bacteria
subsequently invade the appendiceal wall and further propagate a neutrophilic exudate. The
influx of neutrophils causes a fibropurulent reaction on the serosal surface, irritating the
surrounding parietal peritoneum [6]. This results in stimulation of somatic nerves, causing
pain at the site of peritoneal irritation [5].
During the first 24 hours after symptoms develop, approximately 90 percent of patients
develop inflammation and perhaps necrosis of the appendix, but not perforation. The type of
luminal obstruction may be a predictor of perforation of an acutely inflamed appendix.
Fecaliths were six times more common than true calculi in the appendix, but calculi were
more often associated with perforated appendicitis or periappendiceal abscess (45 percent)
than were fecaliths (19 percent). This is presumably due to the rigidity of true calculi as
compared with the softer, more crushable fecaliths [13].
Once significant inflammation and necrosis occur, the appendix is at risk of perforation, which
leads to localized abscess formation or diffuse peritonitis. The time course to perforation is
variable. One study showed that 20 percent of patients developed perforation less than 24
hours after the onset of symptoms [17]. Sixty-five percent of patients in whom the appendix
perforated had symptoms for longer than 48 hours.
CLINICAL FEATURES
Clinical manifestations
History Abdominal pain is the most common symptom, and is reported in nearly all
confirmed cases of appendicitis [18,19]. The clinical presentation of acute appendicitis is
described as a constellation of the following classic symptoms:
Right lower quadrant (right anterior iliac fossa) abdominal pain
Anorexia
Nausea and vomiting
In the classic presentation, the patient describes the onset of abdominal pain as the first
symptom. The pain is typically periumbilical in nature with subsequent migration to the right
lower quadrant as the inflammation progresses [18]. Although considered a classic symptom,

migratory pain occurs only in 50 to 60 percent of patients with appendicitis [8,20]. Nausea and
vomiting, if they occur, usually follow the onset of pain. Fever-related symptoms generally
occur later in the course of illness.
In many patients, initial features are atypical or nonspecific, and can include:
Indigestion
Flatulence
Bowel irregularity
Diarrhea
Generalized malaise
Because the early symptoms of appendicitis are often subtle, patients and clinicians may
minimize their importance. The symptoms of appendicitis vary depending upon the location of
the tip of the appendix (figure 1) (see 'Anatomy' above). For example, an inflamed anterior
appendix produces marked, localized pain in the right lower quadrant, while a retrocecal
appendix may cause a dull abdominal ache [21]. The location of the pain may also be atypical
in patients who have the tip of the appendix located in the pelvis, which can cause tenderness
below McBurney's point. Such patients may complain of urinary frequency and dysuria or
rectal symptoms, such as tenesmus and diarrhea.
Physical examination The early signs of appendicitis are often subtle. Low-grade fever
reaching 101.0F (38.3C) may be present. The physical examination may be unrevealing in the
very early stages of appendicitis since the visceral organs are not innervated with somatic pain
fibers.
However, as the inflammation progresses, involvement of the overlying parietal peritoneum
causes localized tenderness in the right lower quadrant and can be detected on the abdominal
examination. Rectal examination, although often advocated, has not been shown to provide
additional diagnostic information in cases of appendicitis. In women, right adnexal area
tenderness may be present on pelvic examination, and differentiating between tenderness of
pelvic origin versus that of appendicitis may be challenging. High-grade fever
(>101.0F/38.3C) occurs as inflammation progresses. (See "Differential diagnosis of
abdominal pain in adults".)

Patients with a retrocecal appendix may not exhibit marked localized tenderness in the right
lower quadrant since the appendix does not come into contact with the anterior parietal
peritoneum (figure 1) [21]. The rectal and/or pelvic examination is more likely to elicit positive
signs than the abdominal examination. Tenderness may be more prominent on pelvic
examination, and may be mistaken for adnexal tenderness.
Several findings on physical examination have been described to facilitate diagnosis, but these
findings pre-dated definitive imaging for appendicitis, and the wide variation in their
sensitivity and specificity suggests that they be used with caution to broaden, or narrow, a
differential diagnosis. There are no physical findings, taken alone or in concert, that
definitively confirm a diagnosis of appendicitis.
Commonly described physical signs include:
McBurney's point tenderness is described as maximal tenderness at 1.5 to 2 inches from the
anterior superior iliac spine (ASIS) on a straight line from the ASIS to the umbilicus [22]
(sensitivity 50 to 94 percent; specificity 75 to 86 percent [23-25]).
Rovsing's sign refers to pain in the right lower quadrant with palpation of the left lower
quadrant. This sign is also called indirect tenderness and is indicative of right-sided local
peritoneal irritation [26] (sensitivity 22 to 68 percent; specificity 58 to 96 percent [24,27-29]).
The psoas sign is associated with a retrocecal appendix. This is manifested by right lower
quadrant pain with passive right hip extension. The inflamed appendix may lie against the
right psoas muscle, causing the patient to shorten the muscle by drawing up the right knee.
Passive extension of the iliopsoas muscle with hip extension causes right lower quadrant pain
(sensitivity 13 to 42 percent; specificity 79 to 97 percent [27,30,31]).
The obturator sign is associated with a pelvic appendix. This test is based on the principle
that the inflamed appendix may lay against the right obturator internus muscle. When the
clinician flexes the patient's right hip and knee followed by internal rotation of the right hip,
this elicits right lower quadrant pain, (sensitivity 8 percent; specificity 94 percent [30]). The
sensitivity is low enough that experienced clinicians no longer perform this assessment.
Laboratory findings A mild leukocytosis (white blood cell count >10,000 cells/microL) is
present in most patients with acute appendicitis [32]. Approximately 80 percent of patients
have a leukocytosis and a left shift (increase in total WBC count, bands [immature
neutrophils], and neutrophils) in the differential [33-35]. The sensitivity and specificity of an
elevated white blood cell (WBC) count in acute appendicitis is 80 percent and 55 percent
respectively.

Acute appendicitis is unlikely when the WBC count is normal, except in the very early course
of the illness [35-37]. In comparison, mean WBC counts are higher in patients with a
gangrenous (necrotic) or perforated appendix [38]:
Acute 14,500 7,300 cells/microL
Gangrenous 17,100 3,900 cells/microL
Perforated 17,900 2,100 cells/microL (see 'Perforated appendix' below)
Mild elevations in serum bilirubin (total bilirubin >1.0 mg/dL) have been noted to be a marker
for appendiceal perforation with a sensitivity of 70 percent and a specificity of 86 percent
[39]. This compares favorably with a sensitivity and specificity of an elevated WBC of 80
percent and 55 percent respectively.
Imaging studies
Computed tomography findings The following findings suggest acute appendicitis on
standard abdominal computed tomography (CT) scanning with contrast including (image 1
and image 2) [40-42]:
Enlarged appendiceal diameter >6 mm with an occluded lumen
Appendiceal wall thickening (>2 mm)
Periappendiceal fat stranding
Appendiceal wall enhancement
Appendicolith (seen in approximately 25 percent of patients)
Ultrasound findings The most accurate ultrasound finding for acute appendicitis is an
appendiceal diameter of >6 mm (image 3 and image 4) [8,43,44].
Plain radiograph findings Plain radiographs are usually not helpful for establishing the
diagnosis of appendicitis (image 5). However, the following radiographic findings have been
associated with acute appendicitis:
Right lower quadrant appendicolith

Localized right lower quadrant ileus

Loss of the psoas shadow
Free air (occasionally)
Deformity of cecal outline
Right lower quadrant soft tissue density
Magnetic resonance imaging Magnetic resonance imaging (MRI) can assist with the
evaluation of acute abdominal and pelvic pain during pregnancy (image 6) [45,46]. A normal
appendix is visualized as a tubular structure less than or equal to 6 mm in diameter and filled
with airand/or oral contrast material [47]. An enlarged fluid-filled appendix (>7 mm in
diameter) is considered an abnormal finding, while an appendix with a diameter of 6 to 7 mm
is considered an inconclusive finding [47]. (See "Approach to abdominal pain and the acute
abdomen in pregnant and postpartum women" and "Acute appendicitis in pregnancy".)
DIFFERENTIAL DIAGNOSIS A variety of inflammatory and infectious conditions in the right
lower quadrant can mimic the signs and symptoms of acute appendicitis. (See "Differential
diagnosis of abdominal pain in adults".)
Perforated appendix During the first 24 hours after the onset of abdominal pain and
associated symptoms, approximately 90 percent of patients develop inflammation and
perhaps necrosis of the appendix, but not perforation. Once significant inflammation and
necrosis occur, the appendix is at risk for perforation, which leads to localized abscess
formation or diffuse peritonitis. The time course to perforation is variable. One study showed
that 20 percent of patients developed perforation less than 24 hours after the onset of
symptoms [17]. Sixty-five percent of patients in whom the appendix perforated had symptoms
for longer than 48 hours.
A perforated appendix must be considered in a patient whose temperature exceeds 103.0F
(39.4C), the WBC count is greater than 15,000cells/microL, and imaging studies reveal a fluid
collection in the right lower quadrant. (See 'Pathogenesis' above and 'Laboratory findings'
above and "Acute appendicitis in adults: Diagnostic evaluation", section on 'Imaging' and
'Imaging studies' above.)
Cecal diverticulitis Cecal diverticulitis usually occurs in young adults and presents with signs
and symptoms that can be virtually identical to those of acute appendicitis. Right-sided
diverticulitis occurs in only 1.5 percent of patients in Western countries, but is more common

in Asian populations (accounting for as many as 75 percent of cases of diverticulitis). Patients

with right-sided diverticulitis tend to be younger than those with left-sided disease and often
are misdiagnosed with acute appendicitis. Computed tomographic (CT) scanning of the
abdomen with IV and oral contrast is the diagnostic test of choice in patients suspected of
having acute diverticulitis. (See "Clinical manifestations and diagnosis of acute diverticulitis in
adults" and "Nonoperative management of acute uncomplicated diverticulitis", section on
'Right-sided (cecal) diverticulitis'.)
Meckel's diverticulitis Meckel's diverticulitis presents in a fashion similar to acute
appendicitis. A Meckel's diverticulum is a congenital remnant of the omphalomesenteric duct
and is located on the small intestine two feet from the ileocecal valve [48,49]. Meckel's
diverticulitis should be included in the differential diagnosis, as the small bowel may migrate
into the right lower quadrant and mimic the symptoms of appendicitis. If an inflamed
appendix is not found on abdominal exploration for acute appendicitis, the surgeon should
search for an inflamed Meckel's diverticulum. (See "Meckels diverticulum", section on
'Clinical presentations'.)
Acute ileitis Acute ileitis, due most commonly to an acute self-limited bacterial infection
(Yersinia, Campylobacter, Salmonella, and others), should be considered when acute diarrhea
is a prominent symptom. Other clinical manifestations of acute yersiniosis include abdominal
pain, fever, nausea and/or vomiting. Yersiniosis cannot be readily distinguished clinically from
other causes of acute diarrhea that present with these symptoms. However, localization of
abdominal pain to the right lower quadrant along with acute diarrhea may be a diagnostic
clue for yersiniosis. (See "Clinical manifestations and diagnosis of Yersinia infections", section
on 'Acute yersiniosis'.)
Acute yersiniosis presenting with right lower abdominal pain, fever, vomiting, leukocytosis,
and understated diarrhea may be confused with acute appendicitis. At surgery, findings
include visible inflammation around the appendix and terminal ileum and inflammation of the
mesenteric lymph nodes; the appendix itself is generally normal. Yersinia can be cultured from
the appendix and involved lymph nodes. (See "Clinical manifestations and diagnosis of
Yersinia infections", section on 'Pseudoappendicitis'.)
Crohn's disease Crohn's disease can present with symptoms similar to appendicitis,
particularly when localized to the distal ileum. Fatigue, prolonged diarrhea with abdominal
pain, weight loss, and fever, with or without gross bleeding, are the hallmarks of Crohn's
disease. An acute exacerbation of Crohns disease can mimic acute appendicitis and may be
indistinguishable by clinical evaluation and imaging.

Crohn's disease should be suspected in patients who have persistent pain after surgery,
especially if the appendix is histologically normal. (See "Clinical manifestations, diagnosis and
prognosis of Crohn disease in adults".)
Gynecologic and obstetrical conditions The following gynecologic diseases may present
with symptoms and/or clinical findings that are included in the differential of acute
appendicitis:
Tubo-ovarian abscess A tubo-ovarian abscess (TOA) is an inflammatory mass involving the
fallopian tube, ovary, and, occasionally, other adjacent pelvic organs (eg, bowel, bladder).
These abscesses are found most commonly in reproductive age women and typically result
from upper genital tract infection. Tubo-ovarian abscess is usually a complication of pelvic
inflammatory disease. The classic presentation includes acute lower abdominal pain, fever,
chills, and vaginal discharge. However, fever is not present in all patients, some patients
report only low-grade nocturnal fevers or chills, and not all women present in an acute
fashion. Clinical history and CT imaging can help differentiate TOA from acute appendicitis
(picture 1). (See "Epidemiology, clinical manifestations, and diagnosis of tuboovarian abscess",
section on 'Clinical presentation'.)
Pelvic inflammatory disease Lower abdominal pain is the cardinal presenting symptom in
women with pelvic inflammatory disease (PID), although the character of the pain may be
quite subtle. The recent onset of pain that worsens during coitus or with jarring movement
may be the only presenting symptom of PID; the onset of pain during or shortly after menses
is particularly suggestive. On physical examination, only about one-half of patients with PID
have fever. Abdominal examination reveals diffuse tenderness greatest in the lower
quadrants, which may or may not be symmetrical. Rebound tenderness and decreased bowel
sounds are common. On pelvic examination, the finding of a purulent endocervical
discharge and/or acute cervical motion and adnexal tenderness with bimanual examination is
strongly suggestive of PID. Clinical history and CT imaging can help differentiate PID from
acute appendicitis (See "Pelvic inflammatory disease: Clinical manifestations and diagnosis".)
Ruptured ovarian cyst Rupture of an ovarian cyst is a common occurrence in women of
reproductive age and may be associated with the sudden onset of unilateral lower abdominal
pain. The right lower quadrant is most commonly affected, possibly because the rectosigmoid
colon protects the left ovary from the effects of abdominal trauma. The pain often begins
during strenuous physical activity, such as exercise or sexual intercourse, and may be
accompanied by light vaginal bleeding due to a drop in secretion of ovarian hormones and
subsequent endometrial sloughing. Blood from the rupture site may seep into the ovary,
which can cause pain from stretching of the ovarian cortex, or it may flow into the abdomen,
which has an irritant effect on the peritoneum. Serous or mucinous fluid released upon cyst

rupture is not very irritating; the patient may remain asymptomatic despite accumulation of a
large volume of intraperitoneal fluid. On the other hand, spillage of sebaceous material upon
rupture of a dermoid cyst causes a marked granulomatous reaction and chemical peritonitis,
which is usually quite painful. Intraabdominal hemorrhage may be associated with Cullen's
sign (ie, periumbilical ecchymoses). Clinical history and CT imaging can help differentiate a
ruptured ovarian cyst from acute appendicitis (image 7 and image 8). (See "Evaluation and
management of ruptured ovarian cyst".)
Mittelschmerz Mittelschmerz refers to midcycle pain in an ovulatory woman caused by
normal follicular enlargement just prior to ovulation or to normal follicular bleeding at
ovulation. The pain is typically mild and unilateral; it occurs midway between menstrual
periods and lasts for a few hours to a couple of days. Fluid or blood is released from the
ruptured egg follicle and can cause irritation of the lining of the abdominal wall. (See
"Physiology of the normal menstrual cycle".)
Ovarian and fallopian tube torsion Ovarian torsion refers to the twisting of the ovary on its
ligamentous supports, often resulting in impedance of its blood supply (picture 2). Isolated
fallopian tube torsion is uncommon (picture 3). Expedient diagnosis is important to preserve
ovarian function and prevent adverse sequelae. However, the diagnosis can be challenging
because the symptoms are relatively nonspecific.
The most common symptom of ovarian torsion is sudden onset lower abdominal pain, often
associated with waves of nausea and vomiting. Fever, although an uncommon finding in
ovarian torsion, may be a marker of necrosis, particularly in the setting of an increased white
blood cell count. Clinical history and CT imaging can help differentiate the diagnosis from
acute appendicitis (picture 4). (See "Ovarian and fallopian tube torsion".)
Endometriosis Endometriosis is defined as the presence of endometrial glands and stroma
at extrauterine sites. These ectopic endometrial implants are usually located in the pelvis, but
can occur nearly anywhere in the body (picture 5).
Common symptoms of endometriosis include pelvic pain (which is usually chronic and often
more severe during menses or at ovulation), dysmenorrhea, deep dyspareunia, cyclical bowel
or bladder symptoms, abnormal menstrual bleeding, and infertility. There are often no
abnormal findings on physical examination; when findings are present, the most common is
tenderness upon palpation of the posterior fornix. Ultrasound is mostly useful for diagnosing
ovarian endometriomas; it lacks adequate resolution for visualizing adhesions and
superficial peritoneal/ovarian implants, which are more common than endometriomas. (See
"Endometriosis: Pathogenesis, clinical features, and diagnosis".)

Ovarian hyperstimulation syndrome Ovarian hyperstimulation syndrome (OHSS) is an

iatrogenic complication of ovulation induction therapy, and may be accompanied by or
mistaken for cyst rupture. Clinical findings include bloating, nausea, vomiting, diarrhea,
lethargy, shortness of breath, and rapid weight gain.
Severe ovarian hyperstimulation syndrome is characterized by large ovarian cysts, ascites,
and, in some patients, pleural and/or pericardial effusion, electrolyte imbalance
(hyponatremia, hyperkalemia), hypovolemia, and hypovolemic shock. Marked
hemoconcentration, increased blood viscosity, and thromboembolic phenomena, including
disseminated intravascular coagulation, occur in the most severe cases. (See "Pathogenesis,
clinical manifestations, and diagnosis of ovarian hyperstimulation syndrome".)
Ectopic pregnancy Ectopic pregnancy has clinical symptoms and sonographic features
similar to those of a ruptured ovarian cyst. In women with acute pelvic pain or abnormal
vaginal bleeding, a positive pregnancy test strongly suggests the presence of an ectopic
pregnancy if an intrauterine pregnancy cannot be visualized sonographically. If an intrauterine
pregnancy is visualized, then pelvic pain and intraperitoneal fluid could be due to a ruptured
ovarian cyst (eg, corpus luteum cyst, theca lutein cyst) or heterotopic pregnancy. (See "Ectopic
pregnancy: Clinical manifestations and diagnosis", section on 'Heterotopic pregnancy'.)
Acute endometritis Acute endometritis occurs after an obstetrical delivery or, rarely, after
an invasive uterine procedure. The diagnosis is largely based upon the presence of fever,
gradual onset of uterine tenderness, foul uterine discharge, and leukocytosis in an at-risk
setting. (See "Postpartum endometritis" and "Endometritis unrelated to pregnancy".)
Urologic conditions
Renal colic Pain is the most common symptom and varies from a mild and barely noticeable
ache to discomfort that is so intense that it requires parenteral analgesics. The pain typically
waxes and wanes in severity, and develops in waves or paroxysms that are related to
movement of the stone in the ureter and associated ureteral spasm. Paroxysms of severe pain
usually last 20 to 60 minutes. Pain is thought to occur primarily from urinary obstruction with
distention of the renal capsule. (See "Diagnosis and acute management of suspected
nephrolithiasis in adults" and "Acute management of nephrolithiasis in children".)
Testicular torsion Testicular torsion is a urologic emergency that is more common in
neonates and postpubertal boys, although it can occur at any age. Testicular torsion results
from inadequate fixation of the testis to the tunica vaginalis. If fixation of the lower pole of
the testis to the tunica vaginalis is insufficiently broad-based or absent, the testis may torse
(twist) on the spermatic cord, potentially producing ischemia from reduced arterial inflow and

venous outflow obstruction. (See "Causes of scrotal pain in children and adolescents", section
on 'Testicular torsion' and "Evaluation of the acute scrotum in adults", section on 'Testicular
torsion'.)
Epididymitis Epididymitis occurs more frequently among late adolescents, but also occurs in
younger boys who deny sexual activity and is the most common cause of scrotal pain in adults
in the outpatient setting. Several factors may predispose postpubertal boys to develop
subacute epididymitis, including sexual activity, heavy physical exertion, and direct trauma
(eg, bicycle or motorcycle riding). Bacterial epididymitis in prepubertal boys is associated with
structural anomalies of the urinary tract. In acute infectious epididymitis, palpation reveals
induration and swelling of the involved epididymis with exquisite tenderness. More advanced
cases often present with testicular swelling and pain (epididymo-orchitis) with scrotal wall
erythema and a reactive hydrocele. (See "Causes of scrotal pain in children and adolescents",
section on 'Epididymitis' and "Evaluation of the acute scrotum in adults", section on
'Epididymitis'.)
Torsion of the appendix testis or appendix epididymis The appendix testis is a small
vestigial structure on the anterosuperior aspect of the testis (an embryologic remnant of the
Mllerian duct system). The appendix epididymis is a vestigial remnant of the Wolffian duct
that is located at the head of the epididymis. The pedunculated shape of these appendages
predisposes them to torsion, which can produce scrotal pain that ranges from mild to severe.
Most cases of torsion of the appendix testis occur between the ages of 7 and 14 years, and
rarely occur in adults. (See "Causes of scrotal pain in children and adolescents", section on
'Torsion of the appendix testis or appendix epididymis' and "Evaluation of the acute scrotum
in adults", section on 'Torsion of the appendix testis'.)
TREATMENT The management of acute appendicitis in children and adults is discussed in
detail separately. (See "Acute appendicitis in children: Management" and "Management of
acute appendicitis in adults".)
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Here are the patient education articles that are relevant to this topic. We encourage you to
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Basics topics (see "Patient information: Appendicitis in adults (The Basics)").
SUMMARY AND RECOMMENDATIONS Appendicitis is one of the most common causes of
the acute abdomen and one of the most frequent indications for an emergent abdominal
surgical procedure worldwide.
The tip of the appendix can be found in a retrocecal or pelvic location, as well as medial,
lateral, anterior, or posterior to the cecum. Anatomic variability can complicate the diagnosis,
as clinical presentation will reflect the anatomic position of the appendix. (See 'Anatomy'
above.)
Appendiceal obstruction plays a role in the pathogenesis of appendicitis, but it is not
required for the development of appendicitis. (See 'Pathogenesis' above.)
The classic symptoms of appendicitis include right lower quadrant abdominal pain, anorexia,
fever, nausea, and vomiting. The abdominal pain is initially periumbilical in nature with
subsequent migration to the right lower quadrant as the inflammation progresses (see
'Clinical manifestations' above). Patients with appendicitis can also present with atypical or
nonspecific symptoms, such as indigestion, flatulence, bowel irregularity, and generalized
malaise; and not all patients will have migratory abdominal pain.
The differential diagnosis of right lower quadrant abdominal pain includes inflammatory
disease processes (eg, Crohns disease, ruptured cyst), infectious diseases (eg, acute ileitis,
tubo-ovarian abscess), and obstetrical conditions (eg, ectopic pregnancy). (See 'Differential
diagnosis' above.)
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REFERENCES

Williams GR. Presidential Address: a history of appendicitis. With anecdotes

illustrating its importance. Ann Surg 1983; 197:495.

Fitz, RH. Perforating inflammation of the vermiform appendix with special reference to
its early diagnosis and treatment. Am J Med Sci 1886; 92:321.

Jaffe, BM, Berger, DH. The Appendix. In: Schwartz Principles of Surgery, 8th ed,
3 Schwartz, SI, Brunicardi, CF (Ed), McGraw-Hill Health Pub. Division, New York
2005.
4

Buschard K, Kjaeldgaard A. Investigation and analysis of the position, fixation, length

and embryology of the vermiform appendix. Acta Chir Scand 1973; 139:293.

Mulholland, MW, Lillemoe, KD, Doherty, GM, et al. Greenfield's Surgery, 4th ed,
Lippincott Williams & Wilkins, Philadelphia, PA 2005.

Kumar, V, Abbas, AK, Fausto, N. Robbins and Cotran: Pathologic Basis of Disease,
7th ed, Saunders Elsevier, Philadelphia, PA 2007.

Addiss DG, Shaffer N, Fowler BS, Tauxe RV. The epidemiology of appendicitis and
appendectomy in the United States. Am J Epidemiol 1990; 132:910.

8 Birnbaum BA, Wilson SR. Appendicitis at the millennium. Radiology 2000; 215:337.
9 Burkitt DP. The aetiology of appendicitis. Br J Surg 1971; 58:695.
10 Butler C. Surgical pathology of acute appendicitis. Hum Pathol 1981; 12:870.
11

Miranda R, Johnston AD, O'Leary JP. Incidental appendectomy: frequency of

pathologic abnormalities. Am Surg 1980; 46:355.

12

Arnbjrnsson E, Bengmark S. Obstruction of the appendix lumen in relation to

pathogenesis of acute appendicitis. Acta Chir Scand 1983; 149:789.

13

Nitecki S, Karmeli R, Sarr MG. Appendiceal calculi and fecaliths as indications for
appendectomy. Surg Gynecol Obstet 1990; 171:185.

Jones BA, Demetriades D, Segal I, Burkitt DP. The prevalence of appendiceal fecaliths
14 in patients with and without appendicitis. A comparative study from Canada and South
Africa. Ann Surg 1985; 202:80.
15

Lau WY, Teoh-Chan CH, Fan ST, et al. The bacteriology and septic complication of
patients with appendicitis. Ann Surg 1984; 200:576.

16

Bennion RS, Baron EJ, Thompson JE Jr, et al. The bacteriology of gangrenous and
perforated appendicitis--revisited. Ann Surg 1990; 211:165.

17

Temple CL, Huchcroft SA, Temple WJ. The natural history of appendicitis in adults. A
prospective study. Ann Surg 1995; 221:278.

Lee SL, Walsh AJ, Ho HS. Computed tomography and ultrasonography do not improve
18 and may delay the diagnosis and treatment of acute appendicitis. Arch Surg 2001;
136:556.
Rao PM, Rhea JT, Novelline RA, et al. Helical CT technique for the diagnosis of
19 appendicitis: prospective evaluation of a focused appendix CT examination. Radiology
1997; 202:139.

Chung CH, Ng CP, Lai KK. Delays by patients, emergency physicians, and surgeons in
20 the management of acute appendicitis: retrospective study. Hong Kong Med J 2000;
6:254.
21 Guidry SP, Poole GV. The anatomy of appendicitis. Am Surg 1994; 60:68.
22

McBurney, C. Experience with early operative interference in cases of disease of the

vermiform appendix. NY Med J 1889; 50:676.

23

Golledge J, Toms AP, Franklin IJ, et al. Assessment of peritonism in appendicitis. Ann
R Coll Surg Engl 1996; 78:11.

Andersson RE, Hugander AP, Ghazi SH, et al. Diagnostic value of disease history,
24 clinical presentation, and inflammatory parameters of appendicitis. World J Surg 1999;
23:133.
25

Lane R, Grabham J. A useful sign for the diagnosis of peritoneal irritation in the right
iliac fossa. Ann R Coll Surg Engl 1997; 79:128.

Rovsing, NT. Indirektes Hervorrufen des typischen Schmerzes an McBurney's Punkt.

26 Ein Beitrag zur diagnostik der Appendicitis und Typhlitis. Zentralblatt fr Chirurgie,
Leipzig, 1907; 34:1257.
27

Izbicki JR, Knoefel WT, Wilker DK, et al. Accurate diagnosis of acute appendicitis: a
retrospective and prospective analysis of 686 patients. Eur J Surg 1992; 158:227.

28

Alshehri MY, Ibrahim A, Abuaisha N, et al. Value of rebound tenderness in acute

appendicitis. East Afr Med J 1995; 72:504.

Jahn H, Mathiesen FK, Neckelmann K, et al. Comparison of clinical judgment and

29 diagnostic ultrasonography in the diagnosis of acute appendicitis: experience with a
score-aided diagnosis. Eur J Surg 1997; 163:433.
30 Berry J Jr, Malt RA. Appendicitis near its centenary. Ann Surg 1984; 200:567.
31

John H, Neff U, Kelemen M. Appendicitis diagnosis today: clinical and ultrasonic

deductions. World J Surg 1993; 17:243.

32

Silen, W. Cope's Early Diagnosis of the Acute Abdomen, 19th edition, Oxford
University Press 1996. p.70.

33

Coleman C, Thompson JE Jr, Bennion RS, Schmit PJ. White blood cell count is a poor
predictor of severity of disease in the diagnosis of appendicitis. Am Surg 1998; 64:983.

34

Tehrani HY, Petros JG, Kumar RR, Chu Q. Markers of severe appendicitis. Am Surg
1999; 65:453.

Thompson MM, Underwood MJ, Dookeran KA, et al. Role of sequential leucocyte
35 counts and C-reactive protein measurements in acute appendicitis. Br J Surg 1992;
79:822.
36

Grnroos JM, Grnroos P. Leucocyte count and C-reactive protein in the diagnosis of
acute appendicitis. Br J Surg 1999; 86:501.

37 Br J Surg 1999; 86:501.

38

Guraya SY, Al-Tuwaijri TA, Khairy GA, Murshid KR. Validity of leukocyte count to
predict the severity of acute appendicitis. Saudi Med J 2005; 26:1945.

Sand M, Bechara FG, Holland-Letz T, et al. Diagnostic value of hyperbilirubinemia as

39 a predictive factor for appendiceal perforation in acute appendicitis. Am J Surg 2009;
198:193.
Rao PM, Rhea JT, Novelline RA. Sensitivity and specificity of the individual CT signs
40 of appendicitis: experience with 200 helical appendiceal CT examinations. J Comput
Assist Tomogr 1997; 21:686.
41

Whitley S, Sookur P, McLean A, Power N. The appendix on CT. Clin Radiol 2009;
64:190.

42

Choi D, Park H, Lee YR, et al. The most useful findings for diagnosing acute
appendicitis on contrast-enhanced helical CT. Acta Radiol 2003; 44:574.

Kessler N, Cyteval C, Gallix B, et al. Appendicitis: evaluation of sensitivity,

43 specificity, and predictive values of US, Doppler US, and laboratory findings.
Radiology 2004; 230:472.
44

Jeffrey RB Jr, Laing FC, Townsend RR. Acute appendicitis: sonographic criteria based
on 250 cases. Radiology 1988; 167:327.

Spalluto LB, Woodfield CA, DeBenedectis CM, Lazarus E. MR imaging evaluation of

45 abdominal pain during pregnancy: appendicitis and other nonobstetric causes.
Radiographics 2012; 32:317.
46

Oto A, Ernst RD, Ghulmiyyah LM, et al. MR imaging in the triage of pregnant patients
with acute abdominal and pelvic pain. Abdom Imaging 2009; 34:243.

47

Pedrosa I, Levine D, Eyvazzadeh AD, et al. MR imaging evaluation of acute

appendicitis in pregnancy. Radiology 2006; 238:891.

48

Lee TH, Kim JO, Kim JJ, et al. A case of intussuscepted Meckel's diverticulum. World
J Gastroenterol 2009; 15:5109.

Banli O, Karakoyun R, Altun H. Ileo-ileal intussusception due to inverted Meckel's

diverticulum. Acta Chir Belg 2009; 109:516.
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Disclosures
Disclosures: Ronald F Martin, MD Nothing to disclose. Martin Weiser, MD Nothing to
disclose. Wenliang Chen, MD, PhD Nothing to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When
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