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16 Biliary Tract Emergencies
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Acute Pancreatitis
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Abstract
Acute pancreatitis (AP) is a rare entity in
pregnancy, mainly caused by hyperlipidemia
or gallbladder disorders. In many cases,
symptoms of cholelithiasis and biliary
sludge precede the presentation of
AP.Diagnosis is based on clinical presentation, laboratory investigations, and modern
imaging methods such as abdominal magnetic resonance imaging or magnetic resonance cholangiopancreatography. General
management of mild AP in pregnancy is
conservative and supportive, while severe
AP should be treated in the intensive care
unit. Endoscopic or surgical interventions
are common. Biliary AP can be resolved
with urgent ERCP sphincterotomy followed
by laparoscopic cholecystectomy, preferably
in the second trimester when technical conditions are optimal and risk for the fetus and
pregnant woman minimal. Laparoscopic
cholecystectomy can be postponed after
delivery when the third trimester ERCP is
done. Hyperlipidemic AP is treated with
lipid-lowering methods, sometimes even
with a therapeutic delivery. Immediate parathyroidectomy is indicated with primary
hyperparathyroidism-induced AP.One of the
most common types, biliary AP, is associated with better outcomes than non-biliary
causes.
17.1 Historical Perspective
Acute pancreatitis (AP) during pregnancy is
extremely rare. German gynecologist Wilhelm
Joseph Schmitt (1760–1827), working in Wien,
reported the rst case of pregnancy complicated
by hyperlipidemic AP in 1818 [1] in a 30-yearold woman who died in the fourth month of her
eighth pregnancy. William Lawrence (Fig.17.1)
in 1831 [2] described the second case also with
maternal mortality. It is difcult to conrm
whether the AP (macroscopic description without
a denitive microscopic diagnosis) started during
advanced pregnancy. The pregnant woman was
extremely thirsty during advanced pregnancy and
postpartum. The inammation, sepsis, or possible (gestational) diabetes mellitus (GDM) could
be the cause. Mondière suggested a possible
association between AP and pregnancy in 1836
[3]. Lawrence later collected a series of 53 cases.
German author, Marcus, collected 44 cases up to
1930 [4]. Longmade and Edmondson [5] added
nine personal cases. Sheehan, in 1940, rst recognized the association between acute fatty liver
© 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_17
465
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Fig. 17.1 Sir William Lawrence (Cirencester, July 16,
1783–London, July 5, 1867), son of a surgeon, helped the
founding of the Lancet journal, was elected to the Council
of the Royal College of Surgeons in 1828 and became its
President in 1846, and again in 1855. He also became a
Serjeant Surgeon (an ofcer of the Medical Household of
the Royal Household of the Sovereign of the United
Kingdom). (From Wikipedia)
17 Acute Pancreatitis
more common in East Asian countries, including
China, where AP in pregnancy accounts for
4.25% of all (unknown whether only women all
both sexes are included) AP [20] or 1/441 pregnancies [21].
Accurate assessment of disease incidence in
pregnancy is complex. During normal pregnancy,
patients expect some degree of abdominal pain.
Therefore, mild disease may be underreported.
Also, there is an issue with the denition of AP in
pregnancy. Some included 10 months before parturition, which ends up 10 months postpartum
[22], while the standard denition of the postpartum period is 6 weeks [4]. In addition, some
causes are attributed to biliary stones without
denitive conrmation. Biliary sludge and gallstones exist in 10% of people in Western countries. The incidence rises in pregnancy, and it is
questionable that gallbladder stones or sludge
caused AP in some patients without denitive
diagnostic elimination of all other causes. In
some studies, nearly 70% of cases are secondary
to biliary stones or sludge, followed by hyperlipidemia and alcohol abuse in approximately 20%
of cases, respectively [13, 23, 24]. Therefore, the
discrepancy in incidence is due to [25] the
following:
of pregnancy (AFLP) and AP.In 1952, four additional cases were reported in France [6]. In 1955,
Ross suggested a rise in intra-abdominal pressure, such as undue prolonged second stage of
labor, as a pathogenesis of AP in pregnancy [7].
The rst report of postpartum AP seems to be
by Haidlen in 1884 [8] and other early cases by
Watts [9] and Deaver [10]. Joske collected personal series of six patients with postpartum AP
presentations [11].
17.2 Incidence
Incidence varies more signicantly than in the
general population (England, Denmark, and the
United States: 4.8–24.2/100,000 [12]), ranging
from 1/1000 to 1/12,000 pregnancies, and rarely
progresses to the necrotizing form [13–19]. It is
• The rarity of the disease,
• The postpartum period up to 10 months,
• Different decades and countries,
• Underestimation due to underreporting,
• A small number of cases in studies,
• Multiple possible causes are not denitively
excluded.
17.2.1 Age, Trimester, andRace
More and more women become pregnant at a
more advanced age, and the incidence of AP in
the general population increases with age [26].
The mean age in the two largest studies up to
1973 was 24.2 and 27 years, respectively [5].
Until 1951, primipara suffered from AP more
often than multipara. The primipara is even more
prone to AP if she has gallstones [5]. Current
17.2 Incidence
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467
studies show that AP is more frequent in multiparas, 64–75% [13, 27, 28].
The Hispanic population has a higher incidence (0.1%) due to a higher risk for gallstone
disease [29]. Alcohol-induced AP is rare in countries, especially in the Middle East, where alcohol consumption is forbidden.
AP appears more prevalent in advanced gestation, most commonly in the third trimester [23, 24,
30, 31]. The trimester distribution depends on the
population studied and varies from 19 to 28% in
the rst, 21 to 33% in the second, 43 to 78% in the
third, and 2 to 38% in the puerperium [13, 25,
27–29, 32]. The proportion of severe AP (SAP)
also ts the rule that frequency increases with gestational age (1st, 2nd, and 3rd at 0%, 11.1%, and
88.9%, respectively) with a much larger span [32].
The trimester distribution is consistent with (1) a
potential lithogenic effect of estrogen during pregnancy [13, 25], (2) a physiological type of insulin
resistance in the second and third trimesters of
pregnancy [33], (3) a progressive physiologic
increase in both serum cholesterol and triglyceride
concentrations, with peak levels reached at term,
in response to elevated estrogen levels, (4) possible compression effect of the uterus on a biliary
tree, pancreatic vessels and pancreas itself, and (5)
signicant rise in intra- abdominal pressure due to
prolonged second stage of labor [7].
17.2.2 Biliary
During pregnancy, cholelithiasis is the most common cause of AP, accounting for up to 70% of
cases [13, 17, 34]. The biliary cause is also the
most common in puerperium [22]. Pregnancy
increases the incidence of biliary sludge and
stone, which can cause AP (see Sect. 16.1.3).
17.2.3 Hyperlipidemia/Dyslipidemia
Chylomicronemia occurs when plasma triglyceride levels exceed 1000mg/dL.The chylomicro-
nemia syndrome is dened when chylomicronemia
is accompanied by one or more of the following:
• Eruptive xanthoma (see Sect. 17.4): small yellowish papules, frequently with an erythematous base, appearing predominantly on the
buttocks and elbows caused by deposition of
large amounts of chylomicron triglycerides in
cutaneous histiocytes,
• Lipemia retinalis (see Sect. 17.4): the retina
has a salmon-colored, creamy appearance,
and the retinal vessels are white,
• Abdominal ndings: abdominal pain, acute
pancreatitis, or hepatosplenomegaly.
The association of hyperlipidemia with AP
during pregnancy was rst reported in 1818 and
was the rst published case of AP during pregnancy [1]. Until 1970, 101 reports were published, with 15 cases between 1956 and 1996
[35]. Previously, 1.7–6% of AP in pregnancy
were attributed to hyperlipidemia [36, 37].
Currently, AP secondary to hyperlipidemia/dyslipidemia has an estimated incidence of 1/25,000
births [38], or 10–56% of cases [31, 39, 40],
much higher than 1–7% in the nonpregnant population [41, 42].
Failure to investigate chylomicronemia as a
cause of AP leads to underestimating its incidence. First, some cases are declared idiopathic
due to a lack of lipid prole testing. This conrms the importance of triglyceride (TG) levels
pre-screening before initiating estrogen-related
medical treatment such as IVF [43]. Second,
determining the exact etiology of AP may be
complicated by the role of ethanol in precipitating severe hypertriglyceridemia. The same
problem with dening etiology is present in
hypothyroid patients or patients with
DM.Third, within 24–48h of the onset of AP,
in most patients, TG levels fall rapidly because
of fasting, when the supply of chylomicrons
from the intestinal absorption to the blood is cut
off. Also, the therapy with hypocaloric IV uids decreases the secretion of very-low-density
lipoproteins (VLDL) from the liver, further
reducing the TG pool and decreasing its levels
[44]. Therefore, if the lipid prole is not
checked during admission, it could be falsely
negative later. Additionally, the universal mild-
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17 Acute Pancreatitis
to-moderate hyperlipidemia secondary to AP
should not be confused with marked hypertriglyceridemia (HTG) that causes AP [45].
Whether the elevated TG is an epiphenomenon
of the AP or the actual cause of the inammation can be challenging to differentiate. The
serum may be lactescent in 4–20% of the general AP population, and lipid levels increase
above normal in up to 50% of patients with AP
of any cause [46–50]. HTG-induced AP is
equally distributed across trimesters [31].
Approximately one-third of the women developing HTG-induced AP during pregnancy were
nulliparous [13, 51].
17.2.4 Alcohol Abuse
Idiopathic AP in pregnancy is considered alcoholinduced in 12.3–16.5 [25, 52]. Alcohol-induced
AP could be even more prevalent (17.8% overall;
12.3% of 89 AP cases vs. ≤7% in other studies)
[23, 53, 54] due to the inclusion of chronic pancreatitis and the inclusion of Midwestern states
with a high prevalence of alcohol use [55]. Some
countries do not have alcohol-induced AP due to
cultural differences and prohibitions [27]. The
onset of alcohol-induced AP in the general population usually occurs in the fourth decade. The
average alcohol consumption in patients who
develop AP is 150g/day for 10–15 years before
the initial presentation. Alcohol-induced AP is
more commonly diagnosed during pregnancy
probably because pregnant patients seek medical
attention more commonly than female drinkers in
the general population. Again, one must be cautious with the accusation of alcohol use as a cause
due to its interrelation with hyperlipidemia.
17.2.4.1 Pancreatic Pseudocysts
Most pregnant patients with pancreatic pseudocysts are nulliparous (84%), and the majority
(61%) manifest in the third trimester. While some
claim that pancreatic pseudocysts are most frequently associated with alcohol-induced AP in
pregnant and nonpregnant patients, current data
show that hyperlipidemia is the most common
cause (Table 17.6). A signicant past medical
history of alcohol misuse, AP, or both was elucidated in 38% [56]. Although 69% had no identiable medical history, approximately a third had
an undiagnosed predisposing factor—either
familial hyperlipidemia or gallstones [56].
Non-gallstone AP in pregnancy is signicantly more prone to pseudocyst formation
[13, 25, 35, 57–60].
17.2.5 Primary Hyperparathyroidism
In the general population, PHPT is common,
with its greatest frequency in postmenopausal
women, up to 2–3% [61]. The incidence in
women of childbearing age (<40 years) is approximately 8/100,000 per year [62]. Approximately
0.5–1.4% of all PHPT occurs during pregnancy
[63–65]. The most frequent cause of PHPT in the
general population is a single parathyroid adenoma (85%), followed by parathyroid hyperplasia (15–20%) and, very rarely (less than 1%), by
carcinoma [66, 67]. Hunter and Turnbull
described the rst case of PHPT during pregnancy in 1931 [68]. More than 100 cases have
been reported in the English literature between
1931 and 1990 [62] and less than 200 until 2015
[69–74]. Parathyroid adenomas, as in the nonpregnant population, are the most common cause
of PHPT during pregnancy (81.2%) [75]. At least
three different causes may explain the relative
paucity of data: (1) The average age of the initial
manifestation of this disorder is higher than that
17.3 Etiopathogenesis
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of women of childbearing age [61, 66, 67]; (2)
about 80% of nonpregnant individuals with
PHPT are characterized by an asymptomatic
course of this disease [69]; and (3) some symptoms of PHPT may be misinterpreted as a simple
consequence of pregnancy or other gestationrelated disorders, while physiological changes
during gestation may mask some abnormalities
typical to PHPT [73, 76].
There is a 28-fold increased risk of AP in
PHPT patients compared to the general population [77]. Whereas some series have suggested an
association between PHPT and AP, communitybased studies showed no increase in the incidence
of AP among patients with PHPT compared with
matched controls [72, 78]. PHPT is a rare etiology of hypercalcemic-induced AP, causing 0.4–
2% of cases in the general population and
signicantly higher 7–13% during pregnancy
[27, 63, 69–72, 79]. Others found a wide range of
incidences of PHPT-induced AP in the general
population of 1–12% [72, 80–82].
The simultaneous occurrence of PHPT and
AP in pregnancy has only been reported 13 times
until 1998 [70, 83–91]. There were no cases during the rst trimester, and >90% had thyroid adenoma (89%) and only one thyroid carcinoma.
There is an increased incidence of cholelithiasis
in the general population with PHPT [92].
Therefore, the question is the real cause of AP
during pregnancy in some PHPT cases.
17.2.6 Preeclampsia/Eclampsia
Between 1956 and 2007, 15 cases of AP were
thought to be associated with preeclampsia [93].
17.2.7 Pancreatic Neoplasms
Pancreatic neoplasms, both benign and malignant, are uncommon during pregnancy. The most
common are cystic pancreatic lesions, with 13
published cases diagnosed during pregnancy
[94–98]. The rst report was in 1968 by Smithers
etal. [95]. In the general population, pancreatic
mucinous cystic neoplasms occur almost exclusively in females. Only 11 cases of pancreatic
adenocarcinoma [99] and 3 pancreatic neuroendocrine tumors were reported. Pancreatic cancer
manifested as AP in a single case [99] with pancreatic adenocarcinoma.
17.2.8 Acute Fatty Liver ofPregnancy
For the description of acute fatty liver of pregnancy (AFLP), see Sect. 16.2.4.2. Approximately
15% of AFLP patients develop postpartum AP
[100], which could be attributable to pancreatic
ischemia [100].
17.3 Etiopathogenesis
17.3.1 Introduction
Mnemonics for etiology of AP is “IT GET
SMASHED”: Idiopathic, Trauma, Gallstones,
Ethanol, Tumor, Steroids, Mumps, Autoimmune,
Scorpion venom, Hyperlipidemia, ERCP, Drugs.
A comprehensive list of causes in the general
population also applies to the pregnant population, with slightly different incidences
(Table17.1).
470
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17 Acute Pancreatitis
Table 17.1 Causes of acute pancreatitis
Alcohol or methanol abuse (>100g/day for >3 to 5
years)
Choledochal cyst
Cystic brosis
Gallstones
Hereditary (familial) pancreatitis (including a mutation
of the cationic trypsinogen gene)
Hyperlipidemia or hypertriglyceridemia (1000mg/dL)
Hypercalcemia/hyperparathyroidism
Infection (coxsackie B virus, cytomegalovirus, mumps)
Ischemia from hypotension or atheroembolism
Medications (ACE inhibitors, asparaginase,
azathioprine, oral estrogens, antibiotics, 2′,
3′-dideoxyinosine, furosemide, 6-mercaptopurine,
pentamidine, sulfa drugs, valproate, thiazide diuretic,
corticosteroids)
Neoplasm
Pancreatic or periampullary cancer
Pancreas divisum
Peptic ulcers
Preeclampsia/eclampsia
Post-ERCP
Postoperative inammation
Post-renal transplant
Sphincter of Oddi stenosis
Blunt or penetrating trauma
Surgery (ischemia/perfusion/mechanical)
Tropical pancreatitis
Vasculitis
Viral infections
Idiopathic
Elevation of intra-abdominal pressure leading
to high pancreatic ductal pressure [101] and
increased tonus of Oddi’s sphincter may be other
possible mechanisms to induce or promote AP of
any cause.
The trigger events or precipitating factors for
AP in 60% of pregnant women are associated
with an excess high-fat/high-protein diet. The
favored explanation may be that large amounts
of bile/trypsin release can overwhelm the
defense mechanism and activate other enzymes,
resulting in local and systemic complications
[102].
An additional factor in pregnancy is
GDM. Severe diabetic ketoacidosis and hyperglycemia with associated dehydration could trigger AP in pregnancy. DM is a part of a metabolic
syndrome (see Sect. 17.3.5). Idiopathic AP is
diagnosed in 10% of cases [24], with a declining
incidence as the knowledge of genetic causes,
exogenous etiologies, and more precise diagnostic imaging accumulate.
17.3.2 Biliary
During pregnancy, gallstones and biliary sludge
are accused as the most common causes of AP,
causing pancreatic duct/ampulla of Vater obstruction with pancreatic hyperstimulation that
increases pancreatic duct pressure, trypsin reux,
and activation of trypsin in the pancreatic acinar
cells. The enzyme activation within the pancreas
causes autodigestion, followed by local inammation (Fig. 3.2). Pregnancy does not primarily
predispose the pregnant woman to AP, but it does
increase the risk of cholelithiasis and biliary
sludge formation (see Chap. 16) [13]. Biliary AP
occurs several years later (28.2 years) than nonbiliary AP (24.4 years). In both groups, pregnant
women were usually multiparous, and AP was
mainly in the third trimester [24]. Global differences in the distribution of etiologies of AP exist
(see Sect. 17.2), with a tendency for higher incidence during pregnancy than postpartum (Fig.
17.2) [103].
A+B
neutrophilic elastase
o
PLA
complement
kinins
17.3 Etiopathogenesis
https://t.me/medicina_free
471
microlithiasis
high fat
high protein
alcoholic consumption
A,B
activation of macrophages
xygen free radicals
diet
inhibit
or neutrophils
A,B
inhibit
II
2
A,B
A=octreotide
B=herbal mixture
C=
Dan Shen
(Salvia Miltiorrhiza)
bile reflux
pancreatic duct
obstruction
CCK secretion
pancreatic secretion
Oddis sphincter spasm
inhibit
dislocation of bacteria & endotoxin
reactivation of macrophages & neutrophils
systemic inflammatory
response syndrome
(SIRS)
intrapancreatic
duct pressure
activation & release of
pancreatic enzymes
lyosomal enzyme
released to cytoplasm
pancreatic acinar damage
inhibit
A,B
release of activated
pancreatic enzymes
release of inflammatory
aytokines
IL-1, IL-6, IL-8, TNF-α
inflammatory mediators
PA F, LT s, PGs
pancreatic necrosis
& inflammation
intestinal barrier dysfunction
endotoximia
hypercytokinemia
NF-k β
second attack
multi-organ neutrophilic
infiltration
acinar damage
endothelial damage
of microvessels
ET
TXB
2
NO
microcirculatory impairment
increased vascular permeability
ischemia
improve
mitigate
block
B
B
B
improve
inhibit
mitigate
inhibit
B,C
A
C
B
Fig. 17.2 Schematic representation of step-by-step
pathogenesis of (biliary) acute pancreatitis with the possible action of medications. CCK cholecystokinin, NO
multi-organ dysfunction syndrome (MODS)
multi-organ failure (MOF)
nitric oxide, TXB2 thromboxane B2, TNF-α tumor necrosis factor α, PA F platelet-activating factor, PG
prostaglandin
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