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15.6 Dierential Diagnosis
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381
15.6 Dierential Diagnosis
Differential diagnosis is more extensive than in
nonpregnant patients due to the following:
• Less reliable history and physical
examination,
• Higher incidence of additional conditions that
mimic AA.
These conditions are presented as non-
obstetric/nongynecologic and gynecologic/
obstetric conditions (Table15.3).
15.6.1 Round Ligament Pain/
Syndrome
Round ligament pain or syndrome (RLP) is one
of the most common abdominal discomforts of
pregnancy and usually starts in the second trimester of gestation and continues until delivery.
It usually resolves entirely after delivery or early
postpartum. The most common symptoms are
sudden pain in the lower abdomen, usually on the
right side of the pelvic area that can extend to the
groin, and shooting abdominal pain during sudden movements or physical exercise. Pain is sudden and intermittent and lasts a few seconds. The
most common causes are as follows: (1) round
ligament spasm or cramp when the ligament contracts involuntarily. The ligament pulls on the
female reproductive system’s nerve bers and
sensitive structures. Since the uterus tends to
rotate to the right, the pain is often right-sided,
leading to confusion with AA [119]; (2) the
increase in size and weight of the uterus puts
stress on the ligament that holds it, causing round
ligament stretching (see Sect. 19.1.5.2); (3) round
ligament varicosities—enlargement of the blood
vessels of the round ligament, can occur during
pregnancy, causing pain and swelling (see Sect.
19.1.5.1); (4) round ligament/inguinal endome-
triosis (see Sect. 19.1.5.3); and (5) other patholo-
gies of uterine round ligament causing
RLP.However, the diagnosis of RLP is one of
exclusion (see Sect. 19.1.5).
15.6.2 Meckel’s Diverticulitis
Symptomatic Meckel’s diverticulum/diverticulitis (MD) during pregnancy is exceptionally rare
(Fig. 15.8). Wenzl, in 1949, published the rst
case of MD in pregnancy [121]. Approximately
40 cases of MD complicating pregnancy have
been reported since 1949 [122, 123]. The average
maternal age in symptomatic MD is rising—until
Table 15.3 Differential diagnosis of acute appendicitis during pregnancy and puerperium
Non-obstetric/nongynecologic conditions Gynecologic/obstetric conditions
Gastroenteritis Ruptured/hemorrhagic ovarian cyst
Urinary tract infections Adnexal torsion
Pyelonephritis Salpingitis
Nephrolithiasis Tubo-ovarian abscess
Acute cholecystitis Threatened abortion
Acute pancreatitis Placental abruption
(incarcerated) hernia Chorioamnionitis
Bowel obstruction Pelvic inammatory disease
Cecal carcinoma Degenerative broid
Mesenteric adenitis Ectopic pregnancy
Spontaneous rectus hematoma Preeclampsia
Pulmonary embolism Round ligament syndrome/pain
Right lower lobe pneumonia Varicose veins in the parametria
Meckel’s diverticulitis Preterm labor
Sickle cell disease Pelvic endometriosis
Stump appendicitis Metritis
Inammatory bowel disease Ovarian vein syndrome
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Fig. 15.8 Meckel’s diverticulum at the antimesenteric
border of the ileum with a perforation at the tip (white
arrow). Gravid uterus (U). (Reproduced with permission
from [120])
1990, it was 24years (range 17–31) [123], and
after 1990 it raised to 27 [14–34, 38] [122], probably due to increasing maternal age during pregnancy. It is rare during the rst trimester and
equally frequent (48%) in the second and third
trimesters [122].
Presenting symptoms include abdominal pain
(88.9%), nausea or vomiting (59.3%), fever
(18.5%), abdominal distension (18.5%), hematochezia (11.1%), constipation (11.1%), hematemesis (3.7%), diarrhea (3.7%) and asymptomatic
(3.7%) [122]. The most common type of MD presentation is perforation (40–57%) [122, 124],
with an equal incidence of intussusception,
bleeding, inammation, and small bowel obstruction (11.1%) [122]. In the nonpregnant adult population, MD perforation occurs in 7.3–26.8%
[125–127]. In the general population, bleeding is
the most common presentation in patients
younger than 20 years [128, 129] and is rare
beyond 30.
15 Acute Appendicitis
Fig. 15.9 Abdominal CT shows 6.0 × 4.7 cm rimenhancing uid collection with extraluminal air in the
right iliac fossa surrounded by collapsed small bowel
loops. Dilated, uid-lled small bowel loops in the left
lower abdomen indicate small bowel obstruction with a
transition point at the ileal level. (Reproduced with permission from [123])
Before the era of CT and MRI, preoperative
diagnosis is challenging (9% until 2002 [124]
and 7.4% until 2021 [122]). Diagnostic imaging
modalities utilized after 1990 were abdominal
US (40.7%), CT (25.9%), MRI (14.8%), plain
abdominal X-ray (11.1%), and endoscopy
(7.4%). No cases utilized scintigraphy [122].
Even if detected, it mimics AA on the transabdominal US as a noncompressible tubular structure (see Sect. 15.7.3). Although their accuracy is
low, CT and MRI can distinguish between AA
and MD in pregnancy [122]. CT can dene the
pathophysiologic process causing MD
(Fig.15.18) or indirect signs, such as small bowel
obstruction (Fig.15.9). MRI can reveal a thickwalled hollow structure emanating from the distal ileum with inltrative changes, suggesting an
inammation (Fig.15.10).
Treatment follows the principles of incidental
MD in pregnancy (see Sect. 15.9.2).
MD perforation is more common during
pregnancy than in the general adult
population.
15.6.3 Crohn’s Disease
See Chap. 21.
15.6 Dierential Diagnosis
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383
a
Fig. 15.10 (a) Coronal MRI image shows inamed Meckel’s diverticulum (red arrow) and gravid uterus (yellow star).
(b) Axial MRI image shows inamed Meckel’s diverticulum (arrows). (Reproduced with permission from [131])
15.6.4 Urolithiasis/Urinary Tract
Infection
John Osborn Polak (March 12, 1870—June 29,
1931), in 1929, described the difference in the
sequence of events between AA and pyelitis
[132], which is diagnostic. With AA, the pain
could be followed by fever and rarely chills. With
pyelitis, chills come rst, then fever and pain (see
Sect. 27.3.4).
15.6.5 Vomiting ofPregnancy
In 1905, Heaton explained the difference
between AA and vomiting of pregnancy. The
illness may be of all degrees of severity, from
the transient appendiceal colic to the fulminating AA, which proves fatal in a few hours.
In the mild cases, the sickness which ushers in
the illness is liable to be mistaken by both
patient and practitioner for the ordinary vomiting of pregnancy. The use of the clinical thermometer in a doubtful case should prevent
mistake, for the vomiting of pregnancy is
“apyrexial,” and the presence of fever, however slight, should always put us on our guard
and lead us to make a careful examination of
the right iliac region [53]. Unfortunately, low-
b
grade fever is present in 50% of patients with
AA (see Sect. 15.5.2).
15.6.6 Fitz–Hugh–Curtis Syndrome
Perihepatitis (Fitz-Hugh-Curtis syndrome)
results from early bacteremia or retroperitoneal
lymphatic dissemination of C. trachomatis or
gonococcal pelvic infection [133]. The syndrome
is most frequent in young women and more common in the second and third trimesters and puerperium. Inammation in the RUQ produces
perihepatic adhesions. Classically, there is a sudden onset of sharp RUQ pain, often pleuritic in
quality. Nausea and hiccups are occasional.
Physical ndings include RUQ tenderness, an
occasional hepatic friction rub, and fever. Pelvic
examination may be normal or reveal signs of
cervicitis or pelvic inammatory disease. Liver
function tests may be transiently abnormal. A
history of recent pelvic infection suggests the
diagnosis, but the syndrome can be a sequel of
latent or asymptomatic infection. The diagnosis
is further supported by the isolation of gonococcus on cervical culture and the improvement
from appropriate antibiotics [133]. Other conditions should be excluded because specic diagnostic markers are lacking.
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15 Acute Appendicitis
15.6.7 Puerperium-Associated
Diseases
15.6.7.1 Metritis
The most common of these is metritis, the broad
group of postpartum infections of the genital
tract. Metritis is often insidious in onset. Because
of the vague initial manifestations, it is often a
diagnosis of exclusion. Endometritis, or deciduitis, is an infection of the most supercial layer of
the uterus and is the most common site of puerperal infection. Endometritis onset is commonly
2–5days postpartum, and the earliest manifestations are malaise, anorexia, and fever. There may
be no localizing signs or symptoms in mild cases.
The pelvic examination may be normal, even in
severe endometritis. The disease may progress
further to involve the myometrium (myometritis)
and parametrial structures (parametritis) with
extension into the broad ligaments, tubes, ovaries, and pelvic peritoneum [79]. When the parametria are involved, pain and tenderness are
present deep in the groin. Extensive infection
may produce lethargy, chills, high fever, and signicant lower abdominal pain, tenderness, and
rebound. Accompanying paralytic ileus may
cause distention and vomiting. Myometritis and
parametritis are usually accompanied by cervical
motion tenderness and localized peritoneal signs,
rarely generalized peritonitis. The lochia may
provide a clue as to the true nature of the difculty. Within 48 h, the lochia of endometritis
becomes serous, seropurulent, or foul-smelling if
the infection is saprophytic. A are-up of gonorrheal salpingitis seldom begins before the seventh day, and the ndings usually are limited to
the pelvis. A positive history of the previous
infection is important for the diagnosis.
15.6.7.2 Pelvic Thrombophlebitis/
Ovarian Vein Syndrome
Thrombophlebitis and thromboembolic events
are more common in pregnancy, especially puerperium. Ovarian vein thrombosis(syndrome
complicates <0.05% vaginal deliveries and 1–2%
Cesarean sections (CS) [134]. Ovarian vein
thrombosis involves the right ovarian vein in
90%. It is attributed to retrograde ow in the left
ovarian vein and antegrade ow in the right ovarian vein in the postpartum period. This difference
in blood ow may be attributable to the physiologic dextrorotation of the uterus during pregnancy and compression of the right ovarian vein.
Puerperium predisposes to deep vein thrombosis
attributable to sluggish circulation, trauma to the
pelvic vessels during delivery, immobilization,
and estrogen-mediated hypercoagulability.
Other risk factors include abortions, gynecological surgery, malignancy, pelvic inammatory
disease, Crohn’s disease, and infections with
Campylobacter fetus and group A streptococcal
bacteremia. Inherited thrombophilia, primarily
factor V Leiden mutations and protein S deciency, has been reported in 50% of patients with
ovarian vein thrombosis. There are cases of ovarian vein thrombosis associated with antiphospholipid syndrome and heparin-induced
thrombocytopenia-type II.
Pelvic thrombophlebitis, or right ovarian vein
syndrome, commonly presents with abdominal/
pelvic pain (66%), fever (80%), and a tender
midabdominal or RLQ mass [134]. However, the
diagnosis is often complicated by other nonspecic symptoms and signs: back pain, nausea,
vomiting, tachypnea, tachycardia, hypotension,
ileus, and sepsis [135]. It may be difcult to distinguish from metritis but should be considered
after a poor response to appropriate antibiotics or
exclusion of adnexal torsion (see Sect. 6.6).
Diagnosis can be delayed due to fever and elevated laboratory inammatory markers that mislead the diagnosis of AA, urinary tract infection,
or tubo-ovarian abscess [136].
The diagnosis is frequently made after a fever
is nonresponsive to antibiotics for 48 h. Color
Doppler US is the rst diagnostic procedure
[137], but due to low sensitivity and high false
negative and false positive rates, IV contrastenhanced CT is preferred. The sensitivity
(Fig. 15.11) is 100% compared to 92% with
gadolinium- enhanced MRI and 50% of duplex
color Doppler US [139].
Untreated postpartum ovarian vein thrombosis
carries the risk of severe complications like sep-
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Fig. 15.11 Abdominal CT shows thrombosed right ovarian vein (arrow). (Reproduced with permission from
[138] under the CC BY 2.0)
sis and extension into the inferior vena cava.
Septic pulmonary embolism occurs in 11–33%,
with a mortality of 4–5% [140]. Successful treatment includes anticoagulation for 3–6 months
with low molecular weight heparin and antibiotics for 2 weeks. Surgical treatment is reserved
when (1) anticoagulation is contraindicated, (2)
treatment-related complications occur, and (3)
with a high risk for pulmonary embolism—freeoating thrombus, an extension of thrombus, or
recurrent pulmonary embolism despite adequate
medical therapy [141, 142]. Surgical interventions include ligation and splitting the thrombosed ovarian vein and inferior vena cava or
placement of inferior vena cava lters to prevent
pulmonary embolism.
No uniform guidelines exist for the evaluation
of thrombophilia after ovarian vein thrombosis.
Pregnancy and the puerperium are hypercoagulable states, with a predisposition to ovarian vein
thrombosis. The risk factors associated with
postpartum ovarian vein thrombosis include several thrombophilias—antiphospholipid syndrome, lupus anticoagulant, factor V Leiden
mutation, MTFHR C677T deciency, and protein S deciency [143]. However, the American
College of Obstetricians and Gynecologists recommends testing white women with a previous
deep vein thrombosis for the factor V Leiden
mutation and individualizing testing in nonwhite
women [144].
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15.7 Diagnosis
Medicine is a science of uncertainty and an art of
probability.
(Sir William Osler)
The diagnosis of acute appendicitis is more difcult than at other times, as the enlarged uterus renders it almost impossible to explore the right iliac
region satisfactorily.
(John Whitridge Williams, 1903)
Diagnostic workup should be done in a hospital in cooperation with the obstetrician. No signicant difference in the median time from
presentation to rst imaging or surgery, the incidence of negative pathology, or appendiceal rupture exists between women who presented to the
ED or obstetrics triage [145]. The lag time
between arrival to the ED and laparotomy was
signicantly higher in the second half of pregnancy than in the rst half (11.6 vs. 7.7h, respectively) [37].
15.7.1 Laboratory Findings
A pregnant woman’s physiologic leukocytosis,
increased heart rate, and respiratory alkalosis
make her more likely to meet systemic inammatory response syndrome criteria than a nonpregnant woman [146].
Leukocytosis (raised white blood cell count—
WBC) is not diagnostic due to the physiologic
rise in pregnancy, reaching 20,000/mm3 in early
labor [147]. Despite that, a pregnant patient
undergoing appendectomy has an average WBC
value of over 13,000/mm3 compared to 10,500/
mm3 of healthy pregnant women [148–150]. The
values over 16,000/mm3 are highly suspicious
[21, 26, 44, 118, 151] and also indicate appendiceal perforation [109]. Only 60% with perforation had WBC >16,000/mm3 [29]. Different
WBC cutoff values had different sensitivities
and specicities for AA [150]. With suspected
AA and normal WBC levels, serial (every 6h)
WBC measurements [152, 153] or a comparison
with previous WBC values during normal pregnancy is helpful. If WBC values during previous
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normal pregnancy were within normal limits,
then RLQ pain with elevated WBC is a predictor
of AA.
Neutrophil granulocytosis with the left shift
implies acute bacterial infection. Without the left
shift, granulocytosis >80% should raise suspicion
of AA [93]. Even normal values are found with AA
in pregnancy [26, 154]. Neutrophil-to- lymphocyte
ratio (NLR) values are signicantly higher in AA
patients than in healthy pregnant women and pregnant women under acute abdominal observation
[150]. Cutoff values differ from 5.5 to 6.84, result-
ing in different sensitivities and specicities in
most scenarios o>80% [148, 150, 155].
A C-reactive protein (CRP) is normal dur-
ing pregnancy and delivery. After delivery of
normal pregnancy, values increase 10–20-fold
(never >10 mg/L) compared to levels at
admission. Pregnant patients with gestational
diabetes, diabetes mellitus, obesity, or pregnancy-induced hypertension have maximal
CRP levels of 10mg/L [156–159] even despite
racial differences [160]. CRP starts to increase
within 8–12h as a response to inammation.
Its increase is slower than that of WBC and
reaches a maximum level within 24–48 h.
Interestingly, positive cases had negative CRP
values when evaluated <12h from the onset of
pain [118]. Sixty-eight percent with AA had
CRP±10mg/L, but all patients with perforation had elevated CRP (mean 55mg/L) [29].
CRP value increases while the albumin level
decreases in the acute phase response secondary to inammation in pregnant patients. CRP-
to-albumin ratio (CAR) was signicantly
higher in patients who underwent appendectomy after AA diagnosis than in pregnant
women under acute abdominal observation or
healthy pregnant women [150]. Also, the number of lymphocytes was lower, but CRP was
higher in AA patients than in healthy pregnant
women. The number of lymphocytes decreased
while the CRP value increased depending on
the severity of the infection [148, 150, 155].
Lymphocyte-to CRP ratio (LCR) is signicantly lower in a patient with AA than in
healthy pregnant women [150].
15 Acute Appendicitis
Elevated WBC, NLR CRP, CAR, and LCR
levels could be used as supportive parameters for physical examination and anamnesis for AA diagnosis in pregnant patients
[150].
The erythrocyte sedimentation rate is physiologically elevated and less reliable monitoring of
inammatory activity during pregnancy [161].
Leukocyturia (57%) and bacteriuria (41%)
are common with AA [80]. This may represent
concurrent asymptomatic (or symptomatic) bacteriuria, frequent in pregnancy [19]. Other abnormalities such as mild proteinuria or hematuria
are present in up to 19% of pregnant patients
[108].
Puerperal changes in blood components may
be confusing as well. During the rst 10–14days
of the puerperium, WBC counts of 20,000–
25,000/mm3 are not unusual; there is also a predominant increase in neutrophils. The erythrocyte
sedimentation rate may increase to 50–60mm/h.
Reliance on the erythrocyte sedimentation rate or
the WBC count for diagnosing acute infection
may be misleading [79].
15.7.2 Diagnostic Scoring Systems
Isolated clinical signs and blood indices are unreliable for diagnosing AA in pregnancy and lead
to an unacceptable negative appendectomy rate
(NAR), up to 50%, without imaging [37].
Therefore, clinical imaging scoring systems have
been developed to diagnose AA in the nonpregnant population accurately.
15.7.2.1 Alvarado Score
andModications
The most common score in the general population is the Alvarado score (AS) [162]. The mnemonic is MANTRELS (Table 15.4). AS
sensitivity (54.0–96.2%) and specicity (54.0–
74.3%) vary signicantly. AS [163–165] and
modied AS for pregnant patients [166] have
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Table 15.4 Comparison of Alvarado score and modied Alvarado score for pregnant patients
Alvarado Score Modied AS for pregnant patients
Symptoms Score Symptoms Score
Migratory RLQ pain 1 RLQ pain 2
Anorexia 1 Anorexia 1
Nausea/vomiting 1 Nausea/vomiting 1
Signs Signs
Tenderness in RLQ 2 Tenderness in RLQ 2
Rebound tenderness in RLQ 1 Rebound tenderness in RLQ 1
Elevated temperature
(≥37.3°C / ≥99.1°F)
Laboratory Laboratory
Leukocytosis (>10,000/mm3) 2 Leukocytosis (>10,000/mm3) 1
Shift to the left (>75%) 1
Total score 10 Total score 9
Table 15.5 Alvarado score with conrmed acute appendicitis in pregnant (by trimesters) and nonpregnant
Pregnant (%)
Trimester
Statistical method
Sensitivity 93 65 75 79 73
Specicity 50 83 75 80 75
PPD 93 92 75 94 94
NPD 7 35 75 21 13
Accuracy 88 70 75 79 74
Reproduced with permission from [164]
PPD positive predictive value, NPD negative predictive value
First Second Third Total
1 Elevated temperature
(≥37.3°C / ≥99.1°F)
1
Nonpregnant (%)
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been tested in the pregnant population. The difference in comparison to the standard AS is that
migration of pain is not included. Also, the number of points for pain in RLQ is 2 compared to 1
point in the standard AS for the nonpregnant
population. Leukocyte left shift is not included,
and leukocytosis (which could be present in a
normal pregnancy) has only 1 point in modied
AS for pregnant patients. The total score is lower
by 1 point (9 vs. 10) (Table15.4). The positive
predictive value was 60% with AS 5–7 and 100%
with AS 7–9. The sensitivity and specicity of
AS 7 are 80% [163–165].
The AS can be falsely higher in pregnancy due
to physiologic leucocytosis in the late pregnancy
and a higher frequency of nausea and vomiting
during the rst trimester [164, 165]. Also, the
pain localization in the RLQ and the pain migration might vary due to the growth of the uterus
leading to different AS values in pregnancy [164,
165]. The specicity and sensitivity according to
the trimesters are presented in Table15.5.
15.7.3 Transabdominal Ultrasound
The American Colleague of Radiology
Appropriateness Criteria recommends it as the
initial imaging modality for suspected AA in
pregnancy [167]. Most patients are submitted to
the abdominal US preoperatively [17, 168]. Apart
from identifying underlying pathology, it can
identify cervical incompetence [169], obstetric
complications (see Sect. 15.10.4), and fetal status. US criteria are the same as in the nonpregnant population for the diagnosis of AA [170] as
follows:
• Noncompressible appendix,
• Appendiceal diameter>6mm,
• Appendiceal wall thickness≥2mm,
• Free uid around the appendix,
• Complex mass in the area of the
appendix.
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15 Acute Appendicitis
Indirect signs include abnormal uid collections in the pelvic cavity or around the cecum/
appendix. Evaluation of the entire appendiceal
length may be challenging with an enlarged
gravid uterus, and the focal area of AA may be
missed. In many instances, AA is morphologically evident only on its tip, which is sometimes
not visualized [170].
Sensitivities vary dramatically, 18–100% with
higher specicities, 80–100% [22, 80, 93, 148,
161, 168, 170–176]. The positive predictive value
is near 100%. The differentiation between MD
and AA can be difcult because both are noncompressible tubular structures in RLQ
(Fig.15.12).
Fig. 15.12 Transabdominal sonogram shows a tubular
cystic structure, 8×2cm in the right iliac fossa, found to
be giant Meckel’s diverticulitis. (Reproduced with permission from [177])
The accuracy of transabdominal US in a
supine position during late pregnancy is challenging because the enlarged gravid uterus prevents graded compression. In the second half of
pregnancy, the patient should be placed in the left
posterior oblique or left lateral decubitus position, allowing displacement of an enlarged uterus
allowing the graded compression US technique
[171]. High clinical suspicion with a normal or
inconclusive transabdominal US indicates an
abdominal MRI or CT [168].
15.7.4 Transvaginal Ultrasound
There are no Royal College of Obstetricians and
Gynaecologists guidelines about the use of trans-
vaginal US.The transvaginal US can detect the
following [178]:
• Presence and size of adnexal or uterine
pathology ruling out AA,
• Free uid in the pouch of Douglas,
• Pathology in the ileocecal region (cecal
tumors, cecal diverticula, or retroperitoneal tumors),
• AA (aperistaltic, tubular structure measuring ≥6 mm; hyperemia; appendicolith; free uid around the appendix)
(Figs.15.13 and 15.14).
a
Fig. 15.13 Transvaginal imaging of the right adnexa. (a) Transverse view of the appendix. (b) Long view of the appen-
dix measuring 0.7cm. (Reproduced with permission from [179] under the CC BY 3.0)
b
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389
a
Fig. 15.14 Transvaginal imaging of the right adnexa demonstrating appendicitis. (a) Enlarged appendix (AP) with
appendicolith (*). The uterus (UT) is also seen. (b) Hyperemic
Apart from identifying underlying pathology, it can identify cervical incompetence [169]
and other obstetric complications (see Sect.
15.10.4).
Transvaginal Doppler US denes adnexal torsion or vascularized tumors. In nonpregnant
women, 24% with AA were diagnosed by the
transvaginal US after negative transabdominal
US [178]. Some recommend transvaginal US as
the rst US diagnostic tool for female patients
with low abdominal pain [179].
b
appendix (AP) visualized in transverse, appendicolith (*),
right ovary (OV), and uterus (UT) seen. (Reproduced with
permission from [179] under the CC BY 3.0)
The MRI criteria for AA include (Fig.15.15)
the following:
• Appendiceal diameter>7mm,
• Appendiceal wall thickening >2mm,
• Fluid-lled appendix,
• Appendicolith,
• Periappendicular inammation (periappendicular fat stranding and uid),
15.7.5 Abdominal MRI
After the indeterminate US, the European Society
of Urogenital Radiology [180] and the American
College of Radiology [181] recommend abdomi-
nal MRI or CT when MRI is unavailable.
Therefore, indications for abdominal MRI are as
follows:
• The appendix not visualized by abdominal US,
• No other cause of abdominal pain on
US.
The MRI criteria that exclude AA are (1)
appendiceal diameter<6mm or (2) appendiceal
diameter of 6–7mm with no evidence of periappendicitis (Fig.15.16). The second MRI scenario
warrants close clinical follow-up.
MRI has high sensitivity (91.8%) and specicity (97.9%) for AA in pregnant patients [183].
Advantages of MRI for suspected AA in pregnancy include the following:
• Reduced rates of both negative laparotomy
and perforation [184–186],
• Identication of other causes of abdominal
pain [185–188],
• More frequent discharge from the emergency
department [184],
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15 Acute Appendicitis
Fig. 15.15 Axial T2-weighted image shows dilated
appendix (arrow) consistent with acute appendicitis.
(Reproduced with permission from [182])
Fig. 15.16 Coronal T2-weighted image shows normal
appendix (arrow) at 14 weeks gestation. (Reproduced
with permission from [182])
Fig. 15.17 Transverse section of an oral and IV contrastenhanced CT shows a thickened appendix and periappendicular fat stranding (arrow) in 27weeks of pregnancy,
conrming acute appendicitis. (Reproduced with permission from [189])
operative treatment (see Sect. 15.8.1). After the
inconclusive US, abdominal MRI did not lower
the AA perforation rate [186].
15.7.6 Abdominal CT
CT of the appendix is positive for AA with the
following (Fig.15.17):
• Enlarged appendix (maximum
diameter>6mm),
• Periappendiceal inammatory changes
(fat stranding, phlegmon, uid collection, and extraluminal gas).
• Shortened length of stay in non-operated and
operated groups [184, 186],
• Identication of cervical incompetence
[169].
Except for diagnosing AA, MRI accurately
detects the degree of AA inammation for non-
In a pregnant population with AA, sensitivity and specificity are similar to the general
population, over 90% [189–191]. CT established a diagnosis in 30% of cases with an initial negative US [191]. The higher the degree
of appendiceal inflammation, the higher the
sensitivity for detecting AA in pregnancy
[192]. Abdominal CT delineates other condi-
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