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420
Fig. 36.4 Frequency of factors
associated with severe maternal
morbidity (SMM). PPH
postpartum hemorrhage, HTN
D / O hypertensive disorders, VTE
venous thromboembolism [
C. Oxford and M. La Rosa
Frequency of factors associated with SMM
0.60 %
0.60 %
1.20 %
8 ]
2.40 %
1.20 %
6.00 %
0.60 %
19.00 %
20.50 %
PPH
VTE
Table 36.2 MEOWS score [ 10 ]
3 2 1 0 1 2 3
Systolic BP <80 80–89 90–139 140–149 150–159 ≥160
Diastolic BP <90 90–99 100–109 ≥110
Respiratory rate <10 10.0–17 18–24 25–29 ≥30
Heart rate <60 60–110 111–149 ≥150
requirement Room air 24–39 % ≥40 %
O
2
Temperature <34 34–35 35.1–37.9 38–38.9 ≥39
Conscious level Alert Not alert
HTN D/O
Trauma
Acute Cardiopulm Infection Preexisting Medical
47.60 %
AFE/AFLPLatrogenicAcute Neuro
Predictors of Mortality at Admission
In nonpregnant patients, prediction models have been used to
determine the risk of death at admission to the ICU. Among
nonpregnant women, the Acute Physiology and Chronic
Health Evaluation (APACHE), the Simplifi ed Acute
Physiology Score (SAPS), and the Mortality Predictor Model
(MPM) have demonstrated reliable predictive values. None
of these perform well in the obstetric population. The main
reason for the poor performance in gravid and recently
postpartum patients is that they do not account for the normal
physiologic changes of pregnancy or include markers for
pregnancy-associated conditions such as HELLP syndrome
(hemolysis, elevated liver enzymes, and low platelet
syndrome) and often overestimate the risk of maternal
mortality [
Infl ammatory Response Syndrome and Modifi ed Early
Warning scores are 0.9–1.7 and 0.05, respectively, in
obstetric patients and cannot be used to reliably predict ICU
transfer, sepsis, or death in pregnant women.
For this reason, in the United Kingdom (UK), a Modifi ed
Early Obstetric Warning System (MEOWS) was created
9 ]. The positive predictive values of the Systemic
(Table 36.2 ). This tool was developed to better identify women
in risk of clinical deterioration. The area under the curve was
0.96 (95 % CI 0.94–0.96) for the clinical score [ 10 ].
With a universal SMM defi nition by the Joint
Commission and recent advancements in medical technology with machine-based learning, hospital systems can
develop reliable electronic track and trigger Obstetric Early
Warning Systems to respond to early signs of maternal clinical deterioration in an effort to reduce progression of
maternal morbidity to mortality and can be anticipated to
impact other outcomes like maternal length of stay and
readmission rates.
Physiologic Changes in Obstetrics and Clinical Implications
There are well-known physiologic changes during pregnancy
that can affect the management of a patient in the ICU.
Understanding these alterations during pregnancy is a very
important tool to improve maternal and fetal outcomes and
inform management of the critically ill mother.
36 Intensive Care in Obstetrics
421
Cardiovascular
During a normal pregnancy, there is a signifi cant increase of
the blood volume starting at 8 weeks of gestation. During the
fi rst two trimesters, the stroke volume and cardiac output
increase [
approximately 30–50 % in singletons and 50–70 % in
multiple- gestation pregnancies. There is a concomitant
decrease in the systemic vascular resistance (SVR, mediated
by progesterone) and pulmonary vascular resistance (PVR)
on the order of 20 % and 34 %, respectively. The increased
volume and cardiac output do not compensate for the dramatic decrease in SVR, and, as a result, blood pressure
decreases in pregnancy. The blood pressure starts to decrease
as early as 8 weeks, with its nadir in the midtrimester. The
diastolic blood pressure and the mean arterial pressure
(MAP) are the most affected during pregnancy. As blood
volume increases during the course of pregnancy, maternal
blood pressure approaches that of the woman’s prepregnancy
levels. An important concept to keep in mind is that blood
pressure during pregnancy should not be equal or higher than
prepregnancy [
of pregnancy are most often the explanation.
(CVP) and pulmonary artery occlusion pressure (PAOP)
despite the increase in volume, due to the marked
progesterone- mediated decrease in PVR. On the other hand,
there is a decrease in colloidal oncotic pressure, making pulmonary edema more common. Women with preeclampsia
are prone to the development of non-cardiogenic pulmonary
edema because of decreased colloid oncotic pressure and
increased capillary permeability with increased hydrostatic
pressure. Preeclamptic patients may experience very high
afterload at a rate and magnitude far exceeding their baseline
SVR that can lead to cardiogenic pulmonary edema as well
which can be diffi cult to distinguish from peripartum cardiomyopathy. Any peripartum patient with pulmonary edema
and preeclampsia should be evaluated with a transthoracic
echocardiogram to distinguish cardiogenic from noncardiogenic causes.
trophy occur, refl ected in the EKG as left ventricular hypertrophy (wall mass increases up to 50 %) and slight left axis
deviation. Encroachment of the gravid uterus on the diaphragm also physically shifts the heart in a more leftward
direction which also contributes to the left axis deviation
seen on EKG. A right axis deviation on EKG is not normal
in pregnancy and should be further investigated if noted. On
chest X-ray, an increased cardiac silhouette, straightening of
the border of the left side of the heart, and prominence of the
pulmonary conus are seen. All the chambers, in particular
the left atrium, increase in size, making arrhythmias more
common. Finally, there is a mild physiologic pulmonary and
tricuspid regurgitation due to overall cardiac enlargement
11 ]. The cardiac output in pregnancy increases
12 , 13 ]. When it does, hypertensive disorders
There is almost no change in the central venous pressure
During pregnancy, cardiac remodeling and cellular hyper-
from volume engorgement that occurs with the hypervolemic state of pregnancy [ 14 ].
Starting around 20 weeks of gestational age, the uterus is
large enough to cause compression of the aorta and inferior
vena cava (IVC) resulting in supine hypotensive syndrome.
This phenomenon can cause reduced venous return leading
to a 30 % decrease in cardiac output and drop in blood pressure when a gravid patient beyond 20 weeks (or less with
multiple gestations) lies directly fl at on her back. A lateral
tilt relieves aortocaval compression and rapidly improves
cardiac output [ 15 ].
Based on these particular effects during pregnancy, the
American Heart Association (AHA) recommends the following variants when performing the Advanced Critical Life
Support (ACLS) on gravidas with a 20-week or more sized
uterus [ 16 – 18 ]:
• Lateral uterine displacement
• Avoid medications through lower-extremity vascular
access as they may not circulate.
The amount of blood going to the uterus increases with
each trimester. In nonpregnant women, only 2 % of the cardiac output reaches the uterus. However, by the third trimester, 20 % of the cardiac output is shunted to the uteroplacental
circulation. This translates to ~500–700 cc per minute and
explains the massive amount of bleeding that can occur in a
very short period of time in postpartum hemorrhage. During
labor and immediately postpartum, ~300–500 cc of blood
are added to the maternal circulation from the uteroplacental
unit. This “autotransfusion” of labor and dramatic increases
in cardiac output put women with cardiac conditions (particularly valvular disease and pulmonary HTN or stenosis) at
risks for pump failure and arrhythmias, which warrant close
monitoring intrapartum and during the immediate postpartum period. Cardiac output (CO) increases throughout labor
from 17 to 34 % above the baseline nonlaboring state and is
attenuated in women with regional anesthesia. Obstetricians
take advantage of the hemodynamic attenuation afforded
with regional anesthesia in laboring women with known cardiac conditions to allow candidacy for vaginal delivery. The
cardiac output returns to normal around 12 weeks postpartum [ 19 , 20 ].
Heart rate increases slightly in pregnancy as a compensa-
tion for the low SVR, to maintain cardiac output, as early as
7 weeks and increases about 10–20 % above baseline by
term. Tachycardia above this level can be deleterious in
women with certain conditions. For example, in mitral stenosis, when the valve area falls below 1.5 cm 2 , fi lling of the left
ventricle during diastole is compromised and results in a
fi xed cardiac output. These women rely on diastolic fi lling
which is heart rate dependent. Maternal tachycardia can
severely limit LV fi lling in these patients, compromising the
ability to maintain a normal BP, and can result in cardiogenic
422
C. Oxford and M. La Rosa
pulmonary edema and shock as well as poor uteroplacental
blood fl ow leading to potentially harmful fetal effects.
During the second stage of labor, when delivery occurs, a
healthy mother can lose up to 30 % of her blood volume with
little or no change in hemodynamics or hematocrit. This is
due to the gestational hypervolemia that occurs in pregnancy.
The average blood loss during vaginal delivery is ~500 cc
and 1,000 cc with cesarean section. Women with hypertensive disorders of pregnancy, particularly severe preeclampsia, do not expand their blood volume as robustly as normal
gravidas and will show signs of shock earlier with less blood
loss. Postpartum, there is a mobilization of extracellular fl uid
accumulated in pregnancy to the intravascular space and an
expected diuresis that occurs on days 2–3 in vaginal deliveries and 4–5 with cesarean sections. Failure to have the normal postpartum diuresis may lead to high intravascular
volume and pressure resulting in cardiogenic pulmonary
edema.
Invasive Central Monitoring
Pulmonary artery (PA) catheterization is used less commonly
in the ICU as compared to the past and is being replaced by
less-invasive imaging methods (echocardiogram, IVC ultrasound, arterial pressure waveform monitors) to monitor
hemodynamics in critically ill patients. It should be emphasized however that a randomized control trial was performed
showing no survival benefi t in pregnant women with PA
catheter due to the poor correlation between the central
venous pressure and the pulmonary capillary wedge pressure
in pregnant women, in particular if patient has preeclampsia
[ 21 ]. That being said, there remain indications for PA cathe-
ter placement during pregnancy [ 22 ]:
• Hypovolemic shock unresponsive to initial volume resus-
citation attempts
• Septic shock with refractory hypotension or oliguria
• Severe preeclampsia with refractory oliguria or pulmo-
nary edema
• Ineffective intravenous antihypertensive therapy
• Acute respiratory distress syndrome (ARDS)
• Intraoperative or intrapartum cardiac failure
• Severe mitral or aortic valve stenosis
• New York Heart Association (NYHA) class III or IV
heart disease in labor
• Amniotic fl uid embolism
• Adult congenital heart disease
The logistics of invasive monitoring on labor and delivery
can be very challenging due to limited staff available to troubleshoot and interpret data, equipment for monitoring, and
locations where monitors may be available (can be logistically
impossible to labor a woman in the OR who needs central
monitoring in most hospitals with obstetric services).
Oftentimes as a result, women who may benefi t from invasive
monitoring who are in a location without this capability will
end up delivering via cesarean or having a vaginal delivery
without monitoring.
Pulmonary
There are structural and mechanical respiratory changes in
pregnancy. Regarding the structural changes, the nasopharynx becomes edematous with increased mucous secretion
resulting in reduced upper airway dimensions. These changes
make endotracheal intubation more challenging, and low
threshold for early intubation is highly recommended as one
can anticipate a diffi cult airway in pregnancy. Because of
anticipated oropharyngeal edema, the internal diameter of
the endotracheal tube used for intubation of a pregnant
patient should be 0.5–1.0 mm smaller than in nonpregnant
women [ 23 , 24 ].
There are also some changes in the structure of the thorax.
The subcostal angle increases from 68° to 103° (an ~50 %
increase), the transverse diameter of the thorax increases by
2 cm, and the circumference increases by 5 cm. There is also
decreased chest wall compliance.
The mechanical respiratory changes are described in
Table 36.3 . The most signifi cant changes are a decrease in
functional residual capacity (FRC) by 10–25 % in the
third trimester and can exceed the upper limit in obese
women. That in combination with an increase in oxygen
consumption results in overall decreased oxygen reserve
toward the end of pregnancy. The forced expiratory volume in the fi rst second (FEV1), ratio of FEV1 to forced
vital capacity, and peak fl ows remain unchanged during
pregnancy [ 23 ]. The Bohr curve in pregnancy is shifted to
the right, lowers the affi nity of hemoglobin for oxygen,
and results in increased oxygen delivery to the placenta
and maternal tissues.
Table 36.3 Lung volumes in pregnancy
Measurement
Changes during
pregnancy
Respiratory
rate
Unchanged Unchanged Increased
Vital
capacity
Inspiratory
capacity
5–10 %
Tidal
volume
Increases
30–40 %
Inspiratory
reserve
volume
Unchanged Decreased
Functional
residual
capacity
20 %
Expiratory
reserve
volume
Decreased
15–20 %
Residual
volume
Decreased
25 %
Total lung
capacity
Decreased
5 %
36 Intensive Care in Obstetrics
423
There is also a progesterone-mediated increase in
respiratory drive at the level of the medulla and a resultant
increase in tidal volume (VT) and minute ventilation. With
this, pregnancy is a state of chronic respiratory alkalosis with
compensatory metabolic acidosis. Hyperventilation and
decreased PCO 2 are directly related to increased VT not
respiratory rate (RR). The normal PCO
during pregnancy is
2
between 27 and 32 mmHg. If a pregnant woman later in gestation is found to have a PCO 2 consistent with non-gravid
patients, this is considered abnormal and represents CO 2
retention which should be further investigated. The bicarbonate level is normally 18–21 mEq/l to compensate for the
decrease in PCO 2 and does not represent a primary metabolic
acidosis. As a result of this partial compensation, the normal
pH during pregnancy is 7.4–7.45. The increase in MV and
lower PCO 2 are essential to maintain a maternal-fetal CO 2
gradient to allow for fetal CO
The fetal PCO
is approximately 10 mmHg higher than
2
off-loading.
2
maternal when uteroplacental perfusion is normal. It is
important to understand that the fetus develops in a CO 2 -rich
environment and needs the lower maternal CO 2 tension and
the resultant transplacental gradient enabling fetal CO 2 to be
readily diffused across the placenta into the maternal venous
circulation for gas exchange enabling fetal CO 2 to be readily
diffused across the placenta into the maternal venous circulation for gas exchange out of the maternal-fetal unit via the
maternal lungs. Pathologic pulmonary conditions that
increase maternal CO 2 levels will alter the transplacental gradient, allowing for fetal CO 2 retention as well. The fetal pH
is normally 0.1 units lower than maternal pH which is also
important when reviewing mechanical ventilation and
maternal- fetal acid-base interactions.
During a normal labor, especially in the second stage (full
cervical dilation and pushing), the mother tends to moderately hyperventilate in the process, and this drives her CO 2
levels down which increases the maternal-fetal CO 2 gradient
in favor of fetal CO 2 off-loading. That being said, excessive
ventilation can be deleterious. Forced maternal hyperventilation can contribute to fetal acidosis. This has been demonstrated in animal models by Motoyama et al. in 1965: when
the maternal PCO 2 falls to 15–20 mmHg or she becomes very
alkalotic with pH approaching 7.6, uteroplacental vascular
spasm occurs, decreasing circulation and increasing fetal acidosis as oxygen delivery to the fetus is compromised, and
fetal CO 2 is not circulated as well across the placenta [ 25 ].
When the fetus is unable to off-load its CO 2 , in the setting of
inadequate oxygenation, this compromises fetal aerobic (oxidative) metabolism of carbohydrate as an energy source and
converts to the anaerobic pathway where higher levels of lactate are produced above the fetal baseline, and the accumulation of lactic acid leads to metabolic acidosis. In this way,
which is a difference from adults is the fetus can transition
seamlessly from a respiratory to metabolic acidosis.
All of the above must be kept in mind when the question
of parameters for mechanical ventilation arises as permissive
hypercapnia with low-tidal volume ventilation has not been
well studied in obstetric patients. Mechanical ventilation is
almost the same in pregnant and nonpregnant patients with
some exceptions. In pregnancy, PaCO
should be adjusted
2
between 30 and 32 mmHg, maintaining the normal respiratory alkalosis and transplacental gradient. The risk of fetal
acidosis increases as the PCO
approaches 60 mmHg due to
2
uteroplacental vascular spasm, much in the same way as it
occurs with excessive maternal hyperventilation [ 26 ]. It is
important that anyone caring for a pregnant patient who
requires mechanical ventilation understands that extremes of
ventilation are avoided for the benefi t of the mother and
fetus.
Hematologic
In pregnancy, physiologic dilutional anemia is normal. There
is an important increase in the red blood cell mass (around
20 %) but a higher increase in plasma volume. Women gain
an additional 40–50 % of their pre-gravid blood volume, or
approximately 1,300 cc of plasma in a singleton pregnancy
[ 27 , 28 ]. Regarding the white blood cell (WBC) count, there
is a rise during each trimester. During the fi rst trimester, the
upper limit is 9,900/mm 2 , 12,200/mm 2 during the second and
third trimesters, and as high as 30,000/mm 2 during labor and
immediately postpartum [ 29 ]. The WBC changes make the
diagnosis of SIRS or sepsis more diffi cult.
The Sepsis in Obstetrics Score (SOS) shows correlation
with admission to ICU for sepsis, positive blood cultures,
and fetal tachycardia. The cutoff used for sepsis prediction is
≥6, with a sensitivity of 88.9 % and a specifi city of 99.2 %
[ 30 , 31 ]. See Table 36.4 for parameters and Table 36.5 for
scoring.
In pregnancy and the postpartum period, there is a prothrombotic state, which increases the risk of thromboembolic events around sixfold compared to baseline. This is
secondary to an increase of factors I, VII, VIII, IX, and
X. There is also a decrease of protein S (more than C) starting early in pregnancy [ 30 , 32 , 33 ].
Renal
There are a number of important physical and functional
changes of the gravid genitourinary system to keep in context when managing sick pregnant or peripartum patients.
Because of increased plasma volume and fl ow, the kidneys
increase approximately 1 cm in length. The collection system dilates (calyces, pelvis, and ureters), typically greater on
the right due to a slight dextrorotation of the uterus, and, as a
424
Table 36.4 Sepsis in obstetrics score (SOS) parameters [ 30 ]
Variable
Score 4 3 2 1 0 1 2 3 4
Temperature >40.9 39–40.9 38.5–38.9 36–38.4 34–35.9 32–33.9 30–31.9 <30
Systolic BP >90 70–90 <70
Heart rate >179 150–179 130–149 120–129 ≤119
Respiratory rate >49 35–49 25–34 12–24.0 10–11.0 6–9.0 ≤5
% ≥92 % 90–91 % <85 %
Sat O
2
WBC >39.9 25–39.9 17–24.9 5.7–16.9 3–5.6 1–2.9 <1
Immature neutrophils
%
Lactic acid ≥4 <4
High abnormal range Normal
≥10 % <10 %
Low abnormal range
C. Oxford and M. La Rosa
Table 36.5 Sepsis in obstetrics score (SOS) scoring [ 30 ]
Scoring
system Sensitivity Specifi city PPV NPV
SOS 88.90 % 99.20 % 16.70 % 99.70 %
REMS 77.80 % 93.30 % 11.10 % 99.70 %
MEOWS 100 % 77.60 % 4.60 % 100 %
result, imaging studies in the late second and third trimesters
will typically note mild-to-moderate hydronephrosis. This
fi nding can persist up to 4 months postpartum. Severe hydronephrosis is not a physiologic fi nding. Increased urinary stasis from progesterone relaxation of detrusor smooth muscle
and pelvic compression by the expanding uterus contribute
to a higher risk of urinary tract infection (UTI) in pregnant
patients. Symptomatic UTIs and asymptomatic bacteriuria
should be treated in pregnancy. Development of pyelonephritis risks preterm birth, maternal sepsis, and ARDS.
Functionally, there is an increase in the renal plasma fl ow
during pregnancy, which normalizes 12 weeks after the delivery. The creatinine clearance starts to increase as early as
6 weeks of gestation. There is a reduced upper limit of normal
maternal serum creatinine at 0.8 mg/dL due to the increase in
glomerular fi ltration rate (GFR). Blood urea nitrogen (BUN)
levels also decrease in pregnant women [ 34 – 36 ]. Although
pregnant mothers often report increased urinary frequency, the
actual daily urine volume is not signifi cantly altered from nonpregnant patients [ 37 ]. Urinary protein excretion at the 95th
percentile is approximately 260 mg over 24 h and adds validity to the presence of >300 mg of urinary protein a day (which
corresponds well to a urinary protein-to-creatinine ratio of
>0.3), as a criteria establishing the diagnosis of preeclampsia
[ 37 ]. In women with preexisting proteinuria, protein levels in
urine increase even in the absence of preeclampsia. Magnesium
sulfate, the drug of choice to reduce the risk of eclamptic seizure in women with preeclampsia, is almost completely
renally excreted, and the dose or rate administered must be
decreased in gravidas with evidence of renal insuffi ciency
(i.e., creatinine >1.3 mg/dL in pregnancy).
The water retention that occurs in pregnancy is hormonally mediated. Increased estrogen drives renin production
early in pregnancy which increases angiotensinogen
conversion to angiotensins I and II leading to increased
aldosterone levels. Despite the increase fi ltered sodium load
(due to the increase in GFR), increased aldosterone and
deoxycorticosterone in pregnancy create a larger increase in
tubular reabsorption of the fi ltered sodium resulting in a net
retention of ~1 g Na daily. The latter contributes to the gestational hypervolemia of pregnancy. Because greater water is
retained with sodium, there is an overall decrease in serum
sodium concentration in pregnancy down to an average of
136 mmol/l and slightly decreased plasma osmolality from
290 down to 280 mosmol/l.
Glycosuria is common in pregnancy, because there is a
decrease in distal tubular reabsorption of glucose. Spurious
increases in glycosuria are intermittent and do not correlate well
with blood glucose. Hence, glucose can be present in maternal
urine with a normal fi nger stick, and this is physiologic [ 37 ].
Gastrointestinal
There are few changes to the maternal gastrointestinal tract
that signifi cantly impact high-acuity care. The notion of prolonged gastric emptying time associated with increased aspiration rates in pregnancy has been challenged. Gallbladder
stasis does occur and can result in higher rates of stone formation. Otherwise, liver function tests are not signifi cantly
different with the exception of elevated alkaline phosphatase
from placental production and decreased albumin from
plasma dilution (by up to 30 %). Coagulation times and aminotransferase levels are not affected by normal pregnancy;
changes in these values represent pathology.
Pathology in Pregnancy
Cardiac
As previously stated, deaths from maternal cardiac disease
are increasing and now account for up to 50 % of all maternal
36 Intensive Care in Obstetrics
Table 36.6 Antihypertensive medications in pregnancy
Drug Dose Route Frequency Side effect Max dose
Hydralazine 5–10 mg IV/IM 15 min Nausea, emesis,
hypotension, palpitation
Labetalol 20 mg IV 10 min Nausea, emesis,
hypotension,
bronchospasm
Nifedipine 10–20 mg PO 30 min Hypotension, palpitation,
avoid with magnesium
sulfate
Nicardipine 5 mg/h PR Titrate every 5 min Peripheral edema,
tachycardia
Nitroprusside 600–1000 mcg PR/PO Titrate every 5 min Hypotension, increased
intracranial pressure,
rebound hypertension
20 mg IV/30 mg IM
300 mg
50 mg
10 mg/h
4 mcg/kg/min
425
deaths in the ICU. Currently, only approximately 4 % of
pregnancies are complicated by cardiac disease, but this
number is on the rise as the maternal population becomes
older and affected by other comorbidities associated with
cardiac risks. The strongest predictors of maternal complications as outlined by the CARPREG study, prospectively
designed to evaluate pregnancy outcomes in 617 pregnancies
complicated by maternal cardiac disease, are:
• A history of heart failure, transient ischemic attack, cerebrovascular accident (CVA), or arrhythmia
• Prepregnancy New York Heart Association functional
status >class II
• Left heart obstruction (mitral valve area <2 cm 2 , aortic
valve area <1.5 cm 2 , or peak left outfl ow gradient
>30 mmHg)
• Ejection fraction <40 %
In this population, the most commonly encountered com-
plications were pulmonary edema and arrhythmias [ 38 ].
Women with known cardiac disease are also known to be at
risk for heart failure with intolerance of gestational hypervolemia. Patients with known pulmonary hypertension or a
history of peripartum cardiomyopathy without systolic
recovery are advised against pregnancy as maternal death is
prohibitively high in these women. If necessary, supportive
medications can and should be used in pregnancy. Milrinone
is a safe inotrope to use in gravid patients. Sildenafi l or
tadalafi l can also be used in women with symptomatic pulmonary hypertension. ACE inhibitors are contraindicated in
pregnancy but enalapril has been regarded as safe for breastfeeding by the American Academy of Pediatrics in mothers
who delivered term infants.
Preeclampsia-Eclampsia
Preeclampsia is a condition that occurs only in pregnancy. It
is defi ned as elevated blood pressure (SBP > 140 or DBP > 90)
and proteinuria after 20 weeks of gestation. When preeclamptic patients are admitted to the ICU, it is typically for severe
cases with associated refractory hypertension, neurologic
dysfunction (eclamptic seizure, stroke), renal failure, liver
failure, pulmonary edema, HELLP syndrome (hemolysis,
elevated liver enzymes, low platelets), and disseminated
intravascular coagulation [
39 ]. Women with preeclampsia
have a loss of intravascular oncotic pressure. As a result, they
have a total body water overload but with intravascular depletion and tend to have hyperdynamic cardiac function. These
women may have altered renin and aldosterone activity in
pregnancy and may not expand their total blood volume as
robustly as women without preeclampsia. This altered volume state limits the ability of these women to tolerate hemorrhage. Because of low oncotic pressure, leaky capillaries, and
higher hydrostatic pressure, these patients are also predisposed to non-cardiogenic pulmonary edema [ 40 , 41 ].
The fi rst goal in management of preeclampsia with severe
features is to stabilize the mother. Severely elevated blood
pressure in pregnancy (SBP >160 mmHg or/and DBP
>110 mmHg) is associated with stroke and other obstetric
complications such as placental abruption. It is recommended that severe range blood pressure is treated within
15 min of noting the elevation using intravenous antihypertensive agents (Table 36.6 ). Treatment goals and urgency are
also informed by the patient’s baseline state. If the patient
had systolic BPs in the 180s mmHg range consistently prior
to pregnancy, an SBP of 160s mmHg is relatively normal for
her, and dropping her BP rapidly to a normotensive range
can risk decreasing placental perfusion as it is directly correlated with maternal MAP.
Another key point in the management of preeclampsia
with severe features is the prevention of eclamptic seizures.
The Magpie trial showed a signifi cant decrease of seizures in
this population when given magnesium sulfate (therapeutic
range of 4.8–8.4 mg/dL). Again, caution should be used in
patients with impaired renal function, although there is little
risk with commonly prescribed repletion doses for
hypomagnesemia. The signs and symptoms of magnesium
426
Table 36.7 Pharmacologic agents used for uterine atony
Agent Dose Route Frequency Side effect Contraindication
Oxytocin (Pitocin) 10–80 units IV/IM Continuous Nausea, emesis, water
intoxication
Methylergonovine
(Methergine)
15-methyl prostaglandin F2
(Hemabate)
Prostaglandin E2
(dinoprostone)
Misoprostol 600–1,000 mcg PR/PO One dose Tachycardia, fever None
0.2 mg IM/IU 2–4 h Nausea, emesis,
hypertension
0.25 mg IM/IU 15–90 min Nausea, emesis,
diarrhea, fl ushing
20 mg PR 2 h Nausea, emesis,
diarrhea, fever
C. Oxford and M. La Rosa
None
Hypertension,
preeclampsia
Asthma
Hypotension
toxicity are dose dependent with loss of deep tendon refl exes
at serum levels of 8.5–12 mg/dL, respiratory paralysis at
12–16 mg/dL, abnormal cardiac conduction >18 mg/dL, and
cardiac arrest when levels are >30 mg/dL. The half-life of
magnesium sulfate is 4 h in women with normal renal function. Treatment for magnesium toxicity consists of discontinuing the infusion, supportive measures, and administering
on one-gram intravenous of calcium gluconate every
5–10 min as necessary [ 42 – 48 ]. Calcium chloride is appro-
priate to use for patients with impaired hepatic function as
calcium gluconate requires hepatic degluconation for biologic activity, whereas calcium chloride provides immediately available calcium.
Pulmonary edema occurs in 2–3 % of patients with preeclampsia and, as stated above, can be non-cardiogenic.
Treatment includes supportive measures, diuresis, and afterload reduction. Pulmonary edema is considered a sign of
end-organ damage and is an indication for delivery. Patients
with preeclampsia can have oliguric acute kidney injury, and
some reported improved outcomes with the use of a PAC to
guide fl uid management in preeclamptic patients who have
oliguric acute kidney injury unresponsive to volume resuscitation [ 39 ].
Hemorrhage
Causes of hemorrhage in pregnancy are abruption, placenta
previa or accreta, uterine rupture, uterine inversion, and
postpartum hemorrhage. Postpartum hemorrhage is defi ned
as more than 500 ml after a vaginal delivery or more than
1,000 ml after a cesarean section. Hemorrhage is still the
leading cause of maternal death worldwide. In the United
States, there has been a signifi cant decrease in the rates of
maternal death associated with hemorrhage [ 43 , 44 ].
As described above, there is an expansion of blood volume in pregnancy. Because of this, the hypovolemia clinical
signs are almost always delayed. Signs such as tachycardia
and mild hypotension are seen after losing 1,200–1,500 ml
of blood (20–25 % of total volume) [ 43 – 46 ]. Management of
hemorrhage is centered around control of the bleeding source
and volume support. Massive obstetric hemorrhage is managed with blood products based on requirements, and most
hospitals with obstetric services now have hemorrhage protocols to address the rapid bleeding that can occur. Recall
that the uterus consumes 20 % of the cardiac output at term
and can translate to a 500–700 cc per minute blood loss in
obstetric hemorrhage. When hemorrhage is massive and has
not responded to 2 l of crystalloids, the repletion should be
performed in a ratio of 1:1:1 of packed red blood cells, fresh
frozen plasma (FFP), and platelets [ 47 ]. There are medical
and surgical approaches to stop the bleeding. The medications used in the peripartum are oxytocin, misoprostol,
15-methyl prostaglandin, and methylergonovine [ 46 – 48 ].
The doses and contraindications are described in Table 36.7 .
If bleeding has not improved with uterotonic medications,
uterine tamponade devices such as the Bakri balloon ®, Foley
balloons, or packing often stop bleeding. Intraoperatively,
one can place O’Leary stitches to ligate the uterine arteries
for bleeding control and/or use a B-Lynch suture to externally
tamponade the uterus or perform hypogastric artery ligation
with care to avoid the ureters. If the patient is bleeding consistently but slowly and is stable enough to transfer to an interventional radiology suite, then bilateral uterine artery
embolization would be a recommended option. The rate of
success is more than 90 %. One advantage of angioembolization is the potential to use absorbable gelatin sponge
(Gelfoam). This product reabsorbs after 2 weeks, making
future fertility more likely [ 44 , 48 ]. When medical manage-
ment and other surgical or alternative measures fail, hysterectomy may need to be performed [ 49 , 50 ].
Amniotic Fluid Embolism
Amniotic fl uid embolism or anaphylactoid syndrome of
pregnancy is a rare but catastrophic event. The incidence is
around 1 in every 40,000 deliveries, and the mortality is as
high as 60 %. The pathophysiology, although not completely
understood, appears to be secondary to a cascade of abnormal activation of pro-infl ammatory mediator systems similar
to that of the systemic infl ammatory response syndrome, in
36 Intensive Care in Obstetrics
427
association of fetal antigens in maternal circulation during
the delivery process or within 30 min after. The signs and
symptoms associated with this are hypotension, dyspnea,
cyanosis, disseminated intravascular coagulopathy, loss of
consciousness, cardiac arrest (typically PEA arrest), and
seizure-like activity. There are no specifi c treatments or cure
for this entity, and management is supportive. There are case
reports of the use of tranexamic acid in the management of
AFE but more evidence is needed before standards aside
from supportive measures can be endorsed. With an appropriate level of care, the mortality in the United States has
decreased from 60 % to almost 20 % for the cases [
51 ].
Trauma Management
Care of the maternal trauma case is interdisciplinary and
requires high-level communication and coordination of all
service lines responding to the emergency. The ideal team
would have the involvement of emergency department faculty, obstetric or maternal-fetal medicine, neonatology,
obstetric anesthesia, trauma surgery, and the respective nursing support. Understanding the nuances of evaluating these
patients is highly important to maintaining situational awareness and a good outcome. The primary and secondary surveys
should be performed keeping the following caveats in mind:
Primary Survey
• Airway: gravid patients can be expected to have oropharyngeal edema, making securing an airway potentially
diffi cult, and consideration of early intubation in these
patients with an ETT that is 1 mm smaller in internal
diameter is advised. A laryngeal mask airway (LMA) can
be used safely to provide a means to ventilate a patient
who is unable to be intubated; however it is not considered a protected airway.
• Breathing: In the late second to early third trimester, the
uterus displaces the diaphragm upward. If the patient has
a suspected pneumothorax and is visibly pregnant, the
chest tube should be placed higher than in nonpregnant
patients in the third or fourth intercostal space.
• Circulation: leftward uterine displacement with a one- or
two-handed technique is paramount to maintain or augment maternal cardiac output. Avoid lower-extremity
lines in the gravida who is visibly pregnant as iliac compression could compromise circulation of resuscitative
medications. Two large-bore IVs should be placed, and
she should be typed and cross-matched for blood products
early in preparation for any bleeding injuries; placental
abruptions do not always present classically and bleeding
can be concealed. Signs of hemorrhagic shock present
late in pregnant patients, and one should be prepared to
replace blood volume with products. Vasopressors should
be used for those in shock getting volume resuscitation at
the doses for nonpregnant patients. If cardioversion or
defi brillation is required, the voltages used are not different in pregnancy and will not harm the fetus.
• Disability: always consider the postictal state from
eclampsia as a cause for altered mental status or decreased
alertness.
• Exposure: always assess for entry and exit wounds, if
trauma is due to a fi rearm and an exit wound is not present, the bullet could be lodged in the fetus inside the
uterus.
Secondary Survey
It is implicit that the mother is stabilized fi rst before evaluation of the fetus occurs in maternal trauma. The fetus is part
of the secondary survey. Once the primary survey is complete
with said considerations in mind, then a second comprehensive
physical exam is performed where the fetal heart tones can
be checked by Doppler or ultrasound. If the mother is stable
and the pregnancy is viable (23 weeks in some institutions),
then fetal monitoring may be indicated and should be guided
by the obstetric service. Ultrasound is also performed once
the mother is stable to establish placental location, amniotic
fl uid volume, fetal viability, presentation, gestational age,
and estimated fetal weight. A bedside- expanded maternal
focused assessment with sonography for trauma (FAST)
ultrasound can be reliably performed to quickly assess for
evidence of hemoperitoneum, pericardial effusion, and
pneumo- or hemothorax. Lab testing and other imaging (i.e.,
CT or X-rays for orthopedic injuries) occur in the secondary
survey. In hospitals with quick turnover, a high KleihauerBetke result for fetal cells (with HbF) in the maternal circulation is of concern for maternal-fetal hemorrhage, and the
obstetric team should be alerted as the result could inform
delivery timing. Fetal monitoring in the viable pregnancy
may show late decelerations (occur following a contraction)
and can indicate a placental abruption has occurred or is in
process. The obstetric team should be involved as early as
possible in these cases to guide maternal care management
and decisions on fetal expectant management versus delivery. The obstetric team will help guide counseling on possible pregnancy termination in previable cases [ 52 ].
Perimortem Cesarean Section
A perimortem cesarean section is indicated for maternal cardiac arrest and unsuccessful cardiopulmonary resuscitation.
The cesarean section should be started at 4 min of cardiac
428
C. Oxford and M. La Rosa
arrest with the goal to deliver the fetus delivered by 5 min
after maternal arrest for optimal fetal outcomes [
53 ]. If the
pregnancy is beyond 25 weeks gestation, there is a 45 % fetal
and 72 % chance of maternal outcomes historically [
54 – 56 ].
The uterine evacuation can also improve the venous
return. The technique to use is a Pfannenstiel incision with a
low-transverse uterine incision if the lower uterine segment
is well developed or a classical-vertical uterine incision for
preterm or malpresentation [
44 , 49 ].
Summary
Care of the gravid or recently postpartum patient can be challenging if one does not know what to expect in this population. With a better understanding of the common high-acuity
events in pregnancy and the impact of their physiologic alterations, the reader will be better equipped to manage these
patients collaboratively with the obstetric service for the best
outcomes.
References
1. Zwart JJ, Dupuis JR, Richters A, et al. Obstetric intensive care unit
admission: a 2-year nationwide population-based cohort study.
Intensive Care Med. 2010;36:256.
2. Pollock W, Rose L, Dennis CL. Pregnant and postpartum admis-
sions to the intensive care unit: a systematic review. Intensive Care
Med. 2010;36:1465.
3. Zeeman G. Obstetric critical care: a blueprint for improved out-
comes. Crit Care Med. 2006;34(9 suppl):S208.
4. Hoyert DL. Maternal mortality and related concepts. National
Center for Health Statistics. Vital Health Stat. 2007;3(33):4.
5. Creanga, et al. Pregnancy-related mortality in the United States.
Obstet Gynecol. 2015;125:5.
6. Callaghan WM. Overview of maternal mortality in the United
States. Semin Perinatol. 2012;36:2.
7. Souza JP, et al. The WHO maternal near-miss approach and the
Maternal Severity Index Model (MSI): tools for assessing the management of severe maternal morbidity. PLoS One. 2012;7(8):e44129.
10.1371/journal.pone.0044129 .
doi:
8. Crobman, et al. Frequency of and factors associated with severe
maternal morbidity. Obstet Gynecol. 2014;123(4):804–10.
9. Lemeshow S, Teres D, Klar J, et al. Mortality Probability Models
(MPM II) based on an international cohort of intensive care unit
patients. JAMA. 1993;270:2478–86.
10. Carle, et al. Design and internal validation of an obstetric early
warning score. Anaesthesia. 2013;68:354–67.
11. Clapp J, Capeless E. Cardiovascular function before, during and
after the fi rst and subsequent pregnancies. Am J Cardiol. 1997;
80:1469.
12. Clark S, Cotton D, Lee W, et al. Central hemodynamic assessment
of normal term pregnancy. Am J Obstet Gynecol. 1989;161:1439.
13. Granger J. Maternal and fetal adaptations during pregnancy and
integrative physiology. Am J Physiol Regul Integr Comp Physiol.
2002;283:R1289.
14. Bhagwat A, Engel P. Heart disease and pregnancy. Cardiol Clin.
1995;13:163.
15. Thornburg KL, Jacobson SL, Giraud GD, Morton MJ. Hemodynamic
changes in pregnancy. Semin Perinatol. 2000;24(1):11–4.
16. Goodwin AP, Pearce AJ. The human wedge: a manoeuvre to relieve
aortocaval compression during resuscitation in late pregnancy.
Anaesthesia. 1992;47:433.
17. Jones SJ, Kinsella SM, Donald FA. Comparison of measured and
estimated angles of table tilt at Caesarean section. Br J Anaesth.
2003;90:86–7.
18. Kundra P, Khanna S, Habeebullah S, Ravishankar M. Manual displacement of the uterus during Caesarean section. Anaesthesia.
2007;62:460–5.
19. Robson S, Dunlop W, Boys R, et al. Cardiac output during labour.
BMJ. 1987;295:1169.
20. Kerr M. Cardiovascular dynamics in pregnancy and labour. Br Med
Bull. 1968;24:19.
21. Polanczyk C, Rohde L, Goldman L, Cook E, Thomas E,
Marcantonio E, et al. Right heart catheterization and cardiac complications in patients undergoing noncardiac surgery: an observational study. JAMA. 2001;286:309–14.
22. Invasive hemodynamic monitoring in obstetrics and gynecology.
ACOG Technical Bulletin Number 175–December 1992. Int
J Gynaecol Obstet. 1993; 42:199–205.
23. Crapo R. Normal cardiopulmonary physiology during pregnancy.
Clin Obstet Gynecol. 1996;39:3.
24. Schatz M, Zieger R. Diagnosis and management of rhinitis during
pregnancy. Allergy Proc. 1988;9:545.
25. Motoyama E, Rivard G, Acheson F, Cook C. Adverse effect of
maternal hyperventilation on the fetus. Lancet. 1966;1:286–8.
26. The PIOPED Investigators. Value of the ventilation/perfusion scan
in acute pulmonary embolism: results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). JAMA. 1990;
263:2753.
27. Pritchard J. Changes in blood volume during pregnancy and delivery. Anesthesiology. 1965;26:393.
28. Lo F, Kaufman S. Effect of 5α-pregnan-3α-ol-20-one on nitric
oxide biosynthesis and plasma volume in rats. Am J Physiol Regul
Integr Comput Physiol. 2000.
29. Pitkin R, Witte D. Platelet and leukocyte counts in pregnancy.
JAMA. 1979;242:2696.
30. Barton JR, Sibai BM. Severe sepsis and septic shock in pregnancy.
Obstet Gynecol. 2012;120:689.
31. Albright CM, Ali TN, Lopes V, et al. The sepsis in obstetrics score:
a model to identify risk of morbidity from sepsis in pregnancy. Am
J Obstet Gynecol. 2014;211:39.
32. Lockitch G. Clinical biochemistry of pregnancy. Crit Rev Clin Lab
Sci. 1997;34:67.
33. Present P, Comstock GW. Tuberculin sensitivity in pregnancy. Am
Rev Respir Dis. 1975;112:413.
34. Lindheimer M, Davison J, Katz A. The kidney and hypertension in
pregnancy: twenty exciting years. Semin Nephrol. 2001;21:173.
35. Dunlop W. Serial changes in renal haemodynamics during normal
pregnancy. Br J Obstet Gynaecol. 1981;88:1.
36. Ezimokhai M, Davison J, Philips P, et al. Non-postural serial
changes in renal function during the third trimester of normal
human pregnancy. Br J Obstet Gynaecol. 1981;88:465.
37. Yeomans E, Gilstrap L. Physiologic changes in pregnancy and
their impact on critical care. Crit Care Med. 2005;33(10
Suppl):S256–8.
38. Sorensen and on behalf of the Cardiac Disease in Pregnancy
(CARPREG) Investigators, Gordon P, Spears JC, Tam JW,
Amankwah KS, Smallhorn JF, Farine D, Morton S, Kells CM,
Bergin ML, Kiess MC, Marcotte F, Taylor DA, Siu ESC, Sermer M,
Colman JM, Alvarez AN, Mercier L-A, Brian C. Prospective multicenter study of pregnancy outcomes in women with heart disease.
Circulation. 2001;104:515–21.
36 Intensive Care in Obstetrics
429
39. American College of Obstetricians and Gynecologists; Task Force
on Hypertension in Pregnancy. Hypertension in pregnancy. Report
of the American College of Obstetricians and Gynecologists’ Task
Force on Hypertension in Pregnancy. Obstet Gynecol.
2013;122(5):1122–31.
40. LaMarca BD, Gilbert J, Ganger JP. Recent progress toward the
understanding of the pathophysiology of hypertension during preeclampsia. Hypertension. 2008.
41. Zhou CC, Zhang Y, Irani RA. Angiotensin receptor agonistic autoantibodies induce pre-eclampsia in pregnant mice. Nat Med.
2008;14:855–62.
42. LaMarca BD, Ryan MJ, Gilbert JS, Murphy SR, Granger JP.
Infl ammatory cytokines in the pathophysiology of hypertension
during preeclampsia. Curr Hypertens Rep. 2007;9(6):480–5.
43. Pritchard JA, Baldwin RM, Dickey JC, et al. Blood volume changes
in pregnancy and the puerperium. II. Red blood cell loss and
changes in apparent blood volume during and following vaginal
delivery, cesarean section, and cesarean section plus total hysterectomy. Am J Obstet Gynecol. 1962;84:1271.
44. Dildy GA. Postpartum hemorrhage: new management options. Clin
Obstet Gynecol. 2002;45:330.
45. Elbourne DR, Prendiville WJ, Carroli G, et al. Prophylactic use of
oxytocin in the third stage of labour. Cochrane Database Syst Rev.
2001.
46. Prata N, Gerdts C. Measurement of postpartum blood loss. BMJ.
2010;340:c555.
47. Novello A, King JC. Health advisory: prevention of maternal deaths
through improved management of hemorrhage.
www.acog.org/
acog_districts/dist_notice.cfm?recno=1&bulletin=1517
2 May 2006.
48. Bakri YN, Amri A, Abdul Jabber F. Tamponade-balloon for obstetrical bleeding. Int J Gynecol Obstet. 2001;74:139.
49. B-Lynch C, Coker A, Lawal AH, et al. The B-Lynch surgical technique for control of massive postpartum haemorrhage: an alternative to hysterectomy? Five cases reported. Br J Obstet Gynaecol.
1997;104:275.
50. Cho JH, Jun HS, Lee CN. Hemostatic suturing technique for uterine bleeding during cesarean delivery. Obstet Gynecol. 2000;
96:129.
51. Clark SL. Amniotic fl uid embolism. Clin Obstet Gynecol.
2010;53:322.
52. Oxford C, Ludmir J. Trauma in pregnancy. Clin Obstet Gynecol.
2009;52(4):611–29.
53. Mäkikallio K, McElhinney DB, Levine JC, et al. Fetal aortic valve
stenosis and the evolution of hypoplastic left heart syndrome:
patient selection for fetal intervention. Circulation. 2006;113(11):
1401–5.
54. Mattox KL, Goetzl L. Trauma in pregnancy. Crit Care Med. 2005;
33:385–9.
55. Dijkman A, Huisman CM, Smit M, et al. Cardiac arrest in pregnancy: increasing use of perimortem caesarean section due to emergency skills training? BJOG. 2010;117:282.
56. Vanden Hoek TL, Morrison LJ, Shuster M, et al. Part 12: cardiac
arrest in special situations: 2010 American Heart Association
Guidelines for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. Circulation. 2010;122:S829.
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