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16 Biliary Tract Emergencies
16.1.2 Incidence
16.1.2.1 General Population
The prevalence of gallbladder disease in the
general population differs signicantly in different populations and countries. William Mayo
conrmed that gallstones occur three times more
frequently in women [2]. In the USA, 10–15%
of adults have gallstones. In particular, 70% of
Native American women older than 30 develop
cholelithiasis. Mexican American women have a
prevalence of 14%, with Caucasians and Black
women at 4% and 5%, respectively [3]. Chilean
women are at high risk of developing gallstones
[4], and populations of Latin American countries
have a prevalence of gallstones up to 50% in adult
women [5]. In Mexico, the prevalence is 14.3%.
It increases with age—up to 25% after 60years
and 33% after 70years [6].
16.1.2.2 Pregnancy andPuerperium
Complications of gallstones represent the second
most common non-gynecologic condition requiring surgery in pregnancy. The incidence of gallbladder disease in pregnancy is 0.05–0.3%
[7–12]. Asymptomatic gallstones occur in 2.5–
10% during pregnancy and 12% in the early
puerperium versus 1.3% in nonpregnant controls
[4, 13–15]. Approximately 60–69% of pregnant
women with gallstones are asymptomatic [4, 14].
The incidence of acute cholecystitis (AC) during
pregnancy is 1/1000–1/10,000 [16–20].
Approximately 40% of pregnant patients with
symptomatic cholelithiasis require cholecystectomy during pregnancy [21–23]. Cholelithiasis is
the cause of cholecystitis in over 90% of cases.
At least 0.8% of women with gallbladder disease underwent cholecystectomy in the rst postpartum year [24]. It is estimated that more than
32,000 young, otherwise healthy women in the
USA, will require postpartum cholecystectomy
each year [25]. Thus, pregnancy-associated gallbladder disease is a signicant problem in young,
otherwise healthy women.
Despite its relatively uncommon occurrence
during pregnancy, 81% of women with symptoms of gallbladder disease had their rst attack
within 1year of pregnancy [26]. A higher inci-
dence of gallbladder disease (0.39%) is found in
Saudi Arabia. This is attributed to (1) a high number of repeated pregnancies and (2) genetic predisposition because higher percentages (7.5%) of
pregnant women harbor silent gallstones in comparison with 3.5% in Western countries [27].
There is no statistically signicant difference in
the gallstone prevalence rates between Mexicanborn and non-Mexican-born pregnant Hispanic
women in the 20-year to 49-year age group [28].
Surgical gallstone disease during pregnancy is
distributed as follows: biliary colic and AC
(62.7–86.3%), biliary acute pancreatitis (AP)
(3–25.4%), choledocholithiasis (6.8–7.0%), and
acute cholangitis (2.6–5%) [22, 29, 30].
In 1910, almost half (10/25) of patients presented during puerperium [31].
16.1.3 Risk Factors
Pregnancy may constitute a dened period of
subclinical metabolic stress with full clinical presentation revealed later. For example, pregnant
women with gestational diabetes mellitus (DM)
or high blood pressure are at risk of developing
DM or hypertension [32, 33]. A similar phenomenon may happen with gallbladder sludge and
stones [24].
16.1.3.1 Biliary Sludge
Biliary sludge, or microlithiasis, is a mixture of
granules of cholesterol and calcium bilirubinate
crystals up to 2mm in diameter within viscous
bile. Larger clusters are dened as gallstones on
ultrasound (US). Although not sludge becomes
gallstones, sludge is the initial step in gallstone
formation and the earliest recognizable stage of
lithogenesis [34].
Biliary sludge forms in 11–31% of women
during pregnancy and gallstones form in 2–6%
[4, 35–37]. New sludge or stones were found in
30% and 2% of the women at the end of their
pregnancies. The postpartum US revealed the
disappearance of sludge in 61% and the disappearance of stones in 28% [37]. After delivery,
the disappearance of gallstones correlated with a
smaller stone diameter and increasing age [37].
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Therefore, some patients with symptomatic cholelithiasis during pregnancy may not have it after
delivery [36]. These results should be taken with
caution because the sensitivity of US for microscopic sludge is 50–60% [24]. All detected gallstones were<10mm [4, 35].
16.1.3.2 Multiparity
Multiparity is a risk factor due to hormonal
changes that directly inuence gallstone formation [35, 38]. Pregnancy increases the prevalence
from 1.3% in nulliparous women to 12.2% in
multiparous [39]. Approximately 5.1% of women
develop gallbladder disease after one pregnancy,
7.6% after two pregnancies, and 12.3% after
three or more pregnancies [24, 40–42]. After
accounting for the number of children, 12months
of breastfeeding reduces the risk of gallbladder
disease in parous women by 7% [43]. The protective effect of breastfeeding could be from
decreased estrogen levels during lactation [44].
However, other hormonal changes that occur
with lactation may also have an effect. Early marriage and repeated pregnancies until menopause
increase the probability of gallstone disease in
pregnancy. A cross-sectional study found the following incidence of gallstones: in the 21- to
30-year age group, 1.4% in patients having no
pregnancy, 9.6% in patients having one pregnancy, 7.1% in patients having two pregnancies,
6.0% in patients having three pregnancies, and
3.3% in patients having four and more pregnancies; in the 31- to 40-year age group, 0.6% in
patients having no pregnancy, 1.4% in patients
having one pregnancy, 6.0% in patients having
two pregnancies, 8.2% in patients having three
pregnancies, and 12.6% in patients having four
and more pregnancies; in the 41- to 50-year age
group, 0.8% in patients having no pregnancy,
0.6% in patients having one pregnancy, 4.4% in
patients having two pregnancies, 4.4% in patients
having three pregnancies, and 12.9% in patients
having four and more pregnancies; and in the 51to 60-year age group, 0.6% in patients having one
pregnancy, 1.1% in patients having two pregnancies, 2.5% in patients having three pregnancies,
and 14.3% in patients having four and more pregnancies. The risk of gallstone disease increases
with parity, particularly among younger women
[45]. Valdivieso etal. found that 12% of women
immediately after delivery had gallstones compared to 1.3% nulliparous group [4]. The increase
in progesterone secretion, which remains high
during the second and third trimesters, leads to
smooth muscle relaxation and gallbladder dilation and stasis [46]. The incidence of gallbladder
disease in the asymptomatic category was higher
in patients of higher age and parity [31, 47].
Young patients with a higher parity are more
prone to gallbladder disease [15, 47].
On the contrary, some claim no effect or
reduced prevalence by a factor of 40 compared to
nulliparae [14, 48] and that the female-specic
factors of prior pregnancy and the number of previous pregnancies did not show a measurable
inuence on the prevalence of gallbladder stones
[49]. Multiparity could be misinterpreted as a
risk factor instead of age because several pregnancies sometimes include more than 10years.
16.1.3.3 Diabetes Mellitus, Obesity,
andBariatric Surgery
The risk of forming gallbladder sludge or stones
during pregnancy is signicantly higher in obese
(2.3% vs. 0.4% [12]) women (BMI ≥30kg/m2)
[7, 24]. Overweight and obesity are observed in
66% of pregnant and postpartum patients [50].
Insulin resistance, which increases with BMI, is
one possible mechanism linking obesity to gallstones [51–57]. Women who formed gallbladder
sludge or stones were signicantly more insulinresistant. Autopsy studies [41, 55] and epidemiological studies in Mexican Americans [51] and
Caucasian Americans [42] have shown DM to be
a signicant risk factor for gallstones. The independent risk factor for incident sludge or stones
is prepregnancy BMI >25kg/m2 [24, 58]. As the
prevalence of overweight and obesity in young
women increases [59], pregnancy-associated
gallbladder disease may become a signicant
problem.
Despite recognizing weight loss procedures as
risk factors for cholelithiasis [10], the impact of
gestation on the occurrence of biliary disease
after bariatric procedures is vague. The reported
incidence of symptomatic cholelithiasis in the
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16 Biliary Tract Emergencies
general population following bariatric surgery is
up to 15%, depending on the procedure [60]. The
cholecystectomy rate following LAGB, RYGB,
and SG is 6.5%, 9.7%, and 10.1%, respectively
[61].
16.1.3.4 Oral Contraceptives
See Sect. 16.1.4.1.
16.1.3.5 Age
Age (see Sect. 16.1.2.1) and multiparity (see
Sect. 16.1.3.2) are interrelated risk factors for
gallbladder disease in pregnancy.
16.1.3.6 Gallbladder Volume
andFunction
During pregnancy, gallstone and biliary sludge
formation may be related to increased fasting
gallbladder volume [62] or postprandial gallbladder volume [63, 64]. The third mechanism is that
gallstone and biliary sludge formation during
pregnancy could be attributed to gallbladder
motility dysfunction [65, 66]. A direct relationship between gallbladder hypomotility and gallstone and biliary sludge formation during
pregnancy has been shown in a group of healthy
pregnant women [35].
16.1.4 Pathogenesis
16.1.4.1 Estrogens/Progesterone
Cholesterol gallstones are more common in
women than men, and this gender difference
begins during puberty and continues through the
childbearing years [5, 67]. Pregnancy is
associated with an increased percentage of colic
acid, increased cholesterol secretion, increased
bile acid pool size, decreased enterohepatic circulation, and decreased levels of chenodeoxycholic acid [68].
Progesterone
The progesterone-induced smooth muscle relaxation of the gallbladder reduces gallbladder emptying and promotes bile stasis [69, 70].
Progesterone also reduces bile acid secretion and
increases the risk of cholelithiasis and subse-
quent AC [71]. The US in pregnant women shows
a decrease in the gallbladder emptying rate and
increased fasting and residual gallbladder volumes after emptying in the second and third trimesters. Also, incomplete postprandial
gallbladder emptying is present in pregnant
women [63, 66, 72].
Estrogen
Estrogen increases the risk of forming cholesterol gallstones by promoting the hepatic secretion of biliary cholesterol that induces an increase
in cholesterol saturation of the bile [73–76]. Also,
high estrogen levels signicantly enhance the
activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting
enzyme in hepatic cholesterol biosynthesis even
under high dietary cholesterol loads [76, 77].
Furthermore, estrogen could augment the capacity of dietary cholesterol to induce cholesterol
supersaturation of the bile [77, 78], and high
doses of estrogen augment intestinal cholesterol
absorption [78]. During estrogen treatment, cholesterol is synthesized despite its excess availability from the high-cholesterol diet. Loss of
negative feedback regulation of cholesterol biosynthesis results in excess secretion of newly
synthesized cholesterol and supersaturation of
the bile that predisposes cholesterol precipitation
and gallstone formation [76]. Therefore, the most
common type of stone in pregnancy is yellow
cholesterol stones [5, 24]. Additionally, high
estrogen levels induce gallbladder hypomotility
[79] and sphincter of Oddi hypomotility [80].
Since plasma hormone concentrations increase
linearly during gestation, the highest risk of gallstone formation is in the third trimester of
pregnancy.
Also, estrogen could decrease plasma lowdensity lipoprotein (LDL) cholesterol and
increase plasma high-density lipoprotein (HDL)
cholesterol [81, 82]. The decrease in plasma LDL
results from increased hepatic LDL receptor
expression, which increases the clearance of
plasma LDL.Therefore, the increased uptake of
LDL by the liver may result in increased cholesterol secretion into the bile. These alterations
could induce an apparent increase in hepatic out-
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425
put of biliary cholesterol derived from circulating
lipoproteins such as HDL and LDL. However,
LDL cholesterol could have a more negligible
effect on biliary secretion. Figure16.1 illustrates
the potential lithogenic mechanisms of estrogen
through the ESR1 pathway in the liver. There is a
high gallstone/sludge dissolution rate in the rst
month after delivery [84, 85]. The rate of disap-
Estrogen
SREBP-2
The SREBP-2
Responsive Genes
Cholesterol
Biosynthesis
Cholesterol
(+)
(+)
ESR1
(+) (+)
pearance of gallstones and biliary sludge is
15–28% and 39–68%, respectively [37, 86]. After
delivery, the spontaneous disappearance of gallstones is signicantly more frequent in older
women [37]. Speculation is that small gallstones
are ejected from the gallbladder during the postpartum period when gallbladder contraction
restores. It starts as early as 2weeks after deliv-
HEPATOCYTE
Cholesterol 7a-Hydroxylase
Sterol 27-Hydroxylase
(+)
Bile Salt
synthesis
Bile Salts Phospholipid
Canalicular
Membrane
Fig. 16.1 Proposed model is underlying the potential
lithogenic mechanisms of estrogen through the estrogen
receptor 1 (ESR1) pathway in the liver. There is a possible
“estrogen-ESR1-SREBP-2” pathway promoting cholesterol biosynthesis and hepatic secretion of biliary cholesterol in the liver. The negative feedback regulation of
cholesterol biosynthesis (as shown in a dashed line) is
inhibited by ESR1 activated by estrogen, mainly through
stimulating the activity of sterol regulatory elementbinding protein-2 (SREBP-2) with the resulting activation
of the SREBP-2 responsive genes for the cholesterol biosynthetic pathway. Consequently, these alterations induce
ABCG5/G8 ABCB11 ABCB4
Biliary Hypersecretion
Supersaturation of Bile
Gallstones
BILE
GALLBLADDER
excess secretion of newly synthesized cholesterol and
supersaturation of the bile, predisposing cholesterol precipitation and gallstone formation. Moreover, the hepatic
ESR1 activated by estrogen could stimulate ATP-binding
cassette (ABC) transporters ABCG5 and ABCG8 on the
canalicular membrane of the hepatocyte and promote biliary cholesterol secretion. These lithogenic effects of
estrogen are inhibited by the antiestrogenic ICI 182 and
780. Also, the estrogen effects on increasing cholesterol
biosynthesis and promoting cholesterol gallstone formation are, in part, blocked by the deletion of the ESR1 gene.
(Reproduced with permission from [83])
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16 Biliary Tract Emergencies
ery [64] with an increased incidence of AP. In
contrast, most gallstones likely remain in the
gallbladder until dissolved by less lithogenic bile
in older women with reduced gallbladder contractility. Thus, AP associated with pregnancy
usually occurs in young postpartum women and
is usually due to gallstones [37].
16.1.4.2 Insulin
Apart from hormones, insulin resistance is also
responsible for gallstone formation. The exact
mechanisms are not clear. Cholesterol is the primary constituent of gallstones formed during
pregnancy. Cholesterol gallstone formation
requires several pathogenic factors, including
supersaturation of hepatic bile with cholesterol
and altered gallbladder motility.
Hyperinsulinemia and insulin resistance may
affect either of these factors. Hyperinsulinemia
increases cholesterol synthesis via the HMGCoA reductase [87] and increases the hepatic
uptake of LDL cholesterol [88]. Insulin resistance is also associated with lower serum HDL
cholesterol levels, a known risk factor for gallstones [89]. Administration of insulin in DM
increases biliary cholesterol saturation [90].
Biliary cholesterol saturation is higher in
patients with type II DM than in controls [91,
92]. Insulin inhibits basal and cholecystokinin-
stimulated gallbladder motility, and gallbladder
dysmotility is frequent with type II DM [93, 94].
In animal models, nonobese diabetic mice have
diminished gallbladder contractility and rapid
formation of cholesterol crystals [95], while gallbladder contractility correlates inversely with
glucose and insulin levels in obese animals [96].
Insulin resistance is associated with gallbladder
dysmotility in nonobese, nondiabetic humans
[97]. Therefore, even in the absence of obesity,
insulin resistance may lead to gallbladder sludge
and stone formation, either by causing gallbladder dysmotility or altering biliary lipid secretion.
Insulin resistance may be a surrogate for other
undened pathophysiologic mechanisms that
lead to gallstone formation rather than a direct
underlying cause [58].
Diabetics have an increased cholesterol saturation index in the bile compared with nondiabet-
ics [98]. Also, gallbladder fasting volumes are
larger, and gallbladder motility is diminished in
non-insulin-dependent diabetics compared with
nondiabetics [99, 100]. Hyperinsulinemia is
characteristic of noninsulin-dependent DM due
to insulin resistance, and there is an association
between hyperinsulinemia and an increased prevalence of gallbladder disease [51, 53, 54]. Both
hyperglycemia and euglycemic hyperinsulinemia
inhibit CCK-stimulated gallbladder motility [93].
Hyperinsulinemia may also be a key factor
because insulin regulates the Na+-K+ pump,
adversely affecting smooth muscle cells’ ionic
and osmotic homeostasis, including gallbladder
myocytes [101]. The Na+-K+ pump of presynaptic nerve terminals is also regulated by insulin
[101]. Moreover, decreased Na+-K+ pump activity can increase intracellular Na+, increasing the
Na+-Ca2+ exchange, thereby increasing intracellular calcium. Increased intracellular calcium
will alter both smooth muscle tone and the release
of neurotransmitters. Moreover, the gallbladder
myocytes from obese, diabetic mice are foreshortened and respond poorly to cholecystokinin
(CCK) [102].
ations in the density or sensitivity of acetylcholine or CCK receptors or prevent neurotransmitters
from accessing their receptors. To form advanced
glycation end products, sugars can react nonenzymatically with amino groups in proteins, lipids, and nucleic acids [103]. These products
cause covalent cross-linking of the collagen and
protein matrix [103]. The cross-linking of the
matrix may lead to stiffening of the gallbladder
wall itself, limiting its contraction, or may impair
CCK egress through blood vessel basement
membranes, preventing CCK interaction with
neural or myocyte receptors.
16.1.4.3 Diabetes Mellitus, Obesity,
A potential explanation for the differences in
gallbladder dynamics between obese and lean
individuals may be the differences in serum and,
perhaps, gallbladder wall lipids [104]. As a result,
the smooth muscle cell cholesterol/phospholipids
ratio increases, and membrane uidity decreases
Insulin resistance or DM may also affect alter-
andBariatric Surgery
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[104]. Therefore, these obese subjects with high
serum total and LDL cholesterols and triglycerides may also have high gallbladder lipids, which
may play a role in gallbladder function.
The rapid weight loss associated with the bariatric procedure further increases the risk of gallstone
formation due to impaired gastric emptying and
enhanced bile stasis [105, 106]. Pregnancy is associated with a fourfold increased risk of cholecystectomy among reproductive-aged women after
laparoscopic sleeve gastrectomy. Also, over onefourth of the women who conceived after laparoscopic sleeve gastrectomy subsequently underwent
cholecystectomy [61]. Lower gestational weight
gain was the only factor associated with cholecystectomy after laparoscopic sleeve gastrectomy
[61]. The prophylactic administration of ursodeoxycholic after surgery and strict postoperative surveillance is recommended in these patients.
16.1.4.4 Other
A 50% increase in the bile acid pool is associated
with a concomitant steroid-induced increase in
cholesterol secretion during pregnancy. Together
with replacing deoxycholic and chenodeoxycholic bile acids with cholic acid, increased volume
and decreased motility of the gallbladder enhance
the development of biliary stones [26].
16.1.5 Clinical Presentation
16.1.5.1 Medical History
As early as 1911, William Mayo stated that quiescent gallstones often become active during
pregnancy [2]. Symptoms of gallstone disease
during pregnancy are the same as in nonpregnant
patients [4, 107]. An episode of biliary pain usually begins with right upper quadrant or midepigastric pain, which may increase in severity.
Biliary colic begins quite suddenly and may
radiate to the interscapular area, the angle of the
right scapula, or the right shoulder. It may be
precipitated by a fatty meal or by consuming a
large meal following a fasting period. However,
biliary colic occurs in a diurnal pattern, with
pain peaking around midnight. Nausea and vomiting accompany episodes of colic in 50% of
patients. Finally, 70–80% of patients will have a
history of known gallbladder stones, colic
attacks, and fatty food intolerance [16].
Increasing severity of colicky pain, fever, or
chills (rigors) usually implies an underlying
complication, i.e., AC, AP, or cholangitis.
Common bile duct (CBD) stones should be suspected if persistent jaundice is present.
16.1.5.2 Physical Examination
During the physical examination, several signs
could be elicited:
• Direct abdominal tenderness in the upper
right quadrant. Due to somewhat distant locations of the enlarging uterus and gallbladder,
there is no signicant blunting of symptoms
and signs,
• Murphy’s sign (cessation of inspiration during
palpation of the inamed gallbladder) may be
elicited less frequently in pregnant patients
and indicates AC [108],
• Abdominal muscle rigidity is present with gall-
bladder perforation and biliary peritonitis, but
abdominal wall laxity in late pregnancy might
mask the classical signs of peritonitis [109],
• Fever and tachycardia are variably present
and not sensitive signs. The more advanced
the disease, the more pronounced these symptoms and signs are,
• Vomiting and dyspepsia are difcult to differ-
entiate from peptic ulcers. Itching is a sign of
either liver disease or biliary obstruction.
Only women with prepregnancy stones
experience biliary pain [37].
16.1.6 Dierential Diagnosis
Many diseases present with pain in the upper
right abdominal quadrant. However, most of
them could be excluded with good history taking
and clinical examination. The list of the most
common differential diagnoses is presented in
Table16.1.
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Table 16.1 Differential diagnosis of right upper quadrant pain in pregnancy
a
Jaundice
CBD stones Diaphragmatic myocardial
Hepatitis Acute appendicitis
Intrahepatic cholestasis Pancreatitis
Preeclampsia–
eclampsia
HELLP syndrome Pyelonephritis/nephrolithiasis
Acute fatty liver in
pregnancy
Hepatic malignancy Herpes zoster (shingles)
Cholangitis Perihepatitis (Fitz-Hugh–
Hepatic vascular
engorgement
Hepatic hematoma Pleural effusion
a
Jaundice in these conditions is not obligatory
No jaundice
infarction
Symptomatic/perforated
peptic ulcer
Radiculopathy
Curtis syndrome)
Rib fracture/costal margin
pain
Pneumonia
Colon cancer (hepatic exure)
16.1.6.1 Hyperemesis Gravidarum
Hyperemesis gravidarum is intractable nausea
and persistent vomiting associated with weight
loss greater than 5% of prepregnancy body
weight and ketonuria [110]. It occurs in 0.5–1.5%
of pregnancies [110] and is more common in nulliparous than in multiparous women prone to
cholelithiasis and cholecystitis [111].
Hyperemesis gravidarum leads to dehydration,
and hospitalization is usually required for IV
uid therapy [111]. This disorder presents early
in the rst trimester of pregnancy. As a rule,
symptoms resolve before the second part of pregnancy, regardless of therapy. Jaundice is uncommon and, if present, is not associated with
abdominal pain or fever.
Abnormal liver tests are common, but the
exact frequency is unknown. A frequency of 16%
has been found [112]. The most striking abnormality is the elevation of aminotransferases with
ALT levels exceeding AST levels, usually in nonalcoholic and noncirrhotic liver diseases [112].
ALT levels are variable, and hepatitis serologies
are helpful in the differential diagnosis, especially when ALT levels are above ten times the
normal upper limit or when it is the rst affected
pregnancy. The associated drug liver injury
should be checked, especially when jaundice is
present. A liver biopsy is not needed. Pregnancies
complicated by hyperemesis gravidarum have
been associated with transient hyperthyroidism,
which usually requires no specic therapy [111].
16.1.6.2 Perihepatitis (Fitz-Hugh–
Curtis Syndrome)
Perihepatitis results from early bacteremic or retroperitoneal lymphatic dissemination of
Chlamydia trachomatis or gonococcal pelvic
infection [113]. The syndrome is most frequently
seen in young women and is more common in the
second and third trimesters and puerperium.
Inammation in the right upper quadrant produces perihepatic adhesions. Classically, there is
a sudden onset of sharp right upper quadrant
pain, often pleuritic in quality. Nausea and hiccups are occasionally noted. Physical ndings
include tenderness under the right costal margin,
occasional hepatic friction rub, and fever. Pelvic
examination may be normal or may reveal signs
of cervicitis or pelvic inammatory disease.
Liver function tests and cholecystogram may be
transiently abnormal. A history of recent pelvic
infection suggests the diagnosis, but the syndrome can be a sequela of latent or asymptomatic
infection. The diagnosis is further supported by
the isolation of gonococcus on cervical culture
and the improvement after appropriate antibiotics
[113]. Other causes should be excluded because
this syndrome has no specic diagnostic marker.
16.1.6.3 Costal Margin Pain
In 1921, Alexander Tietze rst described a syndrome characterized by a painful afiction of the
costochondral cartilages (the area between the ribs
and costal cartilages) [114]. The cause of the pain
is recurrent, repetitive irritation of the intercostal
nerves, not synovitis of the interchondral cartilage.
These factors support the hypothesis that direct or
indirect trauma is the cause of the syndrome.
Costal margin pain and tenderness due to stretching of muscular attachments are not uncommon
during pregnancy. Upon physical examination, the
pain is produced when the rib margins are displaced upward and anteriorly; thus, the hooking
maneuver can be used to corroborate the diagnosis
(Fig.16.2). Carnett’s sign can be used for conr-
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Fig. 16.2 Schematic illustration of the hooking maneuver. The ngers are hooked beneath the costal margins,
displacing them upward and anteriorly
mation. The patient is asked to lift the head and
shoulders from the examination table to tense the
abdominal muscles. An alternative is to ask the
patient to raise both legs with straight knees. A
painful, positive test increases the likelihood that
the abdominal wall, not the abdominal cavity, is
the source of the pain. If a conduction block is
used for diagnostic purposes, another block may
be performed using long-lasting local anesthesia
with 0.5% bupivacaine. After delivery (ideally
breastfeeding), a combination of local anesthesia
0.5% bupivacaine and 40mg triamcinolone (FDA
class C) can be used. This has been found to relieve
the problem unless further trauma recreates the
pathology. Repeated local anesthesia steroid
blockade may be performed if residual pain persists or reoccurs.
16.1.7 Diagnosis
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16.1.7.1 Laboratory Findings
Clinically suspected biliary colic or AC should
be evaluated in the hospital. Only granulocytosis (left shift) indicates a bacterial infection.
C-reactive protein (CRP) is elevated, and bacterial infection is expected with values
>40mg/L. Serum bilirubin and transaminases
may be elevated, as in nonpregnant women.
Serum alkaline phosphatase is less helpful
because estrogen causes its elevation (levels
may double during normal pregnancy). Serum
amylase levels are elevated transiently in up to
33%. Finally, postprandial plasma levels of
total bile acids progressively increase during
pregnancy.
16.1.7.2 Transabdominal Ultrasound
Adequate transabdominal US visualization of
the gallbladder in pregnancy is 95–98% [47,
115, 116]. The remaining patients, whose
gallbladder could not be visualized initially,
are diagnosed with chronic cholecystitis with
contracted gallbladder and thickened gallbladder wall on the rescan [47]. Gallbladder
sludge (see Sect. 16.1.3.1) is visible as the
accumulation of bile. It is reported in up to
30% of gravid patients, with a similar proportion of women affected by the postpartum
period [24]. The US in early pregnancy confirms the physiological expansion of the gallbladder and the accumulation of stones,
debris, and bile. The US of the gallbladder in
healthy pregnant women shows a decrease in
the emptying rate and an increase in residual
volume after emptying. If gallstones are the
only pathologic finding, the state is defined as
biliary colic. US criteria for AC include the
following:
Pregnancy is comparatively seldom complicated
by jaundice. Notwithstanding the fact that in most
cases jaundice disappears without treatment, too
favorable a prognosis should not be ventured, for
the reason that now and again the condition may
represent the initial symptom of acute yellow atrophy of the liver.
(John Whitridge Williams, 1903)
• Gallbladder calculi,
• Wall thickening (>3mm),
• Pericholecystic uid,
• Sonographic Murphy’s sign (focal tenderness under the US transducer positioned over the gallbladder).
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16 Biliary Tract Emergencies
CBD obstruction should be ruled out because
it changes the therapeutic approach. It is suspected or conrmed by the following ndings:
• CBD >7mm in diameter,
• Dilation of intra- and extrahepatic ducts,
• Gallbladder calculi smaller than cystic
duct diameter.
Abdominal pain from suspected urolithiasis is
better evaluated with US.Although the diagnosis
of calculus is complicated by pregnancy-related
hydronephrosis, the addition of the color Doppler
US of the bladder to identify ureteral jets and the
transvaginal US to detect stones in the distal third
of the ureter helps in the evaluation [117].
16.1.7.3 Endoscopic Ultrasound
See Sect 16.2.5.5.
16.1.7.4 Magnetic Resonance
Cholangiopancreatography
Magnetic resonance cholangiopancreatography
(MRCP) helps differentiate CBD stones from
intrahepatic cholestasis of pregnancy (see Sect
16.2.4.1) because the clinical and biochemical
presentation of these two entities overlaps [118].
MRCP is indicated when dilation of intrahepatic
and extrahepatic ducts (Fig.16.3) is present on
the transabdominal US (see Sect. 16.2). It can
also differentiate between CBD stones and
external compression due to Mirizzi syndrome
(Fig. 16.4). Additionally, the pancreas is frequently obscured by overlying bowel gas on US
evaluation. MRCP better evaluates the pancreas
Fig. 16.3 CBD stones in the second trimester of pregnancy. Magnetic resonance cholangiopancreatography
shows distal common bile duct obstruction due to a calculus (arrowhead), gravid uterus (curved arrow), and physi-
ological right hydronephrosis and hydroureter (arrows).
(Reproduced with permission from [119])
ab
Fig. 16.4 Obstructive jaundice at 36weeks of gestation
with right upper quadrant pain. (a) Coronal T2-weighted
single-shot fast spin-echo image shows distended gallbladder with cholelithiasis (arrow) and intrahepatic biliary dilation (arrowheads). (b) Thin-slice MRCP shows that the
distal CBD is normal in caliber, and the inamed and distended gallbladder compressed the common hepatic duct.
Reconstruction of thin-slice MRCP demonstrates the distended gallbladder fundus compressing the proximal CBD
(arrow), causing intrahepatic biliary dilation, and a normal
caliber distal CBD (arrowheads), consistent with Mirizzi
syndrome. MRCP magnetic resonance cholangiopancreatography, CBD common bile duct. (Reproduced with permission from [120] under the CC Attribution License)
16.1 Acute Cholecystitis/Biliary Colic
https://t.me/medicina_free
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for edema, the pancreatic duct for obstruction in
biliary AP, and the peripancreatic tissues for
inammation.
16.1.8 Treatment
16.1.8.1 Historical Perspective
In 1890, Robert Barnwell Rhett, Jr. (Fig.16.5),
wrote of a cholecystotomy on a pregnant woman.
In 1893, Boorse mentioned a case of pregnancy
complicated by the expression of biliary calculi.
In 1893, Willien reported a cholecystotomy in the
third month of pregnancy. In 1895, Vineberg
reported two cases of AC in the puerperium and
found only four previously published cases. In
1895, Davis AB reported a case of cholecystectomy in the seventh month without interrupting
the pregnancy. Ploger, in 1910, gave a record of
42 cases; 22 had puerperal biliary colic, and in 19
of these, it was the rst attack. The remaining 20
attributed the beginning or increase in the sever-
Fig. 16.5 Robert Barnwell Rhett Jr. (Huntsville, 1853–
Charleston, 1901), President of the Medical Society of
South Carolina and Dean of the Charleston Medical
School, performed the rst cholecystotomy on a pregnant
patient in 1890. (Reproduced with permission from [121])
ity of their gallstone pains to some pregnancy
[122]. Peterson collected 25 cases complicating
pregnancy, including his case, and 10 complicating the puerperium. These are cases proved by
operation or by nding calculi in the stool [31].
Otherwise, he could have included 20 cases of
Huchard and 51 of Berline-Herwig. Since 1910,
Green reported 2 cases following a miscarriage
[123]; Branson, 4 cases [124]; Audebert, 1 case;
and Graham, 6 cases, a relatively meager list
when the frequency of gallstone operation is considered [125]. Schroeder said that 90% of operated women had borne children. Peterson found
that 75% had children. Grube proves that of 657
cases of gallstone, 613 cases had children. There
were 183 married and 33 unmarried or sterile
women [126]. Grube concisely states that pregnancy produces changes in the biliary system: (1)
stasis of the bile, (2) increase in cholesterin in the
bile, (3) protein decomposition, (4) cell desquamation, and (5) hyperemia of the mucosa of the
bile ducts [126]. He agrees with Hofbauer that
cholelithiasis is due to the above processes plus
bacterial infection and says that investigations of
the liver of women who have died during or just
before or after labor all of the conditions mentioned earlier are characteristic of pregnancy
[127]. M’Nee and Ashoff found that some forms
of stones originate in the aseptic and uninamed
bladder. M’Nee believed there is a denite relationship between gallstones and pregnancy, considering that the most common age of onset
corresponds to the period of childbearing and the
number of cases of gallstones in women who
have borne children [128]. He believed that the
pressure of the uterus causes stasis. He also found
that the cholesterme contents of the bile were
greatly increased in ve women who died during,
just before, or after labor. These ndings coincide
with those of Grube. Peterson says that in pregnancy, it is signicant that in nearly one-third of
the cases the period of onset is at that time of gestation when the uterus is approaching the level of
the umbilicus, sending the intestines upward, and
when the growing fetus is beginning to hamper
the eliminative powers of the liver. In the puerperium, in one-half of the cases, the attacks occurred
during the rst 7 days postpartum, suggesting
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