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mmHg
Supine
IAP (mmHg)
Semirecum bent
3.1 Physiology andPathophysiology
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47
knee-elbow positions, even −2 to −4 mmHg.
During pregnancy, IAP rises slightly though not
in proportion to the increase in the size of the
uterus, until the last month, when usually the
abdominal muscles are stretched beyond their
ability to respond, and there is usually a fall of
pressure below normal. The R.H. Paramore
obtained further evidence through rectal manometry in 1913 [10]. The data were extracted for the
standing, supine, left lateral, and knee-chest positions. The highest IAP mean value is in the standing position, and the lowest positive IAP mean
value is in the left lateral position. The knee-chest
position (inversion of the abdominal orientation)
Fig. 3.1 (a) Mean
intra-abdominal pressure
by position and
gestational age
transrectally.
(Reproduced with
permission from [17]
under the CC
BY-NC-ND 3.0), and
(b) 1h post-Cesarean
section intravesically
(signicantly lower in
supine position) [18]
35
30
25
20
15
10
5
0
–5
–10
produced a negative pressure mean value
(Fig.3.1). There is an issue with accurate measurement because the probes inserted in the lower
abdomen (rectum, bladder) could produce a
higher IAP in the lower than in the upper abdomen. Also, the IAP measured from the second
trimester onwards may not be an accurate marker
of actual IAP [19]. This is partly due to the
compression of the gravid uterus on the bladder,
falsely raising the IAP.
Recently, intravesical measurements in
healthy term parturients obtained under spinal
anesthesia before elective Cesarean section (CS)
found the median IAP in a leftward tilted position
Left lateral
Supine
Stand
Knee-chest
–22 wks26–30 wks31–36 wks37–40 wks
Not pregnant
[N = 26; not pregnant = 2, pregnant = 24; PP= postpartum]
35
30
25
20
15
10
5
0
9
–6 wks
PP2
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3 Increased Intra-abdominal Pressure
to be 22±2.9mmHg (range 15–29mmHg) [20].
These IAP values are actually in the threshold
range for ACS if organ failure were also present
[21]. However, the methodology could have created some bias, leading to overestimating IAP
values. The dermatome level of spinal anesthetic
was unknown, leading to possible underrelaxed
abdominal wall muscle, and 50 mL instead of
25mL was instilled in the bladder. After neonatal
delivery, the IAP dropped signicantly to a
median IAP of 16mmHg (range 11–24mmHg)
[20]. Another issue is the unspecied degree of
left lateral tilt during the IAP measurements,
making it difcult to reconcile if these measurements reected the actual IAP or the weight of
the gravid uterus on the bladder itself. There is
debate about the degree of tilt required to minimize compression of the IVC by the uterus [22,
23]. Under spinal anesthesia, there was signi-
cantly higher IAP in the supine position than the
left lateral tilt of 10°, with the reference point
held constant by placing the bladder pressure
transducer in a line adjacent to the patient on an
intravenous pole [19]. Compressing the bladder
by the gravid uterus falsely elevates the IAP values when fully supine. Also, there is a concern
regarding the positioning of ventilated patients
fully supine to measure IAP while increasing
aspiration risks [24–26]. Sensory block under
spinal anesthesia, at least at the level of T6, leads
to paralysis of abdominal muscles, altered wall
compliance, and changes in IAP.These ndings
may not be replicable in critically ill patients
without a spinal block.
Left lateral tilt has become the standard of
care in CS, particularly after spinal anesthesia, to both facilitate CS and alleviate
potential aortocaval compression while
supine [22]. A tilt of 15° is generally recommended [22].
Proposed normal IAP raises with pregnancy
progression. Obstetrics-specic IAP values for
diagnosing IAH and ACS are presented in
Table3.1. These values are based partly on nor-
Table 3.1 The IAP in healthy pregnancy [27]
Gestational age Mean IAP (mmHg)
<20weeks 5–7
20–26week 8–10
27–32week 11–12
>32weeks 13–14
Postpartum 8–10
IAP intra-abdominal pressure
mal abdominal compliance and the volume of the
fetus. IAH in pregnancy is a sustained or repeated
pathological elevation in IAP ≥14mmHg. ACS
in pregnancy is a sustained IAP >25mmHg associated with new organ failure/dysfunction.
Women with preeclampsia have a slightly higher
IAP than healthy pregnant women and may have
signs/symptoms of end-organ failure. Postpartum
patients with IAH may have the severity graded
using the same scale as nonpregnant adults
(Table3.2).
Guidelines group pregnancy and morbid obesity as chronically compensated states of IAH
[28]. Unlike pregnancy, chronic obesity is the
deposition of fat diffusely throughout the abdominal cavity and does not last a xed period. This
anatomical difference could be signicant, given
that the standard of measurement of IAP uses the
intravesical pressure as a surrogate, the location
of which rests in the pelvis.
3.1.4 Pathophysiology ofIAH/ACS
3.1.4.1 Physical Laws ofIAP
inPregnancy
The relationship between IAP and pregnancy is
dened by the equation DIAP = DIAV/Cab
(change in IAP=change in intra-abdominal volume/abdominal compliance) [29]. This equation
considers the magnitude or volume of the abdomen in the supine position, which is appropriate
for critically ill patients [29]. Abdominal compliance or elasticity is a volume change divided by a
change in pressure (L/mmHg) and describes tolerance to increases in intra-abdominal volume [29].
However, pregnant women are mobile, and IAP in
pregnancy varies with position [10, 18–20, 30].
Therefore, the equation is expanded to incorporate
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49
Table 3.2
Denition Diagnostic criteria
IAP is the steady-state pressure concealed within the
abdominal cavity
IAP is approximately 5–7mmHg in critically ill adults
IAH is a sustained or repeated pathological elevation in
IAP ≥12mmHg
ACS is a sustained IAP >20mmHg (with or without an
APP <60mmHg) that is associated with new organ
dysfunction/failure
APP=MAP– IAP
A polycompartment syndrome is a condition where
two or more anatomical compartments have elevated
compartmental pressures
Abdominal compliance is a measure of the ease of
abdominal expansion, which is determined by the
elasticity of the abdominal wall and diaphragm
The open abdomen requires a temporary abdominal
closure due to the skin and fascia not being closed after
laparotomy
Reproduced with permission from [28]
ACS abdominal compartment syndrome, APP abdominal perfusion pressure, IAH intra-abdominal hypertension, IAP
intra-abdominal pressure, MAP mean arterial pressure
Denitions and diagnostic criteria for IAP, IAH, and ACS
The reference standard for intermittent IAP
measurements is via the bladder with a maximal
instillation volume of 25mL of sterile saline
IAP should be expressed in mmHg and measured at
end-expiration in the supine position after ensuring that
abdominal muscle contractions are absent and with the
transducer zeroed at the level of the midaxillary line
Grade I, IAP 12–15mmHg
Grade II, IAP 16–20mmHg
Grade III, IAP 21–25mmHg
Grade IV, IAP >25mmHg
Primary IAH or ACS is a condition associated with
injury or disease in the abdominopelvic region that
frequently requires early surgical or interventional
radiological intervention
Secondary IAH or ACS refers to conditions that do not
originate from the abdominopelvic region
Recurrent IAH or ACS refers to the condition in which
IAH or ACS redevelops following previous surgical or
medical treatment of primary or secondary IAH or ACS
It should be expressed as the change in intra- abdominal
volume per change in IAP
the unique vector dynamics of the maternal abdomen, as vector force more accurately describes
both volume magnitude and force direction (consideration of weight due to gravity): VF=VM+D
(vector force = volume magnitude + direction)
[29, 31]. Hence, applied to pregnancy, the formula
is DIAP-P=DIAVF/Cab (change in IAP in pregnancy = change in abdominal vector force (volume+direction)/abdominal compliance).
The formula DIAP = DIAV/Cab assumes a
curvilinear relationship between abdominal volume and pressure dependent on abdominal wall
compliance [29]. Following the initial linear
slope, an exponential increase in pressure occurs
once the critical volume is attained. This formula
and curvilinear relationship reect the principle
of Laplace’s Law, which addresses the relation-
ship between radius (volume), pressure, and wall
tension [31]. The greater the radius (volume), the
greater wall tension is required to withstand
internal uid pressure. Based on these principles
and at constant atmospheric pressure, the formula
DIAP-P=DIAVF/Cab assumes a similar curvilinear relationship between abdominal vector
force and IAP-P, dependent on abdominal wall
compliance.
IAP in women during the latter stages of pregnancy increases into the range of IAH, perhaps
leading to a reduced “buffer” for the pressure to
increase before ACS for any underlying cause of
IAP.Mulier found a linear relationship between
IAP and volume to calculate the abdominal wall
elastance [32] and even decreased signicantly
with increased age and gravidity [33].
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3 Increased Intra-abdominal Pressure
The IAP in nonpregnant, healthy adults ranges
from 0 to 7mmHg and increases to 10–11mmHg
in critically ill, non-obstetric patients [34]. A sustained IAP increase of ≥12 mmHg represents
IAH (Table3.2); IAP >20mmHg associated with
new-onset organ dysfunction represents ACS
[28]. Abdominal perfusion pressure is estimated
by subtracting IAP from mean arterial pressure,
and values >55 to 60 mmHg suggest adequate
abdominal organ perfusion better than relying on
mean arterial pressure or IAP alone. However,
current recommendations do not support using
abdominal perfusion pressure to guide resuscitation and uid management for ACS [28].
3.1.4.2 Digestive System
Pathophysiology
IAH/ACS results in hemodynamic shifts, including decreased venous, arterial, and microcirculatory ow and increased systemic resistance
resulting in ischemia-reperfusion injury [29].
This compromised microcirculatory ow and
oxidative stress cause epithelial damage and
disruption of the mucosal integrity in the intestinal epithelium, leading to intestinal permeability
[35, 36]. Epithelial integrity is further compromised by losing intercellular tight junction integrity and loss of intestinal barrier function [37].
This leads to the translocation of LPS endotoxin
from Gram-negative bacteria to the mesenteric
lymph nodes, the portal vein, and the liver [35,
36]. The exposure of Kupffer cells to LPS endo-
toxin initiates a cytotoxic immune response.
Multiple proinammatory cytokines mediate the
endotoxic effects of LPS in the systemic circulation. This results in a systemic inammatory
response, oxidative stress, and subsequent multiorgan failure [38, 39]. The LPS response is mediated by the liver, while the placenta mediates the
immune response characteristic of preeclampsia.
In addition to intestinal ischemia-reperfusion
injury resulting in mucosal epithelial injury, the
loss of barrier function may be caused by two
environmental factors: abnormal exposure to
enteric and pathogenic bacteria and small intestine exposure to dietary gliadin [40, 41].
Therefore, intestinal permeability is caused by
(1) intestinal ischemia-reperfusion injury, (2)
exposure to enteric pathogenic bacteria, and (3)
dietary gliadin.
3.1.4.3 IAH/ACS andtheFetus
Despite the limited understanding of maternal
IAH, even less is known regarding its effects on
the fetus. IAH decreases uterine blood ow and
induces compensatory fetal hypertension [42],
such as during laparoscopy, even with inert gasses rather than CO2. In a gravid rabbit model,
intra-amniotic pressure (IAMNP) was linearly
related to IAP (IAMNP = IAP × 0.8 + 2.0).
Further, the elevation of IAMNP to 15.6cmH2O
via the elevation of the IAP (to 17cmH2O) altered
the contractile properties of the fetal bladder
[43]. One hypothesis regarding the fetal- placental
unit is that elevated IAMNP is translated to elevated fetal IAP, both inuenced by the elevations
of maternal IAP [44]. Through this mechanism,
elevated fetal IAP could result in increased urethral resistance, the chronicity of which could
lead to abnormal development of the bladder
detrusor muscles, resultant dysfunctional voiding
in children, and possibly urinary tract anomalies
[44].
In addition to increased IAP, pregnant rats
exposed to LPS had higher serum TNF-α levels.
TNF-α mediated inammation resulted in [45,
46]: (1) decient trophoblastic invasion and spi-
ral artery remodeling, (2) altered uteroplacental
hemodynamics and increased average spiral
artery resistance index, (3) placental nitrosative
stress, (4) increased maternal mean arterial pressure, (5) maternal renal structural alterations,
including mesangial hypercellularity, occlusion
of capillary loops; and (6) signicant maternal
elevation of protein:creatinine ratios and proteinuria, (7) fetal death in a dose-dependent manner
within 3–4h of LPS exposure, (8) fetal growth
restriction in the surviving fetuses, and (9) maternal coagulopathy in cases of fetal death.
3.2 Etiopathogenesis
IAH/ACS in pregnancy presumes a causal pathway, which may be intrinsically or environmentally triggered (Fig.3.2). This hypothesis includes
LPS Translocation to liver via
ab
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DIAP-P = DIAVF/C
Increased Abdominal Vector Force
Intra-Abdominal Volume Maternal
Normal gestational growth
Multiple gestation
Fetal macrosomia
Acute abnormal uterine distention
Obesity
Decreased Abdominal Compliance
Maternal anthropometrics
Progressive gestational age (third trimester)
Maximum abdominal expansion obtained
Primigravida
Habitation at high elevation, sudden drop in P
Sustained or Increasing IAP
(Absolute thresholds unknown)
Cardio-vascular Kidney
• Compression inferior vena cava
• Venous outflow obstruction
• Decreased venous return
• Decreased Cardiac output
• Compression of aorta
• Increased systemic resistance
• Maternal hypertension
• Impaired micro-circulatory flow
• lschemia reperfusion injury
ARDS = Acute respiratory distress syndrome; CD14 = cluster of differentiation14; COX-2 = cyclooxygenase 2; DIC - disseminated intravascular coagulopathy;
HELLP = hemolysis, elevated liver enzymes, low platelets; IAP - intra-abdominal pressure; ICAM-1 = intercellular adhesion molecule-1; iNOS = inducible nitric
oxide synthase; LMIC = Iow & middle income countries; LPS = lipopolysaccharide; PATM = atmospheric pressure; MCP-1 = monocyte chemotactic protein-1;
MD2 = myeloid differentiation co-receptor 2; MIP-1a = macrophage inflammatory protein-1a; NFkB - nuclear factor kappa-light-chain-enhancer of activated B
cells; PLA2 - phospholipase 2; ROS - roactive oxygon species; sEng - soluble endoglin; sFlt1 - solube fms-like tyrosine kinase-1; TLR4 - tolHike receptor 4;
TNF-a = tumor necrosis factor a; IL = interleukins; VCAM-1 = vascular cell adhesion molecule-1
*TNF-a = TNF-a plus other proinflammatory cytokines, chemokines and enzymes
IAP-P=lAVF/ C
[Change in intra-abdominal pressure in pregnancy = change in abdominal vector force (volume + direction)/abdominal compliance]
ab
position
Standing
Supine
ATM
• Compression renal vein
• Venous outflow obstruction
• Decreased renal perfusion
• Decreased glomerular filtration
• Glomerulosclerosis
• Increased renin, angiotensin,
aldosterone
• Proteinuria
• Oliguria, anuria
• Acute kidney injury
Increased Intestinal Permeability
(Zonulin Upregulation)
Intestinal ischemia reperfusion injury
Gut microbiome complex in pregnancy
Decreased peristaisis
Dysbiosis
Contaminated drinking water (LMIC)
Dietary gliadin
Placental *TNF-a Exposure
• <22 weeks-deficient
trophoblastc invasion, spiral
arterial remodeling
• Elevated sFlt1, sEng & other
antiangiogenic proteins
• Ischemia reperfusion injury
• Apoptosis, foam cells, fibrin
Hepatic-Splanchnic Multi-Organ Dysfunction
• Compression portal vein, increased
portal pressure, blood flow stasis, &
decreased intestinal mucosal perfusion
• Decreased splanchnic arterial flow
• Intestinal & hepatic ischemia
reperfusion injury
• Loss of intestinal barrier function,
intestinal permeability
• LPS translocation & Kupffer cell
activation (see above)
mesenteric lymph nodes and
*TNF-a
portal vein
Cytotoxic Immune Response
• LPS DNA Transcription
TLR4-MD2-CD14 pathway activation
NFkB (Kupffer cells)
• Pro-inflammatory Cytokines:TNF-a,
IL-6, IL-lb, IL-4, IL-5
• Chemokines: IL-8, MCP-1, MIP-1a,
• Enzymes: INOS, COX-2, PLA2, VCAM-1,
ICAM-1, E-selectin, eicosanoicds, ROS
• Systemic inflammatory response
• Apoptosis, foam cells, fibrin,
atherosclerotic plaque deposits
• DIC, HELLP, hepatocellular
necrosis, hepatic rupture
Poly-Compartment Syndrome
• Increased thoracic pressure &
ARDS
• Increased intra-cranial pressure
& seizures
*TNF-a
Fig. 3.2 Intra-abdominal hypertension in pregnancy etiology pathway. (Reproduced with permission from [17] under
the CC BY-NC-ND 3.0)
the relationship between independent and dependent variables, the temporal-spatial positioning
of etiological factors, and the role of genetic
factors.
Preeclampsia is part of a spectrum of hypertensive disorders of pregnancy, dened as the presence of arterial hypertension (blood pressure BP
≥140/90mmHg) on 2 occasions, at least 6h apart,
but without evidence of end-organ damage, of a
woman who was normotensive before 20weeks’
3.2.1 Nonoperative Conditions
gestation and proteinuria (>0.3g/24h). With preexisting essential hypertension, preeclampsia is
3.2.1.1 Preeclampsia
François Mauriceau (Fig.3.3) noted the preponderance of ‘toxemia’ of pregnancy in primiparas
in 1694 and described some preeclampsia clinical manifestations [48]. In the 1900s, Paramore
suggested uncompensated elevated IAP as a possible etiologic factor in the development of preeclampsia [10, 49]. He also hypothesized that
nulliparous and muscular women were prone to
spastic abdominal wall tone resulting in elevated
IAP, compromising perfusion pressure to the
abdominopelvic viscera [10, 49].
diagnosed if systolic BP has increased by
30 mmHg or if diastolic BP has increased by
15mmHg [50]. Patients with preeclampsia have
low colloid osmotic pressure with signicant third
spacing resulting in elevated IAP.When sustained
or increasing, IAP in pregnancy ≥12mmHg leads
to hemodynamic shifts, intestinal ischemia-reperfusion injury, translocation of LPS endotoxin to
the liver, systemic cytotoxic immune response,
multi-organ dysfunction, and poly-compartment
syndrome [17]. The pathophysiology of preeclampsia is shown in Fig.3.4.
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Clinical symptoms and organ failure that
can be seen in patients with preeclampsia
are similar to those of patients with IAH.
3 Increased Intra-abdominal Pressure
angiogenic toxins, causing widespread endothelial dysfunction [53] and generalized inammation. The worldwide incidence in pregnancy is
3–5% [50].
The endothelial dysfunction leads to increased
vascular permeability and possible hypoalbuminemia, which cause the third spacing of uids
resulting in signicant intra-abdominal uid collections. The uid extravasation causes relative
intravascular depletion, which may cause
decreased urine output. Immediate postpartum
IAPs are higher than those in the normal postoperative population [18] and more prominent in
pregnancies complicated with arterial hypertensive disorders of pregnancy/HELLP syndrome.
The combination of higher IAPs and abnormal
renal function may falsely lead the physician to
diagnose ACS.This may, in turn, lead to unnecessarily aggressive management options.
Therefore, preeclampsia should be ruled out
when IAP/IAH accompanies proteinuria after the
20th week of gestation.
Fig. 3.3 François Mauriceau (Paris 1637–Paris 1709)
received his training in obstetrics at the Hôtel- Dieu. He
was a leading obstetrician in seventeenth-century Europe.
In 1668, he published Traité des Maladies des Femmes
Grosses et Accouchées, a book that helped establish
obstetrics as a science. (Reproduced with permission from
[47] under CC PD-Art tag)
The antepartum (18.3cmH2O vs. 13.3cmH2O)
and postpartum IAP levels were signicantly
higher in preeclampsia than in healthy pregnant
patients [52]. Abdominal hypertension was identied in>80% of preeclamptic patients. Those
with severe preeclampsia with oliguria had the
highest IAP level [52].
These clinical manifestations have been well
described as early as the mid-1600s [48]. The
most common hypothesis is that abnormal placentation occurs during the myometrial trophoblastic invasion in the second trimester [50],
leading to placental ischemia and the release of
3.2.1.2 HELLP Syndrome
HELLP is considered a severe variant of preeclampsia and manifests as a syndrome of hemolysis, elevated liver enzymes, and low platelet
count [53]. Due to hormonal inuences during
pregnancy, the abdominal wall is slowly stretched,
increasing its compliance and reducing the potential for increased IAP caused by the expanding
uterus. Spontaneous rupture of a hepatic subcapsular hematoma (see Sect. 26.1) is a complication
of HELLP syndrome and results in intraabdominal hemorrhage. Continued intraperitoneal hemorrhage and uid resuscitation can lead
to IAH and ACS, along with hemorrhagic shock
[54].
3.2.1.3 Ovarian Hyperstimulation
Syndrome
Ovarian hyperstimulation syndrome (OHSS) is
an uncommon but increasingly common complication of ovulation induction for assisted reproduction [55, 56]. Other risk factors are presented
in Table3.3.
The mechanism is thought to be mediated by
vasoactive cytokines in response to exogenous
Progressively Increasing IAP
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Fig. 3.4 Presumed
pathophysiology of
preeclampsia/eclampsia
(purple—direct effects
on venous ow; blue—
increased pressures;
green—direct effects on
the fetus; orange—
clinical signs; yellow—
end effects of increased
IAP; red—lifethreatening systemic
outcomes). IAP
intra-abdominal
pressure, sFLT placental
soluble fms-like tyrosine
kinase 1, PlGF placental
growth factor, VEGF
vasoactive endothelial
growth factor, SIRS
septic inammatory
response syndrome,
ARDS adult respiratory
distress syndrome, IVC
inferior vena cava, JGA
juxta-glomerular
apparatus, ACE
angiotensin-converting
enzyme, ICP intracranial
pressure [51]
Uterine venous flow fetal growth
IVC compression
Diffuse splanchnic
compression
renal venous flow
portal venous flow
splenic venous flow
Placental fetal ischemia
sFLT, inflammation
vaso-constriction
PIGF, VEGF
Lower body edema
renal, portal, splenic
venous flow
plasma, blood volume
venous capacitance
Glomerulopathy, focal
glomerulosclerosis
JGA activation
RAAS
hepatopedal flow
Hypersplenism
hepatofugal flow
SIRS
Multi-system organ
failure / ARDS
Proteinuria
Hypertension
Thromboeytopenia,
hemolysis
Hepatic & splenic
ischemia/necrosis
transaminases
uric acid
53
Table. 3.3
of ovarian hyperstimulation syndrome
Young age (<35years)
Low body mass index—asthenic habitus
Polycystic ovarian syndrome
History of atopy or allergies
Previous episode of OHSS
Pregnancy
Higher or repeated doses of exogenous human
chorionic gonadotropin
Gonadotropin-releasing hormone—agonist protocol
Use of Clomiphene citrate
Increased number of developing follicles (>35)
≥14 oocytes retrieved
Elevated serum estradiol (>2500pg/mL)
Reproduced with permission from [57]
intrathoracic
pressure
Risk factors associated with the development
Upper body edema
Lung compression
jugular venous flow
SIRS / ARDS
PaO2, PaCO
ICP
2
Seizures
human chorionic gonadotropin administration
[58]. Vascular endothelial growth factor increases
vascular permeability by reducing the colloid
osmotic gradient favoring leakage to the extravascular space [55, 59]. This “third spacing”
leads to intravascular volume depletion, resulting
in hypotension. In its most severe form, massive
and rapid accumulation of abdominal ascites
results in an overt ACS [58]. Because hypotension leads to decreased venous pressure and
reduced venous return, a decreased cardiac output might be expected; however, studies have
found the cardiac output increased in OHSS
while mean arterial pressure and peripheral vas-
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3 Increased Intra-abdominal Pressure
cular resistance decreased [60]. These ndings
implied the accompanying arterial vasodilation
in OHSS [61]. Hypotension affects organ function. Reduced kidney perfusion leads to a reduced
glomerular ltration rate and can result in oliguria (Fig.3.5). Transvaginal oocyte retrieval can
inoculate infection to ascitic uid [62]. The compliance of the abdominal wall gradually increases
in patients with OHSS with larger ascites volumes needed to result in the same drop in IAP
[6]. The compliance can be calculated by the
change in intra-abdominal volume divided by the
change in IAP (see Sect. 3.1.4.1).
3.2.1.4 Obesity
Obesity causes chronically elevated IAP
(7–14mmHg) [6], and prepregnancy body mass
Fig. 3.5 Pathophysiology of ovarian
hyperstimulation
syndrome. (Reproduced
with permission from
[57])
index (BMI) signicantly correlates to elevated
post-CS IAP [18]. However, no evidence exists
that the effects of pregnancy and obesity on IAP
are additive [27].
3.2.1.5 Obstetric/Gynecologic
Conditions
A pathological increase in intra-abdominal volume is seen with multiple gestations, fetal macrosomia, polyhydramnios, fetal/placental hydrops,
and large hydatidiform moles [63, 64].
Like OHSS, rapid growth in abdominal girth,
dyspnea, abdominal pain, and other overt symptoms of ACS in other gynecological conditions
must also be considered in the differentials.
Patients undergoing ovulation induction are also
at increased risk of ovarian torsion and ectopic
Overian
Hyperstimulation
Capillary Leakage
“Third Spacing”
Tissue Edema Hypovolemia
Ascites
Hydrothorax
Compartment
Syndrome
Release of
Vasoactive factors
Decreased Organ
Perfusion
Liver/Renal
Impairment
Hemoconcentration
Hypercoagulability
Thromboembolic
Events
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pregnancy [56]. Meigs’ syndrome, solid ovarian
tumors associated with hydrothorax and ascites,
has been described similarly to OHSS in presenting with symptoms of ACS [65].
3.2.2 Operative Conditions
Normal postoperative pressures following
abdominal surgery range from 3 to 15mmHg in
the general population [66]. There is a lack of
information about IAP in an entirely female and
obstetric population.
3.2.2.1 Laparoscopic
Pneumoperitoneum
Laparoscopy during pregnancy potentially
exposes the fetus to risks from (1) trocar placement, (2) the effects of CO2 on the developing
fetus and the long-term effects of this exposure
with the signicant fetal loss, and (3) consequences of the increased intra-abdominal pressure on the fetus (See Chap. 4).
Several intraperitoneal access techniques for
delivering pneumoperitoneum exist. One is
using an open (Hasson) technique under direct
vision. Another is a Veress needle inserted
2–4cm above the uterus on the left or the RUQ
in the midclavicular line approximately 1–2cm
below the costal margin (Palmer’s point). Veress
needle can be inserted under the guidance of the
US.Some claim a higher risk of perforation of
intra- abdominal organs or pneumoamnion, especially in advanced pregnancy [67, 68]. An optical trocar (under direct vision) can be used for
entering the abdomen after pneumoperitoneum
created by the Veress needle, as in bariatric surgery. Optical trocars can be used even without
pneumoperitoneum.
The use of elective laparoscopy in the rst trimester of pregnancy is controversial [69] because
of the unknown effects of the CO2 pneumoperitoneum on the developing fetus [70, 71].
55
There is no increased risk for obstetric outcomes with elective laparoscopy [72, 73].
At the same time, the greater fetal loss in
emergency surgery is attributed to intraperitoneal inammation or bleeding without changes in obstetric outcomes between
the open and laparoscopic approaches [74].
As a general principle, when the fetal- maternal
unit is stressed, the mother is “conserved” at the
expense of the fetus. For example, during pregnancy, the normally decreased maternal PaCO2
may ensure adequate transplacental CO2 diffusion from the fetus to the mother for subsequent
pulmonary excretion. CO2 pneumoperitoneum
may cause maternal and subsequent fetal hypercarbia due to the mother’s decreased maternal
ventilation and increased transperitoneal CO2
absorption. Experiments on pregnant sheep with
CO2 pneumoperitoneum of 15mmHg showed a
drop in pH into the acidemic range both in the
mother and the fetus [70]. After 30min, a steady
state is reached. Hyperventilating the mother
brings the pH of both back to normal ranges.
There were no changes in PaO2. Fetal hemodynamic effects included increased mean heart rate
and a mean arterial pressure. After deation, pH,
heart rate, and BP turned to normal. Under the
same conditions, nitrous oxide as insufating gas
showed no effects on fetal blood-gas values, heart
rate, and BP.This indicates that fetal tachycardia
and hypertension are caused by hypercarbia, not
increased IAP.The conclusion was that the pneumoperitoneum is not a signicant risk to a healthy
fetus. It induces progressive, albeit reversible,
fetal hypercarbia, acidosis, and tachycardia when
pneumoperitoneum pressures exceed 15mmHg.
These effects were minimized using low pneumoperitoneum pressures or nitrous oxide as the
insufation gas [70]. The potentially deleterious
effects of short-term fetal hypercarbia are
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3 Increased Intra-abdominal Pressure
unknown. However, in high-risk mothers prone
to hypercarbia (e.g., chronic lung disease, massive obesity), precautions to decrease maternal
hypercarbia by using low-pressure pneumoperitoneum (≤12 mmHg) or nitrous oxide as the
insufation gas might be considered. Nitrous
oxide has been safely employed during gynecologic laparoscopy.
Others conrmed that an IAP ≤15mmHg has
no risks. The intrauterine pressure during uterine
contractions and coughing (representing intermittent and short periods) is higher [75–77].
Nitrous oxide requires the presence of either
hydrogen gas or methane (such as from colonic
origin) to be combustible during electrosurgical
procedures [70].
The introduction of gas into the peritoneum
(closed cavity) has two immediate effects: (1) an
increase in IAP and (2) gaseous exchange leading
to equilibrium with gases in the blood [78].
Increased IAP can decrease cardiac output by
several mechanisms, including direct alteration
of venous resistance in the inferior vena cava,
total peripheral resistance, and mean systemic
pressure [78]. Impaired venous return via compression of the inferior vena cava is of particular
concern in the second half of pregnancy since the
enlarged uterus can also limit venous return. The
uterine compression of the vena cava can be minimized by lateral tilt (see Sect. 3.1.3). The CO2
absorbed across the peritoneal surface rst equilibrates within the bloodstream with a longer
operative time with the skeletal muscle, viscera,
and nally, bone. Patients undergoing a prolonged laparoscopy are at risk of maintaining
hypercarbia and acidosis postoperatively until all
excess CO2 is eliminated from the tissue.
Hypercarbia and respiratory acidosis can be
monitored to some extent by capnography, which
measures end-tidal CO2 concentration in the
endotracheal tubes. If a rise in end-tidal CO2 is
detected, CO2 elimination via the alveoli can be
increased using controlled hyperventilation. The
limitation of capnography is that while it is sensitive, end-tidal CO2 is not foolproof in estimating
CO2 arterial pressure. When a ventilationperfusion mismatch is present, and the ventilation is greater relative to perfusion, gas from such
ventilation will contain less pCO2 than the actual
PaCO2, resulting in falsely normal or low endtidal CO2 readings [79]. A similar discrepancy
between end-tidal CO2 and PaCO2 and subsequent acidosis has been demonstrated in laparoscopy patients with compromised cardiopulmonary
status [80]. Monitoring arterial PaCO2 and pH is
preferable to limit the risk of hypercarbia and acidosis for such patients. The close monitoring of
CO2 is also important, considering the potential
direct effect of CO2 in increasing the mean arterial pressure and total peripheral resistance index,
leading to increased afterload and limiting cardiac output [81].
Limited studies of pneumoperitoneum in
pregnant sheep have demonstrated increased fetal
arterial BP, tachycardia, and respiratory acidosis,
only partially corrected with alteration in ventilator settings based on maternal capnography
results [70, 82]. Intraperitoneal CO2 pressures of
≤12 mmHg are recommended to prevent fetal
acidosis [83]. CO2 pneumoperitoneum created a
minimal impact on the patient and the fetus when
IAP ≤15mmHg is used [70, 84]. Some authors
use a pneumoperitoneum of 10 mmHg—low
enough to be in the safe range and high enough to
gain adequate visualization for a safe procedure
[85, 86].
Questions arise regarding the risk of decreased
uterine blood ow due to increased IAP from
insufation and the possibility of fetal CO2
absorption. CO2 used to create pneumoperitoneum could lead to fetal CO2 absorption with
potential subsequent fetal acidosis. This could be
minimized with IAP maintenance <12 mmHg
and minimizing operative time. Clinical and
experimental studies found no substantial adverse
effects on the fetus when the maximal pneumoperitoneum pressure was limited to 10–12mmHg,
and the operation was less than 60min [84, 87].
Sheep fetus has sufcient placental ow reserves
or compensatory responses to maintain adequate
gas exchange during a 1h, 20mmHg pneumoperitoneum [88]. Others stress the importance of
absorbing carbon monoxide through the peritoneum, produced using monopolar energy. The
absorbed carbon monoxide can produce carboxyhemoglobin and methemoglobin that compete
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