Acute Appendicitis in Adults - Clinical Manifestations and Differential Diagnosis - UpToDate

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11/5/2021 Acute appendicitis in adults: Clinical manifestations and differential diagnosis - UpToDate

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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: Apr 2021. | This topic last updated: Jan 19, 2021.

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 emergency
abdominal surgical procedure worldwide [1,2].

The clinical manifestations and differential diagnosis of appendicitis in adults will be reviewed
here. The diagnostic evaluation and management of appendicitis in adults and appendicitis in
pregnancy and children are discussed separately. (See "Acute appendicitis in adults: Diagnostic
evaluation" and "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].
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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

The incidence of acute appendicitis is approximately 100 per 100,000 person-years. The precise
rate varies between 98 and 110 per 100,000 person-years in several large population studies
from North America [7-9] and Europe [10]. The incidence of acute appendicitis has been
decreasing since the 1970s for unknown reasons [8,10,11].

Appendicitis occurs most frequently in the second and third decades of life. The incidence is
highest in the 10-to-19-year-old age group and lowest in children ≤9 years [7,8]. 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].

The incidence of perforated appendicitis is approximately 29 per 100,000 person-years in both


the United States and South Korea [12]. There are also more cases of perforated appendicitis in
men than women (31 versus 25 per 100,000 person-years) [8]. The incidence of perforated
appendicitis has been rising despite a fall in the overall incidence of acute appendicitis [11].

One report from Washington State suggested that acute appendicitis is not randomly
distributed across geographic subunits [8]. Socioeconomic advantages, such as higher income
and secondary education, were strongly associated with a lower incidence of acute appendicitis.
The geographic clustering of perforated appendicitis is only half as strong as that of acute
appendicitis.

PATHOGENESIS

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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 [3,13-16].
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 [17].

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 [18,19].

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 to T10 are stimulated,
leading to vague central or periumbilical abdominal pain [13]. 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 "Well-differentiated neuroendocrine tumors of the appendix".)

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 progresses, 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 [20]. Common
organisms involved in gangrenous and perforated appendicitis include Escherichia coli,
Peptostreptococcus, Bacteroides fragilis, and Pseudomonas species [21]. 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].
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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 [18].

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 [22]. 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 [23,24]. 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 [23]. Although considered a classic symptom,
migratory pain occurs only in 50 to 60 percent of patients with appendicitis [13,25]. Nausea and
vomiting, if they occur, usually follow the onset of pain [26]. 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

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● 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 [27]. 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 101.0°F (38.3°C) 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 [28]. 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 (>101.0°F/38.3°C)
occurs as inflammation progresses. (See "Causes 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) [27]. 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 predated 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 [29]
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(sensitivity 50 to 94 percent; specificity 75 to 86 percent [30-32]).

● 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 [33] (sensitivity 22 to 68 percent; specificity 58 to 96 percent [31,34-36]).

● 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 [34,37,38]).

● The obturator sign is associated with a pelvic appendix. This test is based on the principle
that the inflamed appendix may lie 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 [37]).
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 [39]. Approximately 80 percent of patients have
a leukocytosis and a left shift (increase in total white blood cell (WBC) count, bands [immature
neutrophils], and neutrophils) in the differential [40-42]. The sensitivity and specificity of an
elevated WBC count in acute appendicitis are 80 and 55 percent, respectively.

Acute appendicitis is unlikely when the WBC count is normal, except in the very early course of
the illness [42,43]. In comparison, mean WBC counts are higher in patients with a gangrenous
(necrotic) or perforated appendix [44]:

● Acute − 14,500±7300 cells/microL


● Gangrenous − 17,100±3900 cells/microL
● Perforated − 17,900±2100 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 [45].
However, the test is not discriminatory and generally not helpful in the evaluation of patients
suspected of acute appendicitis

Imaging exams — Representative images of appendicitis are shown in this section. The choice
of imaging examination for the diagnosis of acute appendicitis is discussed in detail separately.

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(See "Acute appendicitis in adults: Diagnostic evaluation", section on 'Imaging'.)

Computed tomography findings — The following findings suggest acute appendicitis on


standard abdominal computed tomography (CT) scanning with contrast including ( image 1
and image 2) [46-48]:

● 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) [13,49,50].

Plain radiograph findings — Plain radiographs are usually not helpful for establishing the
diagnosis of appendicitis ( image 5).

Magnetic resonance imaging — Magnetic resonance imaging (MRI) can assist with the
evaluation of acute abdominal and pelvic pain during pregnancy ( image 6) [51,52]. A normal
appendix is visualized as a tubular structure less than or equal to 6 mm in diameter and filled
with air and/or oral contrast material [53]. 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 [53]. (See "Approach to acute abdominal pain in pregnant
and postpartum women" and "Acute appendicitis in pregnancy".)

DIAGNOSIS

Appendicitis is suspected in patients who present acutely with right lower quadrant
pain/tenderness and leukocytosis but only confirmed on histologic finding of a surgical
specimen. Diagnostic evaluation of appendicitis is discussed in detail in a separate topic. (See
"Acute appendicitis in adults: Diagnostic evaluation", section on 'Imaging'.)

DIFFERENTIAL DIAGNOSIS

A variety of inflammatory and infectious conditions in the right lower quadrant can mimic the
signs and symptoms of acute appendicitis. (See "Causes of abdominal pain in adults".)

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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 [22]. 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 103.0°F


(39.4°C), whose WBC count is greater than 15,000 cells/microL, and whose imaging studies
reveal a fluid collection in the right lower quadrant. (See 'Pathogenesis' above and 'Laboratory
findings' above and 'Imaging exams' above and "Acute appendicitis in adults: Diagnostic
evaluation".)

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 intravenous 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 "Acute colonic diverticulitis: Medical management", 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 [54,55]. 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 "Meckel's 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
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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 Crohn's 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 tubo-ovarian 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 approximately one-half of patients with
PID have fever. Abdominal examination reveals diffuse tenderness greatest in the lower
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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. Intra-abdominal 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 and
picture 3). Isolated fallopian tube torsion is uncommon ( picture 4). 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
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blood cell count. Clinical history and CT imaging can help differentiate the diagnosis from acute
appendicitis . (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".)
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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 "Kidney stones in adults: Diagnosis and acute management
of suspected nephrolithiasis" 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 "Acute scrotal pain 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 "Acute scrotal pain in adults".)

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
Müllerian 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 "Acute scrotal pain in adults",
section on 'Other etiologies'.)

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SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Appendicitis in adults".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade
reading level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading
level and are best for patients who want in-depth information and are comfortable with some
medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a
variety of subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topics (see "Patient education: 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 emergency abdominal surgical procedure worldwide. (See
'Epidemiology' above.)

● 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

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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; not all patients will have migratory abdominal pain.

● Appendicitis is suspected in patients who present acutely with right lower quadrant
pain/tenderness and leukocytosis but only confirmed on histologic finding of a surgical
specimen. Diagnostic evaluation of appendicitis is discussed in detail in a separate topic.
(See "Acute appendicitis in adults: Diagnostic evaluation", section on 'Imaging'.)

● The differential diagnosis of right lower quadrant abdominal pain includes inflammatory
disease processes (eg, Crohn's disease, ruptured cyst), infectious diseases (eg, acute ileitis,
tubo-ovarian abscess), and obstetrical conditions (eg, ectopic pregnancy). (See 'Differential
diagnosis' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

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importance. Ann Surg 1983; 197:495.
2. Fitz RH. Perforating inflammation of the vermiform appendix with special reference to its
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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.
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and Practice, 4th ed, Lippincott Williams & Wilkins, Philadelphia 2005.

6. Kumar V, Abbas AK, Fausto N. Robbins & Cotran Pathologic Basis of Disease, 7th ed, Saund
ers Elsevier, Philadelphia 2007.
7. 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. Golz RA, Flum DR, Sanchez SE, et al. Geographic Association Between Incidence of Acute
Appendicitis and Socioeconomic Status. JAMA Surg 2020; 155:330.

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9. Luckmann R. Incidence and case fatality rates for acute appendicitis in California. A
population-based study of the effects of age. Am J Epidemiol 1989; 129:905.
10. Ilves I, Paajanen HE, Herzig KH, et al. Changing incidence of acute appendicitis and
nonspecific abdominal pain between 1987 and 2007 in Finland. World J Surg 2011; 35:731.
11. Livingston EH, Woodward WA, Sarosi GA, Haley RW. Disconnect between incidence of
nonperforated and perforated appendicitis: implications for pathophysiology and
management. Ann Surg 2007; 245:886.
12. Lee SL, Shekherdimian S, Chiu VY. Effect of race and socioeconomic status in the treatment
of appendicitis in patients with equal health care access. Arch Surg 2011; 146:156.
13. Birnbaum BA, Wilson SR. Appendicitis at the millennium. Radiology 2000; 215:337.
14. Burkitt DP. The aetiology of appendicitis. Br J Surg 1971; 58:695.
15. Butler C. Surgical pathology of acute appendicitis. Hum Pathol 1981; 12:870.
16. Miranda R, Johnston AD, O'Leary JP. Incidental appendectomy: frequency of pathologic
abnormalities. Am Surg 1980; 46:355.
17. Arnbjörnsson E, Bengmark S. Obstruction of the appendix lumen in relation to
pathogenesis of acute appendicitis. Acta Chir Scand 1983; 149:789.

18. Nitecki S, Karmeli R, Sarr MG. Appendiceal calculi and fecaliths as indications for
appendectomy. Surg Gynecol Obstet 1990; 171:185.
19. Jones BA, Demetriades D, Segal I, Burkitt DP. The prevalence of appendiceal fecaliths in
patients with and without appendicitis. A comparative study from Canada and South Africa.
Ann Surg 1985; 202:80.
20. Lau WY, Teoh-Chan CH, Fan ST, et al. The bacteriology and septic complication of patients
with appendicitis. Ann Surg 1984; 200:576.
21. Bennion RS, Baron EJ, Thompson JE Jr, et al. The bacteriology of gangrenous and perforated
appendicitis--revisited. Ann Surg 1990; 211:165.
22. Temple CL, Huchcroft SA, Temple WJ. The natural history of appendicitis in adults. A
prospective study. Ann Surg 1995; 221:278.
23. Lee SL, Walsh AJ, Ho HS. Computed tomography and ultrasonography do not improve and
may delay the diagnosis and treatment of acute appendicitis. Arch Surg 2001; 136:556.

24. Rao PM, Rhea JT, Novelline RA, et al. Helical CT technique for the diagnosis of appendicitis:
prospective evaluation of a focused appendix CT examination. Radiology 1997; 202:139.
25. Chung CH, Ng CP, Lai KK. Delays by patients, emergency physicians, and surgeons in the
management of acute appendicitis: retrospective study. Hong Kong Med J 2000; 6:254.

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26. Takada T, Inokuchi R, Kim H, et al. Is "pain before vomiting" useful?: Diagnostic
performance of the classic patient history item in acute appendicitis. Am J Emerg Med
2021; 41:84.
27. Guidry SP, Poole GV. The anatomy of appendicitis. Am Surg 1994; 60:68.

28. Takada T, Nishiwaki H, Yamamoto Y, et al. The Role of Digital Rectal Examination for
Diagnosis of Acute Appendicitis: A Systematic Review and Meta-Analysis. PLoS One 2015;
10:e0136996.

29. McBurney, C. Experience with early operative interference in cases of disease of the
vermiform appendix. NY Med J 1889; 50:676.
30. Golledge J, Toms AP, Franklin IJ, et al. Assessment of peritonism in appendicitis. Ann R Coll
Surg Engl 1996; 78:11.
31. Andersson RE, Hugander AP, Ghazi SH, et al. Diagnostic value of disease history, clinical
presentation, and inflammatory parameters of appendicitis. World J Surg 1999; 23:133.
32. 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.
33. Rovsing, NT. Indirektes Hervorrufen des typischen Schmerzes an McBurney's Punkt. Ein
Beitrag zur diagnostik der Appendicitis und Typhlitis. Zentralblatt für Chirurgie, Leipzig,
1907; 34:1257.
34. 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.

35. Alshehri MY, Ibrahim A, Abuaisha N, et al. Value of rebound tenderness in acute
appendicitis. East Afr Med J 1995; 72:504.
36. Jahn H, Mathiesen FK, Neckelmann K, et al. Comparison of clinical judgment and diagnostic
ultrasonography in the diagnosis of acute appendicitis: experience with a score-aided
diagnosis. Eur J Surg 1997; 163:433.
37. Berry J Jr, Malt RA. Appendicitis near its centenary. Ann Surg 1984; 200:567.
38. John H, Neff U, Kelemen M. Appendicitis diagnosis today: clinical and ultrasonic deductions.
World J Surg 1993; 17:243.
39. Cope Z, Silen W. Cope's Early Diagnosis of the Acute Abdomen, 19th ed, Oxford University P
ress, New York 1996. p.70.

40. 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.
41. Tehrani HY, Petros JG, Kumar RR, Chu Q. Markers of severe appendicitis. Am Surg 1999;
65:453.
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42. Thompson MM, Underwood MJ, Dookeran KA, et al. Role of sequential leucocyte counts
and C-reactive protein measurements in acute appendicitis. Br J Surg 1992; 79:822.
43. Grönroos JM, Grönroos P. Leucocyte count and C-reactive protein in the diagnosis of acute
appendicitis. Br J Surg 1999; 86:501.
44. 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.
45. Sand M, Bechara FG, Holland-Letz T, et al. Diagnostic value of hyperbilirubinemia as a
predictive factor for appendiceal perforation in acute appendicitis. Am J Surg 2009;
198:193.
46. Rao PM, Rhea JT, Novelline RA. Sensitivity and specificity of the individual CT signs of
appendicitis: experience with 200 helical appendiceal CT examinations. J Comput Assist
Tomogr 1997; 21:686.
47. Whitley S, Sookur P, McLean A, Power N. The appendix on CT. Clin Radiol 2009; 64:190.

48. 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.
49. Kessler N, Cyteval C, Gallix B, et al. Appendicitis: evaluation of sensitivity, specificity, and
predictive values of US, Doppler US, and laboratory findings. Radiology 2004; 230:472.
50. Jeffrey RB Jr, Laing FC, Townsend RR. Acute appendicitis: sonographic criteria based on 250
cases. Radiology 1988; 167:327.
51. Spalluto LB, Woodfield CA, DeBenedectis CM, Lazarus E. MR imaging evaluation of
abdominal pain during pregnancy: appendicitis and other nonobstetric causes.
Radiographics 2012; 32:317.
52. 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.
53. Pedrosa I, Levine D, Eyvazzadeh AD, et al. MR imaging evaluation of acute appendicitis in
pregnancy. Radiology 2006; 238:891.

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

Variations in the position of the appendix

Graphic 64911 Version 2.0

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Blood supply to the colon and rectum

The blood supply to the colon originates from the SMA and the IMA. The SMA arises approximately 1
cm below the celiac artery and runs inferiorly toward the cecum, terminating as the ileocolic artery.
The SMA gives rise to the inferior pancreaticoduodenal artery, several jejunal and ileal branches, the
middle colic artery, and the right colic artery.
As a general rule, the middle colic artery arises from the proximal SMA and supplies blood to the
proximal to midtransverse colon. However, it occasionally provides the predominant blood flow to
the splenic flexure.
The right colic artery supplies blood to the mid-distal ascending colon. In anatomical studies, the
right colic artery arises independently from the SMA in 28 percent of individuals, which is depicted in
this figure. More frequently, the right colic artery arises with, or as a branch of, the middle colic,
ileocolic, or left colic arteries. The right colic artery is absent in 13 percent of individuals. [1]
The ileocolic artery supplies blood to the distal ileum, cecum, and proximal ascending colon.
The IMA arises approximately 6 to 7 cm below the SMA. The IMA gives rise to the left colic artery and
sigmoid arteries continuing as the superior rectal (hemorrhoidal) artery. It is largely responsible for
supplying blood distal to the transverse colon.

SMA: superior mesenteric artery; IMA: inferior mesenteric artery.

Reference:
1. Bergman RA, Thompson SA, Afifi AK, Saadeh FA. Compendium of Human Anatomic Variation: Text, Atlas,
and World Literature, Urban & Schwarzenberg, Baltimore, MD 1988.

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CT normal appendix

Normal appendix. Images of the pelvis from a CT with intravenous and oral contrast
shows an appendix (arrow) that is air-filled with double-layer wall thickness of <6 mm.

CT: computed tomography.

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CT acute appendicitis

Acute appendicitis. Images of the pelvis (A and B) from a CT with intravenous and oral contrast shows a
thickened appendix (arrow) containing an appendicolith and surrounding fluid indicating inflammation.

CT: computed tomography.

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Normal appendix by ultrasound imaging

The gray scale ultrasound (A, and magnified in B) and Doppler image (C) of the appendix are projected in the
transverse plane. Images A and B show a normal appendix measuring almost 6 mm in maximum transverse
dimension (arrow). The appendix was compressible and no hyperemia was demonstrated (arrow) on the Doppler
image (C). These findings are consistent with a normal appendix by ultrasound.

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Acute appendicitis ultrasound

The patient is a 19-year-old female who presented to the emergency department with right lower quadrant pain.
The gray scale ultrasound of the appendix is projected in the longitudinal (A) and transverse planes (B). A
noncompressible appendix measures almost 20 mm in diameter, consistent with a diagnosis of acute appendicitis.
The echogenic mucosal and submucosal portions of the wall have become discontinuous (arrows) suggesting
disruption as a result of sloughing. Luminal air (arrowheads) results in posterior shadowing.

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Appendicolith on abdominal films

This plain film of the abdomen reveals a 1.2 cm calcific density, an appendicolith. The
patient presented with right lower quadrant pain and was diagnosed with acute
appendicitis.

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Magnetic resonance image of appendicitis in pregnancy

T2-weighted magnetic resonance image of a woman with appendicitis at 9 weeks of


gestation. The appendix was fluid-filled and measured 7 mm (arrow). The gestational
sac (gs) is seen lower in the pelvis.

Courtesy of Deborah Levine, MD.

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Tubo-ovarian abscess

Gross intraoperative photograph of a left tubo-ovarian abscess in a patient with pelvic


inflammatory disease.

Courtesy of Mitchel Hoffman, MD.

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Ruptured ovarian cyst

Computed tomography. Arrows indicate free blood within peritoneal cavity surrounding
liver and spleen.

Courtesy of William J Mann, Jr, MD.

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Adnexal mass

Computed tomography. Arrow indicates poorly defined adnexal mass, which at exploration was
ruptured corpus luteum cyst and clot.

Courtesy of William J Mann, Jr, MD.

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Torsion of salvageable ovary

Ovarian and tubal torsion demonstrating marked vascular engorgement as well as


increased size and distension. Anatomy was restored, and both structures were
salvaged despite nonviable appearance. The thick arrow shows the torsed, enlarged
ovary (viable). The dashed arrow shows the enlarged fallopian tube (viable). The arrow
shows the enlarged fimbria of the fallopian tube (viable).

Reproduced with permission from: Pediatric and Adolescent Gynecology, 6th ed, Emans SJ, Laufer
MR, Goldstein DP (Eds), Lippincott Williams & Wilkins, Philadelphia 2012. Copyright © 2012
Lippincott Williams & Wilkins. www.lww.com.

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Torsion with viable ovary

Enlarged viable left ovary found torsed upon laparotomy demonstrating a dark, dusky
appearance secondary to venous lymphatic congestion in the setting of continued
arterial perfusion. The solid arrow denotes the viable ovary; the dashed arrow denotes
the viable fallopian tube.

Reproduced with permission from: Pediatric and Adolescent Gynecology, 6th ed, Emans SJ, Laufer
MR, Goldstein DP (Eds), Lippincott Williams & Wilkins, Philadelphia 2012. Copyright © 2012
Lippincott Williams & Wilkins. www.lww.com.

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Tubal torsion demonstrating severe distension of the distal tube

Reproduced with permission from: Pediatric and Adolescent Gynecology, 6th ed, Emans SJ, Laufer MR,
Goldstein DP (Eds), Lippincott Williams & Wilkins, Philadelphia 2012. Copyright © 2012 Lippincott
Williams & Wilkins. www.lww.com.

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Peritoneal endometriosis

The peritoneum in this woman with endometriosis is studded with reddish, irregularly
shaped implants.

Reprinted with permission. Copyright 1990 Syntex Laboratories, Inc. All rights reserved.

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Contributor Disclosures
Ronald F Martin, MD Nothing to disclose Martin Weiser, MD Consultant/Advisory Boards: PrecisCa
[Gastrointestinal surgical oncology]. Wenliang Chen, MD, PhD Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.

Conflict of interest policy

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