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Acute Appendicitis
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15
Abstract
Acute appendicitis is the most common nonobstetric operative emergency during pregnancy. It amounts to 25% of operative
indications for the acute abdomen during
pregnancy and puerperium. Pain in the right
lower quadrant is the most reliable symptom,
and abdominal tenderness is almost always
present. Fever and tachycardia are not sensitive signs. Leukocytosis is not diagnostic
because elevated levels are found during
pregnancy, especially in the early labor in
normal pregnancy. Neutrophil granulocytosis
is diagnostic as it is a sign of bacterial infection. Graded abdominal ultrasound is the
diagnostic procedure of choice with less
accuracy in the third trimester with no guidelines about the use of transvaginal ultrasound. Magnetic resonance imaging is the
diagnostic procedure of choice in cases when
an abdominal ultrasound is not diagnostic.
Nonoperative antibiotic treatment is increasingly used with excellent outcomes during
pregnancy. A laparoscopic approach is
increasingly used without adverse fetal outcomes. Fetal mortality in uncomplicated
appendicitis is low and raises several times
when perforation and diffuse peritonitis
develops. Maternal mortality is almost 0%
and increases with the delay in surgery for
more than 24h, which is the most common
situation in the third trimester when the diagnosis is often delayed and inaccurate.
15.1 Historical Perspective
It proves fatal to a woman in a state of pregnancy
if she is seized with any acute diseases.
(Hippocrates)
In 1836 (reference unavailable), Stumpf
described a rupture of the cecum in a pregnant
woman, which could be a perforated acute appendicitis (AA). Ofcially, the rst case was in 1848,
when Henry Hancock (Fig.15.1), the President
of the Medical Society of London, presented a
paper to that society describing the treatment of a
30-year-old woman, in her fth pregnancy, 7
months pregnant bearing twins in the Charing
Cross Hospital in London [2]. She developed
abdominal pain, had preterm labor on the fourth
day with a live newborn for 20h, and developed
a tender mass in the lower right abdomen. She
was seen by Hancock 12days after the disease
had started. She had a distended, tender abdomen, particularly in the lower right quadrant
(RLQ). Hancock prescribed opium and poultices.
Two days later, her condition was much worse,
with a palpable mass in the RLQ.The incision
was made above and parallel to Poupart’s ligament over the palpable mass. During exploration,
offensive pus and bubbles of gas escaped. After
2 weeks, she felt pain around the wound, and
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
G. Augustin, Acute Abdomen During Pregnancy, https://doi.org/10.1007/978-3-031-26021-6_15
371
372
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Fig. 15.1 Henry Hancock (1809–1880). Lithograph by
T.H. Maguire, 1849. (Reproduced with permission from
[1] under the CC BY 2.0)
after wound exploration, Hancock found two
fecaliths. He postulated that fecaliths had escaped
by ulceration from the diseased appendix. From
that time, her improvement was rapid, and she
made a good recovery.
Wiggin, in 1892, reported the rst case of
preoperative diagnosis and an operation advised
at a time when the life of both mother and infant
could have been saved. Unfortunately, the
patient’s friends refused the operation. Petersen,
in 1893, recorded the rst postpartum case of
AA on the seventh day following labor at term,
with rupture of the abscess into the bowel and
recovery without operation [3]. In 1894, Paul
Fortunatus Mundé (1846–1902), a gynecologist
from Mount Sinai Hospital in NewYork, published the rst successful case from the USA
[4], treating appendiceal abscess but with the
premature delivery of a dead child. Spirtos
et al. published the earliest series of laparoscopic appendectomies (LA) during pregnancy
in 1987 [5].
15 Acute Appendicitis
15.2 Incidence
Appendicitis seems to be favored by pregnancy /
L’appendicite semble favorisee par la grossesse.
(Dieulafoy)
Appendicitis or epityphlitis (epi - + Greek
typhlon = cecum +− itis, inammation) is the
most common non-obstetric cause of acute abdomen during pregnancy and puerperium. Between
1913 and 1926, approximately 2–2.5% of the
women who presented with symptoms of AA
were pregnant [6, 7]. Since 1935, the incidence of
AA during pregnancy was 1/2000 [8], while
between 1944 and 1959, the incidence was
1/1000 [9, 10]. The report from 1972 claimed
1/704 [11]. The conclusion was that AA is a disease of modern civilization caused by a sedentary
life and a high-residue esh diet [12]. Current
incidence estimates range from 1/181 to 1/8770
pregnancies. AA amounts to 25–30% of operative indications for the acute abdomen in pregnancy [13–32]. The rate of AA during pregnancy
in the most recent four population-based studies
is 1/1000–1/4167 pregnancies [22, 27, 33, 34].
The highest incidence is in Taiwan—1/181 [13]
and varies signicantly between countries and
even between regions and hospitals in the same
country (Table 15.1). Although no references
specically address postpartum AA, most studies
group AA in pregnancy and the puerperium
because of the anatomic and physiological
continuum [38]. In the USA (2002–2015), there
Table 15.1 Comparative incidence of acute appendicitis
in pregnancy between countries
Country Incidence
Taiwan [13] 1:181
Pakistan [25, 35] 1:346–1:1135
Germany [24] 1:499
Sweden [29] 1:776
Chile [36] 1:1028
Israel [37] 1:1055
Saudi Arabia [28] 1:1102
Turkey [15] 1:1312
Jordan [31] 1:1644
Brazil [32] 1:2580
Mexico [30] 1:8770
14
=–10.6(–10.8,–10.5)*
Rates per 10,000 maternal hospitalizations
AppendicitisAcute Appendicitis
15.3 Risk Factors
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373
APC
12
APC
10
8
6
4
2
0
APC
APC
AAPC - Average annuak percentage change from 2002-2015
2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2015 2015
- Annual percentage change from 2002-2011
02-11
- Annual percentage change from 2011-2015
11-15
=–2.4(–2.5,–2.4)*
02-11
=–2.3(–2.3,–2.2)*
02-11
AAPC=–5.0(–5.0,–5.1)*
Year
AAPC=–4.7(–4.8,–4.7)*
APC
APC
=–10.6(–10.8,–10.5)*
11-15
11-15
Fig. 15.2 USA trends in rates of all appendicitis and acute appendicitis per 10,000 maternal hospitalizations (2002–
2015). (Reproduced with permission from [39])
was a 5% average annual decrease in AA rates,
with a steep decline in overall appendicitis and
AA rates after 2011 (Fig. 15.2). The trimester
analysis is presented in Sect. 15.3.2.
15.3 Risk Factors
15.3.1 Age andMultiple Pregnancies
A higher incidence of AA in pregnancy than other
causes is multifactorial (Table 15.2). The incidence of AA and childbearing are strongly related
to a younger age. Ninety percent of pregnant
women are <30years [40], correlating with the
peak incidence of AA in the general population
[41]. The incidence of AA shows regional varia-
tions and a secular trend with a decreasing incidence in the general population. Secular and
Table 15.2 Risk factors for acute appendicitis during
pregnancy
Age<30years
Multiple pregnancies
Second trimester (perforated and negative)
Black and Hispanic women
Nonobese
Attacks of appendicitis before pregnancy
(pregnancy-induced) constipation
Medicaid insurance
regional variations are related to the incidence of
childbirth. The inuence of these variations on the
incidences of AA and pregnancy is complex,
making it difcult to determine the expected incidence of AA during pregnancy for comparison
purposes. Early marriage and repeated pregnancies till menopause increase the probability of an
AA in pregnancy.
374
10.0
Odds Ratio (log scale)
Months prepartumMonths postpartum
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15 Acute Appendicitis
15.3.2 Trimester
It seems that AA is more common in the second
trimester with an incidence of 35–50% [24–26,
42, 43] (the rst 30%, the second 45%, and the
third 25% [22, 40, 44, 45]), but there is no proof
that pregnancy affects the overall incidence [46].
Figure 15.3 compares appendectomies across
trimesters of pregnancy to matched controls
[47]. Patients who had undergone appendectomy
were less likely to be pregnant at the operation
than controls. This inverse relation depended on
the gestation period and the underlying diagnosis at the operation. Corroborating results from
previous reports, the highest incidence of AA
and appendectomy was found in the second trimester of pregnancy. This pattern was seen for
perforated AA and negative explorations,
whereas for non-perforated AA, the strength of
the inverse relation increased continuously
throughout the pregnancy. This result suggests
that pregnancy may protect against AA
(Fig.15.3). In the largest study to date, a national
representative cohort of almost 1.6 million childbearing women, pregnant women during the
antepartum period were 35% less likely to be
diagnosed with AA than the time outside pregnancy (Fig.15.4), with the lowest risk reported
during the third trimester.
Results were unchanged after adjusting for
age and calendar year. Furthermore, there is no
increased risk of AA in the puerperium than outside pregnancy among women aged 15–34.
However, the risk increased almost twofold in
older women during the latter postpartum [33]. It
is possible that AA during pregnancy, at term,
and in the puerperium is lower or underestimated.
First, it could be an unrecognized mild, selflimiting disease [48–50]. Mild attacks could be
interpreted as the ordinary discomforts of pregnancy, and the severe cases in the puerperium
were probably regarded as types of puerperal
sepsis. Also, these attacks could be interpreted as
intestinal colic, renal colic, ureteropyelitis,
threatened miscarriage, salpingitis, and tubal
pregnancy. The second is the issue of AA during
term labor. Sometimes, labor is induced by
inammatory changes due to AA (see Chap. 4)
[49]. The third is potentially reduced incidence,
especially in the third trimester, because of the
protective (immunomodulatory) effect of pregnancy (see Sect. 15.4.1) [47]. This fact dates back
Fig. 15.3 Comparison
of gestational age in
women who had an
appendectomy compared
with matched controls.
The relation is expressed
as the odds ratios
according to conditional
logistic regression.
(Reproduced with
permission from [47])
1.0
0.1
7
6
5
4
3
2
7
6
5
4
3
2
Perforated
Non-perforated
Negative exploration
Perpartum
9 to 8
8 to 7
7 to 6
6 to 5
5 to 4
4 to 3
3 to 2
2 to 1
1 to 0
Partus
Post-partum
0 to 1
1 to 2
2 to 3
16
Rate of AA (95% Cl) per 10,000 person-years
Time period
15.4 Pathogenesis
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14
12
10
8
6
4
2
0
Outside pregnancy I trimester II trimester III trimesterearly postpartumlater postpartum
Fig. 15.4 Absolute rates of acute appendicitis per 10,000 person-years by trimesters and the early and later postpartum
period in England. (Reproduced with permission from [33])
375
to 1921 with the conclusion that in the last few
weeks of gestation and during labor, it is very
rare [51]. It was found at term in 1% [52].
pathogen or by an inammatory response triggered by an infectious agent or some other stimulus. Geographical differences in the incidence of
AA and secular trends in the general population
have been related to the differences in ber
15.3.3 Other
dietary intake and hygiene standards [57, 58].
A signicantly higher proportion of Black and
Hispanic women have AA during pregnancy
15.4.1 Immunologic Changes
[34]. In 1905, conservatively treated suspected
acute or chronic appendicitis had a signicantly
higher incidence of AA during pregnancy, up to
50% (see Sect. 15.4) [48, 53, 54]. Pregnant
women with AA were less likely to be obese and
more commonly had Medicaid insurance [34].
Constipation is a risk factor in the nonpregnant
and pregnant population [55]. Constipation, a
major risk factor, was recognized in 1897 when
R.Abramhams collected 15 cases [56].
During pregnancy, a range of physiological
changes may inuence the pathogenesis of
AA. The implantation requires a T-helper cell
type 1 (Th1) response, followed by a shift toward
a Th2 phenotype for the main duration of pregnancy and a Th1 milieu toward partition [59].
This shift toward a Th2-dominated immunity
results in a depressed cellular inammatory
response and increased humoral immunity [60].
There is an overall decrease in proinammatory
cytokine trajectories in the innate and adaptive
15.4 Pathogenesis
arms of the immune system and an increase in
counter-regulatory cytokines as the pregnancy
One mechanism of AA is the mechanical obstruction of the appendiceal lumen, either due to fecal
stasis, kinking peritoneal adhesions, or infectioninduced swelling of the mural lymphoid tissue.
Another mechanism is a breakdown of the appendiceal mucosal barrier by the direct invasion of a
progresses [61]. Because AA is an inammatory
process, the inverse relationship between pregnancy and AA could suggest that a Th1-mediated
inammatory response is partly responsible [62].
This mechanism inuences only the inammatory and not obstructive type of AA.
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15 Acute Appendicitis
Moreover, cigarette smoking has a proinammatory effect [63] and is associated with an
increased AA risk in the general population [64].
Because pregnancy may motivate women to quit
smoking [65, 66], this could also partially contribute to the lower risk of AA observed during
pregnancy. Inammatory markers have a dosedependent and temporal relationship to smoking
and smoking cessation. The smoking-associated
inammatory response returns to normal 5years
after smokers quit [67].
15.4.2 Anatomical/Physiological
Changes
In the general population, the incidence of AA is
higher in men. It has been suggested that the vascular anastomoses in women between the blood
vessels of the appendix and the ovarian vessels
on the right side may induce comparative immunity. These anastomosing channels relieve appendiceal congestion and inammation by carrying
some blood into systemic circulation [53]. This
mechanism does not have any effect on the
obstructive form of AA.
Progression of AA may be more fulminating
in pregnancy. Increased pelvic vascularity and
displacement or kinking (especially if partly
xed) of the appendix by the growing uterus may
hasten obstruction or strangulation. An increased
local lymphatic drainage and interference with
omental migration due to the enlarged uterus may
favor the systemic spread of the inammatory
process. Braxton Hicks contractions prevent the
formation of adhesions, thereby promoting early
diffuse peritonitis [20, 40, 68, 69]. Also, suppura-
tion takes place higher in the abdomen. The
abdomen can handle suppuration much better in
the lower than in the upper parts. When inammation and suppuration occur, abdominal viscera
localize the process by encircling it. In pregnancy, the intestines and greater omentum are
dislocated. Also, the abdominal viscera strive to
localize the process, decreasing its movements.
At the same time, the uterus does the reverse
increasing the possibility of spreading suppuration and making diffuse peritonitis more likely.
The adnexa and appendix are brought closer with
the ascent of the uterus. Infection in either may
cause a corresponding inammation in the other
by contiguity. In 1900, the communication by
lymphatics, by a peritoneal fold of Clado, the
appendicular ovarian ligament was claimed. This
is a fold of the peritoneum, prolonged outward
from the infundibulopelvic ligament to the mesoappendix [70].
Another possibility for the spread of localized
infection is immediately after delivery. The
expulsion of the fetus and sudden contraction of
the uterus promote abscess rupture. König and
Muret made early observations of this phenomenon [71].
15.4.3 Recurrent/Chronic
Appendicitis
Pregnancy does not predispose to the rst attack
of AA [48, 53–55] but increases the risk of recurrent AA during the same pregnancy. Théodore
Tufer, in 1897, reported a woman with three
successive pregnancies accompanied by appendiceal attacks [72]. The esection of the appendix,
which contained a concretion, was curative.
Recurrent attacks in pregnancy could be the
result of vascular engorgement of the appendix,
constipation commonly associated with pregnancy, the toxemias of pregnancy, the encroachment of the uterus in the early months of
pregnancy and puerperium, and the occasional
stretching or breaking down old inammatory
adhesions, binding the appendix to the uterus and
its appendages. Although without proper analysis, Melford B.Jorgensen in 1952 stated that (1)
recurrent AA is relatively frequent in pregnancy,
and as the pregnancy advances, the attacks
become increasingly more severe, with more difculty in diagnosis and the surgical procedure
more difcult; and (2) AA is likely to recur in
pregnancy if there has been a previous attack
[73]. The history of AA was present in up to 15%
s
15.5 Clinical Presentation
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377
[42]. Recurrence of AA occurs even after antibiotic treatment during (2.9%) the same pregnancy
[42, 74, 75] or after (5.9%) delivery [42], with an
overall recurrence of 8.8% [42].
15.4.4 Female Sex Hormones
A relation with female sex hormones has been
proposed because of a lower incidence among
women and incidence variations during the menstrual cycle, but with inconsistent results [76, 77].
This observation was presented rst by Le Genre
in 1897. Childbearing constitutes a period of
many hormonal uctuations. The dynamic maternal immune responses to normal pregnancy have
evolved out of the need to support a semiallogenic fetus throughout the pregnancy without
signicant infectious or inammatory impediment to the mother.
Fig. 15.5 Height of the
fundus at comparable
gestational dates varies
greatly. The most
common heights are
shown. A convenient
rule of thumb is that at
5months gestation, the
fundus is usually at or
slightly above the
umbilicus [78]
15.5 Clinical Presentation
15.5.1 Medical History
The approach to pregnant patients with abdominal pain is similar to nonpregnant patients.
However, the anatomical/physiological
pregnancy- related changes must be considered
when interpreting history and physical examination ndings. The uterus enlarges about 20 times
during pregnancy resulting in stretching of supporting ligaments and muscles and pressure on
other intra-abdominal structures and layers of the
anterior abdominal wall (Fig.15.5). Immediately
after delivery, the uterus assumes a 15–16-week
size [79]. At 1week postpartum, the uterine fundus returns to the pelvis and is the size of a
12-week gravid uterus. After the rst week, uterine involution occurs more slowly, reaching prepregnancy size within 6weeks (Fig.15.6).
Weeks
Weeks
38
38
40
40
36
36
32
32
28
28
Fundal height is
measured in
centimerters from
the pubic symphsi
to the top most
portion of the
uterus
22
22
16
16
12
12
Pubic
Pubic
symphysis
symphysis
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15 Acute Appendicitis
• Extensive differential diagnosis with the
addition of pregnancy-related diseases,
• Working diagnosis of systemic
infection,
• Obstetric complications could be the
rst sign of non-obstetric intraperitoneal
infection.
1st day
2
3
4
5
6
7
8
9
10
Fig. 15.6 Postnatal shrinking of the uterus
During the rst 6months of pregnancy, symptoms and signs of AA are the same as in nonpregnant women, but diagnostic difculties remain
due to the following:
• Blunting/masking of symptoms and
signs (abdominal distension, intraabdominal organ dislocation, diminished tissue response to inammation),
• Possible changes in appendiceal location as pregnancy advances,
• Nausea, vomiting, and abdominal pain
of normal pregnancy, especially in the
rst trimester,
Constant abdominal pain is the most common
symptom [17], and RLQ pain, present in 67–84%,
is the most reliable symptom [17, 20, 21, 29, 40,
80]. The incidence of RLQ pain decreases during
trimesters (100%, 80%, and 60%, respectively)
[81]. Rates of pain localized in the RUQ range
from 10 to 42% [40, 82, 83] and are most common during the third trimester [25]. Classical
pain migration is found in 50–70% [29, 84]. After
the third month of pregnancy, the pain could
change location and migrate progressively
upward and laterally, reaching the level of the
right iliac crest at the end of the sixth month of
pregnancy. Füth, in 1905 and 1913, described the
displacement of the cecum and appendix upward
[82, 83]. At that time, Hoffman, in 1920, stated
that the appendix is below the iliac crest in 90%
of pregnant women and that the exact position of
the cecum during pregnancy can be dened only
by abdominal X-rays with barium enema [85].
Paul Schumacher, in 1929, conrmed these ndings by X-rays with IV glucose administration
[86]. Baer etal. [87] showed by barium enema
that the growing uterus progressively displaces
the appendix out of the pelvis after the third
month, into the upper right quadrant, by as much
as two ngerbreadths above McBurney’s point,
with a counterclockwise rotation of the tip
(Fig. 15.7). The appendix returns to its normal
position by postpartum day 10. The original
description by Charles Heber McBurney is that
pressure is applied by one nger “exactly between
1½ and 2 inches from the anterior spinous process of the ileum on a straight line drawn from
that process to the umbilicus.” This landmark
corresponds to the areas of the inamed appendix
irritating the abdominal peritoneum over the T11
and T12 dermatomes. The pain and hyperesthesia
15.5 Clinical Presentation
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Fig. 15.7 Change of the location of the appendix during
pregnancy according to Baer etal. [87]. (Springer illustration from second edition of Acute Abdomen During
Pregnancy)
are present over McBurney’s point despite the
possible upward displacement of the appendix
[88]. Others did not conrm the upper displacement of the appendix using physical examination, imaging techniques, or intraoperatively [26,
85, 89–93]. Positional changes may be hampered
by adhesions that restrict the free movement of
the appendix, especially the retrocecal (subserosal) position. Hodjati and Kazerooni found a signicant positional change (>2cm) of the appendix
in 15–23% [92]. This discrepancy is partly due to
the different extents of cecal xation. MRI studies conrmed the upward displacement of the
appendix in the term pregnant woman [94, 95].
379
The most challenging interpretation of abdominal pain is immediately before, during, and
immediately after the labor. With uterine contractions before labor, AA is likely when severe
abdominal pain remains between contractions or
persists after delivery [50].
Abdominal pain aggravated by fetal movements is sometimes detected [55, 96, 97]. One of
the rst mentions of this symptom was by Emil
Jerlov in 1929 [95], William Marbury in 1933
[98], and Urban Maes in 1934 [55].
Nausea is nearly always present, and vomiting
in 70–87% of patients [93]. These symptoms are
exaggerated due to the following: (1)
progesterone- induced delayed gastric emptying
and (2) pressure of the enlarged uterus on the hollow viscus. Symptoms could be misleading
because many women with normal pregnancies
have these symptoms, especially in early pregnancy [29]. AA is likely with new-onset nausea
(the period of nausea and vomiting in early pregnancy is primarily self-limiting and conned to
the rst trimester).
Anorexia is present in 1/3 to 2/3 of pregnant
while almost universal in nonpregnant patients
[19, 20, 99]. New-onset anorexia should raise
suspicion, especially with other symptoms and
signs suggestive of AA.
An atypical clinical picture is most common
in the second trimester [24]. RUQ pain (12%),
uterine contractions, dysuria (20%), and diarrhea
could mask AA [26, 28, 46, 80].
In pregnancy with obstetric complications,
such as miscarriage [53] or preterm labor [100–
102], and abdominal or pelvic pathology symp-
toms, AA should be excluded rst, which could
cause these obstetric complications. Obstetric
complications from AA in pregnancy were
pointed out in the nineteenth century [103–105].
15.5.2 Physical Examination
A growing pregnant uterus could displace a
mobile cecum with the appendix. (Partly)
xed cecum or retrocecal (subserosal)
appendix cannot be displaced.
The abdominal wall changes during pregnancy,
with muscle tone reduction and skin elasticity to
accommodate the enlarging uterus. The abdominal wall tone remains lax for several weeks postpartum, returning to a near-nonparous level in
6–7weeks. The chronic stretching of the parietal
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15 Acute Appendicitis
peritoneum by the growing uterus, particularly in
the third trimester, decreases the number of
afferent sensory nerve bers of the peritoneum
per square. A high circulatory level of adrenocorticoids in pregnancy diminishes the tissue
response to inammation, masks the early signs
of infection, and hinders localization. Increased
parietal and visceral peritoneum separation by an
enlarging uterus causes decreased perception and
localization of somatic pain. These changes make
clinical localization of inamed appendix
unreliable.
The hallmarks of acute surgical disease,
abdominal guarding, and rigidity do not occur or
are attenuated during the early puerperium. This
is responsible for the delay in proper diagnosis.
There is no single and reliable sign for the
diagnosis of AA in pregnancy. Some classic signs
of AA, such as Rovsing’s or Psoas’ sign, have no
diagnostic value for AA in pregnancy [28].
An abdominal mass may be missed on physical examination because of the enlarged gravid
uterus [106].
On direct palpation, abdominal tenderness
in the RLQ is always present [80, 93, 107].
Rebound tenderness is present in 55–93% [25,
80, 93, 99, 108, 109] and abdominal muscle
rigidity in 50–65% [25, 44]. These two signs are
more common during the rst trimester. In the
second and the third trimesters, as the abdominal
wall distends, the anterior abdominal wall is distanced from the inamed appendix losing the
ability to elicit guarding and rigidity [46, 110].
Rovsing’s sign is variable, present in 18–60%
[21, 25, 109, 111], while trimester distribution is
unknown. A positive sign in the third trimester
could be due to the separation of the abdominal
wall from the colon, without the possibility of its
compression.
The psoas’s sign (Obraztsova’s sign) is less
frequent during pregnancy (5–50% [109, 112])
compared to nonpregnant patients with AA [19].
Obturator’s sign is found in 21% of patients
[109].
Rectal or pelvic tenderness may occur in early
pregnancy but is unusual in late pregnancy as the
appendix is dislodged from its pelvic location
and shielded by the enlarged uterus [109, 113].
Therefore, <50% had tenderness on rectal examination [108, 109].
Alders’ sign can differentiate AA from tuboovarian pathology with RLQ pain in pregnancy
and puerperium [114]. The point of maximal tenderness is determined while the patient is supine.
Then, roll the patient onto the left side. If pain
shifts toward the center, then it may be tuboovarian. The problem in pregnant patients in the
third trimester is that the enlarged uterus does not
allow the tubo-ovarian complex to shift its position. This sign is helpful if the uterus is not large
enough to be palpable abdominally. It may be
misleading when a uterine lesion has become
xed by adhesions to the anterior abdominal
wall. In acute salpingitis, the result will depend
on the presence or absence of perisalpingitic
adhesions. Approximately 36% of patients with
proven AA had positive Alders’ sign [109] without comparing trimesters.
Aaron’s sign is a referred pain or discomfort
in the precordial or epigastric region when continuous rm pressure is applied over McBurney’s
point [115].
Bryan’s sign is abdominal pain produced by
shifting the gravid uterus to the right; by some,
the most reliable sign [116].
The mean maximal axillar temperature is
37.2–37.9°C but could be >39°C with perforation and diffuse peritonitis [17, 69, 93].
Approximately 50–70% of pregnant patients
with AA have a low-grade fever [25, 93, 108,
117]. This incidence of elevated temperature is
not different from the normal pregnant population, the nding is also true for tachycardia [45,
117], and both are not sensitive signs [26, 118],
predicting only perforation and peritonitis.
Pregnant patients with low-grade fever also have
leukocytosis, complicating the denitive diagnosis [93].
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