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placenta, so its use should be avoided unless it is considered
absolutely essential.
22
e role of myocardial biopsy in PPCM remains unclear.
Histological classication for the diagnosis of PPCM is
currently lacking. Previous studies have reported evidence
of myocarditis, progressive death of cardiac myocytes, and
destruction of the cytoskeleton in myocardial biopsies of
patients with PPCM. Additionally, cardiac catheterization
is rarely indicated in PPCM. Le cardiac catheterization is
only indicated when coronary artery disease is suspected as
a possible etiology for the cardiomyopathy. e information commonly obtained with right heart catheterization
(i.e., cardiac pressures) can be obtained via less invasive
methods including ECG and cardiacMRI.
B- type natriuretic peptide (BNP) and N- terminal proBNP (NT- proBNP) increase nearly twofold in pregnant
women compared with nonpregnant women as early as
the rst trimester and does not signicantly uctuate during pregnancy.10 Patients with PPCM frequently have BNP
or NT- proBNP values that are up to ve times higher than
those in normal pregnant women.9 One study found a BNP
< 100 pg/ mL had a negative predictive value of 100% for
identifying cardiac events during pregnancy in women with
heart disease.23 Serum markers for inammation and oxidative stress may provide further support for the diagnosis of
PPCM. Although CRP and high sensitivity CRP (hs- CRP)
are usually normal or mildly increased in pregnancy, they
have been reported to be signicantly elevated in patients
with PPCM.10 Interferon- γ decreases during normal preg-
nancy but increases with PPCM.8 A marker for oxidative
stress, oxLDL increases incrementally during normal pregnancy but is signicantly elevated in women withPPCM.
MEDICAL MANAGEMENT OFPERIPARTUM
CARDIOMYOPATHY
Management of PPCM follows current heart failure guidelines, with careful consideration of the implications of specic therapies during pregnancy and lactation (Table 46.1).
Treatment of heart failure in the peripartum period focuses
on maintenance of adequate oxygenation, optimization of
ventricular function, and avoidance of thrombotic complications. Severe cases of PPCM may require mechanical
circulatory support including intra- aortic balloon counterpulsation pump (IABP), extracorporeal membrane oxygenation (ECMO), implantation of a le ventricular assist
device (LVAD), or even heart transplantation. erapies
TABLE46.1 PREGNANCY AND LACTATION RISK ASSOCIATED
WITHMEDICATIONS COMMONLY USED INTHE TREATMENT
OFHEART FAILURE
Medication
FDA Pregnancy
AAP Lactation Rating
Category*
Diuretics
Furosemide
Hydrochlorothiazide
Spironolactone
ACE Inhibitors
Lisinopril
Captopril
Enalapril
Angiotensin Receptor
Blockers
Losartan
Valsartan
Peripheral Vasodilators
Hydralazine
Nitroglycerin
Nitroprusside
Beta- blockers
Metoprolol
Bisoprolol
Carvedilol
Inotrope
Dobutamine
Dopamine
Milrinone
Epinephrine
8
Norepinephrine
Anticoagulation
Unfractionated heparin
Enoxaparin
Warfarin
FDA=US Food and Drug Administration
AAP=American Academy of Pediatrics
Category B:Animal reproduction studies have failed to demonstrate a risk to the fetus, and
there are no adequate and well- controlled studies in pregnantwomen.
Category C:Animal reproduction studies have shown an adverse effect on the fetus, and
there are no adequate and well- controlled studies in humans, but potential benets may
warrant use of the drug in pregnant women despite potentialrisks.
Category D:There is positive evidence of human fetal risk based on adverse reaction data
from investigational or marketing experience or studies in humans, but potential benets
may warrant use of the drug in pregnant women despite potentialrisks.
Category X:Studies in animals or humans have demonstrated fetal abnormalities and/
or there is positive evidence of human fetal risk based on adverse reaction data from
investigational or marketing experience, and the risks involved in use of the drug in pregnant
women clearly outweigh potential benets.
C
B
C
D
D
D
D
D
C
C
C
C
C
C
B
C
C
C
C
C
B
X
Unknown Risk
UnknownRisk
Breast- Feeding
Compatible
Unknown Risk
Breast- Feeding
Compatible
Breast- Feeding
Compatible
Unknown Risk
Unknown Risk
Breast- Feeding
Compatible
UnknownRisk
Unknown Risk
Breast- Feeding
Compatible
UnknownRisk
Unknown Risk
Unknown Risk
UnknownRisk
UnknownRisk
UnknownRisk
Unknown Risk
Unknown Risk
UnknownRisk
Breast- feeding
Compatible
326 SECTION B. CARDIAC CRISES
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327
directed at the underlying cause of PPCM have been
explored, but universal acceptance of a specic “targeted
therapy” for PPCM is lacking.
outcomes in dilated cardiomyopathies and may be protective against tachyarrhythmias.25 Beta1- selective blockers
(metoprolol and bisoprolol) are preferred over nonselective
beta blockers (propranolol). Beta2- receptor blockade may
OXYGENATION
facilitate contractions by inhibiting uterine smooth muscle
relaxation. Beta1 blockers are generally considered safe dur-
ing pregnancy (risk category C).10 ere are some reports
Patients presenting with severe heart failure may require
the administration of supplemental oxygen, with a goal of
maintaining oxygen saturation (SpO2) > 95%. Adequate
oxygenation may necessitate use of noninvasive ventilation
(CPAP/ BiPAP) or intubation with mechanical ventilation.
suggesting that antepartum Beta blocker use is associated
with intrauterine growth restriction and preterm birth.14
Newborns born to mothers receiving beta blockade should
be closely monitor for transient bradycardia, hypoglycemia,
and respiratory depression.
Positive end- expiratory pressure (PEEP) is instrumental in
preventing alveolar collapse, increasing lung compliance,
and counteracting hydrostatic uid ow into the alveoli.
VASODILATORS
Vasodilators improve LV function by reducing aerload,
PHARMACOLOGIC THERAPY
Proper treatment of PPCM can range from that similar to
patients with systolic heart failure in the general population
all the way to acute, invasive therapies for PPCM that presents or worsens acutely around delivery.
decreasing preload, and optimizing intracardiac lling pres-
sures. Hydralazine is considered safe during pregnancy and
is the primary vasodilator used in the antepartum period.
Intravenous nitroglycerin may be necessary in the setting
of high cardiac lling pressures with decompensated heart
failure. Uteroplacental blood ow is not autoregulated—
precipitous decreases in blood pressure may compromise
placental perfusion.
DIURETICS
Diuretics are commonly administered to optimize ventricular function by reducing preload. Intravenous administration should be considered in the setting of orid volume
overload leading to pulmonary congestion and/ or peripheral edema. Furosemide is preferred over thiazide diuretics in the peripartum period.10 Diuretic- induced volume
depletion can lead to decreased uterine perfusion and oligohydramnios. Fetal amniotic uid volume should be monitored in parturients receiving diuretics.
NEUROHORMONAL BLOCKADE
24
Impeding the renin- angiotensin system with angiotensinconverting enzyme inhibitors (ACE- Is) and angiotensin II
receptor blockers (ARBs) has been shown to improve mortality in heart failure.25 Due to the high rate of teratogenic
eects, including renal agenesis, oligohydramnios, and fetal
DIGOXIN
Digoxin is an inotropic and dromotropic agent used for
the treatment of tachycardia (atrial brillation with rapid
ventricular response and/ or persistent heart failure symp-
toms despite treatment with beta blockers and vasodilators.
Digoxin crosses the placenta and is considered risk category
C.Digoxin level must be carefully monitored to avoid inad-
vertent toxicity.
INOTROPES
Inotropes may be indicated in the setting of low cardiac
output with hypoperfusion and/ or refractory pulmonary
edema. Specic intravenous inotropes used in PPCM include
dobutamine (risk category B), milrinone (risk category C),
or dopamine (risk category C). Evidence guiding the use of
inotropic agents in acute decompensated PPCM is lacking.
death, ACE- Is and ARBs are contraindicated during preg-
26,27
nancy.
ing lactation due to the low transfer into breast milk.10 e
ACE- I therapy should continue for as long as the LV function remains impaired.
PPCM. Beta blockers have been shown to improved
Captopril and enalapril are considered safe dur-
Beta blockade should be considered in women with
ANTICOAGULATION
Women with PPCM are particularly vulnerable to throm-
botic complications due to the additive risks of pregnancy-
induced hypercoagulability and decreased cardiac output.
Although the incidence of thromboembolic complications
PERIPARTUM CARDIOMYOPATHY 327
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in PPCM is unknown, anticoagulation should be considered for all women with an LVEF < 35% during the peripartum period. Of note, an LV thrombus is detected in
up to 17% of women at the time of PPCM diagnosis.28
Unfractionated heparin and low molecular weight heparin
(risk category C) do not cross the placenta and are the preferred mode of anticoagulation in the antepartum period.
structures, promoting vasoconstriction, and impairing
cardiomyocyte function.14 Small, preliminary studies have
demonstrated bromocriptine prevents the formation of
PPCM in animal models and leads to improvement in
LV function in patients with PPCM.
14,17
Bromocriptine
impairs lactation, and its use in the treatment of PPCM is
still controversial.
Warfarin (risk category D) should be avoided during pregnancy but is considered compatible with breastfeeding.
OBSTETRIC MANAGEMENT OFPERIPARTUM
CARDIOMYOPATHY
INVASIVE THERAPY
e timing and mode of delivery in parturients with PPCM
Severe PPCM unresponsive to pharmacotherapy may
require mechanical circulatory support. During pregnancy,
IABPs, ECMO, and LVADs are not recommended and
should only be initiated following delivery. Since PPCM
can dramatically improve within the postpartum period,
prolonged circulatory support has been used as a bridge to
recovery, dramatically reducing the percentage of PPCM
patients requiring transplantation from 33% to 7%.11 Heart
transplantation is reserved for severe cases in patients who
are refractory to optimal medical treatment and mechanical
circulatory support.
Ventricular arrhythmias have been reported in up to
20% of patients with PPCM.29 In addition, sudden cardiac
death (SCD) has been reported in PPCM patients with
decreased LV function, as well as in patients with subsequent normalization of their EF.10 ere are currently no
is usually determined by the maternal functional status
and obstetric indications. Vaginal delivery is preferred in
medically optimized patients with well- compensated heart
failure. e second stage of labor may be assisted with forceps or vacuum extraction to avoid the adverse hemodynamic consequence of repeated and/ or prolonged Valsalva
maneuvers. Cesarean delivery may be necessary for clinical
scenarios requiring expedient delivery including maternal cardiorespiratory compromise and/ or fetal distress.
Although cesarean delivery is associated with increased
hemodynamic perturbations, greater blood loss, enhanced
risk of postoperative infections, and greater frequency
of postpartum thrombophlebitis, it may be indicated in
severe, decompensated heart failure. Regardless of the
mode of delivery, the anesthetic technique should be tai-
lored to minimize hemodynamic uctuations.
guidelines for the placement of implantable cardioverter
debrillators (ICD) in patients with PPCM. e benet of
ICD placement must be weighed against the evidence that
ANESTHETIC MANAGEMENT
LV function returns to normal in many PPCM patients
within 6 months. Patients with persistent heart failure
symptoms despite optimal medical treatment for 6months
and those whose EF remains <30% may be candidates for
ICD implantation for primary prevention ofSCD.
10
Appropriate intrapartum anesthetic management of PPCM
depends on the mode and urgency of delivery, as well as the
physiologic condition of the parturient. Anesthetic guide-
lines include avoidance of myocardial depression, main-
tenance of normovolemia, and prevention of increased
TARGETED THERAPY
ventricular aerload. Routine monitors should include
continuous ECG, noninvasive blood pressure, and pulse
oximetry. In the setting of decompensated heart failure,
Several groups have attempted to mitigate cardiac injury
and improve symptomatology through therapies directed
against proposed pathophysiologic mechanisms of PPCM.
e most promising targeted therapy is bromocriptine,
an inhibitor of prolactin (PRL) (Figure 46.1). Inhibition
of PRL decreases the production of the 16kDa PRL fragment implicated in inhibiting endothelial cell proliferation,
inducing endothelial cell apoptosis, disrupting capillary
invasive blood pressure and central venous pressure moni-
toring may be indicated. Regardless of the mode of deliv-
ery, close attention should be directed at maternal position.
Lateral decubitus position relieves uterine compression of
the IVC and allows unobstructed venous return.
Neuraxial anesthesia is generally preferred for both
vaginal and cesarean deliveries. Neuraxial anesthesia blunts
sympathetic stimulation characteristic of labor and delivery.
328 SECTION B. CARDIAC CRISES
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329
Mitigation of sympathetic stimulation limits plasma catecholamine surges, decreases aerload, and increases venous
capacitance. Epidural anesthesia is favored over a singleshot spinal technique. e signicant decrease in systemic
vascular resistance (SVR) accompanying spinal anesthesia
may compromise coronary perfusion and further contribute to cardiac dysfunction. Adequate labor analgesia and/
or surgical anesthesia should be accomplished with slow
a signicant increase in aerload. e combined inuences
of blood loss and autotransfusion can lead to dramatic
uctuations in central blood volume for approximately 24
hours following delivery. Women with severe reductions in
LV systolic function are at increased risk of developing heart
failure symptoms during this period. Cardiac complications
in the immediate postpartum period include pulmonary
edema, tachyarrhythmias, and pulmonary/ systemic emboli.
titration of neuraxial local anesthetics and opioids. Low
concentrations of local anesthetics are recommended for
labor analgesia.
General anesthesia may be indicated for obstetric and/
PROGNOSIS WITHPERIPARTUM
CARDIOMYOPATHY
or patient factors including, but not limited to, emergency
cesarean section, coagulopathy, and/ or intracranial/ neuraxial pathology. e specic challenge of general anesthesia includes maintaining hemodynamic stability despite
the stimulating eect of laryngoscopy and surgery and the
myocardial depressant eects of volatile and intravenous
anesthetics. e hypertensive response of laryngoscopy
can be mitigated with opioids. Short- acting opioids (remifentanil, alfentanil, and fentanyl) should be considered
until delivery of the fetus. If high- dose narcotics are used
for maternal induction, neonatal resuscitation should be
expected following delivery. Intravenous induction agents
(i.e., propofol) and volatile anesthetics may compromise
myocardial contractility and reduce SVR. Inotropes (dobutamine, dopamine) may be necessary to optimize cardiac
output and systemic perfusion. Regardless of the specic
technique, anesthesia for cesarean delivery should optimize
hemodynamic stability by avoiding arrhythmias, maintaining myocardial contractility, and preventing acute changes
inSVR.
POSTPARTUMCARE
Compared to individuals with other causes of cardiomyopa-
thy, women with PPCM are more likely to have myocardial
recovery, dened as improvement in LVEF to ≥ 50%.
30,31
Published data regarding recovery of LV function vary
widely, ranging from 23% to 54%.14 Dierences in reported
LV recovery rates may be due to environment inuences,
genetic dierences, social factors, and follow- up period
variations. e 6- month recovery rate was only 23% in 176
patients with PPCM from South Africa;32 whereas patients
of the United States have a reported recovery ranging from
45% to 78%.19 Goland et al. demonstrated that African
Americans have a decreased rate of LV recovery compared
to Caucasians with PPCM, 40% versus 61%, respectively.33
Recovery usually occurs between 3 and 6months postpar-
tum but might occur as late as 48months. Some dispari-
ties in recovery rates may be due to inconsistencies in the
follow- up period.
Peripartum cardiomyopathy is associated with signicant morbidity and mortality. Mortality for PPCM in the
United States ranges from 0 to 16.5%;
5,7,28,31,34
whereas
a single tertiary center in Turkey reported a mortality
rate of 30% over 4years of follow- up.35 Morbidity can be
substantial and includes severe heart failure, cardiogenic
Following delivery the patient should recover in a critical
care environment with continuous hemodynamic monitoring, careful uid management, and adequate analgesia.
Cardiac output can increase by 80% above prelabor values
immediately aer delivery due to autotransfusion and relief
of inferior vena cava (IVC) compression. e increase in preload is partially counteracted by blood loss during delivery,
with an estimated blood loss of 400 mL for vaginal delivery
and 800 mL for cesarean section. In the setting of postpartum hemorrhage, uterotonic agents should be used cautiously due their associated side eects. Oxytocin (Pitocin)
can cause a marked decrease in SVR and has an antidiuretic
eect at higher doses. Ergometrine (Methergine) may cause
shock, and arrhythmias.19 In addition, women with a history of PPCM are at increased risk of adverse events during
a subsequent pregnancy compared with pregnant women
without PPCM.
36– 38
e risk of recurrence in subsequent
pregnancies is high, and LVEF, once improved, can worsen
again. Women at greatest risk are those who have not
had full myocardial recovery (EF < 50%).37 In a study of
44 women who recovered from PPCM and subsequently
became pregnant, LVEF deterioration was more frequent
in those with a partial recovery than in those with complete
recovery (44% vs. 21%).37 Of note, women with a history of
PPCM with subsequent full myocardial recovery by ECG,
may have decreased contractile reserve as measured by
PERIPARTUM CARDIOMYOPATHY 329
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dobutamine stress ECG.39 erefore, great caution should
be exercised in women with a history of PPCM during subsequent pregnancies.
CASE- BASED LEARNING DISCUSSION
1. How would you evaluate this patient? Would you
request any ancillary tests and/ orlabs?
2. What would your initial management of this patient
entail? What medications would you administer? How
would you monitor this patient?
3. e patient becomes increasingly tachypneic and
tachycardia. SpO2 is 85% on 100% O2 administered via
facemask. Noninvasive blood pressure measurement is
80/ 50. How would you further evaluate and manage
this patient?
4. Six months postpartum, the patient’s EF has recovered
to 55%. She is interested in becoming pregnant again.
What is her risk of reoccurrence?
5. During the patient’s second pregnancy she develops
PPCM at 38 weeks gestation. She presents dyspneic
and tachycardic to the labor and delivery suite.
Echocardiogram reveals an EF of 15%. e fetal heart
tracing is concerning for repetitive late decelerations.
e obstetric team would like to proceed with a
cesarean delivery. What is your preferred anesthesia
technique? What monitors would you use? What are
your intraoperative concerns?
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7. Elkayam U, Akhter MW, Singh H, etal. Pregnancy- associated cardiomyopathy: Clinical characteristics and a comparison between
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15. Patten IS, Rana S, Shahul S, etal. Cardiac angiog enic imbalance leads
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16. Hilker- Kleiner D, Kaminski K, Podewski E, etal. A cathepsin Dcleaved 16 kDa form of prolactin mediates postpartum cardiomyopathy. Cell. 2007;128(3):589– 600.
17. Sliwa K, Blauwet L, Tibazar wa K, etal. Evaluation of bromocriptine in
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18. Sliwa K, Hilker- Kleiner D, Petrie MC, et al. Current state of
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29. Diao M, Diop IB, Kane A, etal. Electrocardiographic recording of
long duration (holter) of 24 hours during idiopathic cardiomyopathy
of the peripartum. Archives Mal Coeur Vaiss. 2004;97(1):25– 30.
30. Cooper LT, Mather PJ, Alexis JD, etal. Myocardial recovery in
peripartum cardiomyopathy: Prospective comparison with recent
onset cardiomyopathy in men and nonperipartum women. Journal
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31. Felker GM, ompson RE, Hare JM, etal. Underlying causes and
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32. Blauwet LA, Libhaber E, Forster O, etal. Predictors of outcome
in 176 South African patients with peripartum cardiomyopathy.
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33. Goland S, Modi K, Hatamizadeh P, Elkayam U. Dierences in
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34. Brar SS, Khan SS, Sandhu GK, etal. Incidence, mortality, and racial
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35. Biteker M, Ilhan E, Biteker G, Duman D, Bozkurt B. Delayed recovery in peripartum cardiomyopathy: AN indication for long- term
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37. Elkayam U, Tummala PP, Rao K, etal. Maternal and fetal outcomes
of subsequent pregnancies in women with peripartum cardiomyopathy. New England Journal of Medicine. 2001;344(21):1567– 71.
38. Fett JD, Fristoe KL, Welsh SN. Risk of heart failure relapse
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47.
PERIPARTUM EMBOLISM
Elizabeth M.S. Lange and PalomaToledo
AMNIOTIC FLUID EMBOLISM
CASE
A 31- year- old G2P1 at 36 weeks is undergoing cesarean
delivery under epidural anesthesia for arrest of dilation
following induction of labor for twin gestation and preeclampsia when she experiences sudden onset of shortness
of breath.
MECHANISM
Amniotic uid embolism (AFE) was historically believed to
be due to embolism of squamous cells, mucin, meconium,
and amorphous eosinophilic material into the maternal circulation. Current evidence suggests that emboli alone are
insucient to precipitate this event. While the pathophysiology remains poorly understood, the most likely mechanism is a systemic inammatory response associated with
the inappropriate release of endogenous inammatory
mediators, including arachidonic acid metabolites (i.e.,
thromboxane, prostaglandins, leukotrienes, endothelins).1
e exact trigger for the reaction in women with AFE is
unknown.
RISK FACTORS
Amniotic uid embolism has been associated with obstetric
factors such as abnormal placentation, placental abruption,
eclampsia, multiple gestation, induction of labor, articial or spontaneous rupture of membranes, and operative
delivery.
AFE include older age and race or ethnicity.
2– 6
Maternal demographic factors associated with
2,3
Amniotic
uid embolism has been described following antepartum
abdominal trauma,7 aer rst- trimester abortions,8 during
the second trimester,9 at the time of delivery,6 and in the
postpartum period.
10
ASSESSMENT (PRESENTING SIGNS AND
SYMPTOMS)
e classic presentation of AFE includes acute respiratory
distress, cardiovascular collapse, and coagulopathy near
the time of delivery in the absence of other diagnoses, and
it remains a diagnosis of exclusion.
1,6,11
e scope of syndromes that may accompany AFE is broad and is shown
in Box 47.1.
1,6,11
e extensive dierential diagnosis for
AFE should include nonobstetric, obstetric, and anesthetic
causes (Table 47.1). Even though the time course and clinical presentation of many of the competing diagnoses overlap, only AFE and massive placental abruption result in a
relatively sudden onset consumptive coagulopathy aer
maternal collapse.
Amniotic uid embolism most oen occurs during
2,6
labor.
Maternal symptoms typically occur rst; however, in some instances, fetal heart rate changes, such as
bradycardia or variable decelerations, may precede maternal symptoms.6 Presentation of AFE is biphasic. During
the initial phase, acute pulmonary hypertension results in
right ventricular failure, a decrease in cardiac output, and
ventilation- perfusion mismatch leading to hypoxemia.
Right ventricular failure leads to right ventricular dilation,
which bulges into and compresses the le ventricle, thereby
impeding le ventricular lling and eventually decreasing
cardiac output.
12,13
Endogenous catecholamine release may
produce a brief period of systemic hypertension and uterine
tachysystole that precedes hypotension or cardiac arrest.6
Aprofound shunt may be found on arterial blood gas analysis and patients can demonstrate severe hypoxemia despite
high levels of inspired oxygen.
6
A second phase commences when right ventricular
function improves,13 typically 15 to 30 minutes aer the
initial event. Le ventricular failure oen persists in the second stage, and is accompanied by decreased systemic ventricular resistance, decreased le ventricular stroke index,
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TABLE47.1 FEATURES OFAMNIOTIC FLUID EMBOLISM
BOX 47.1 DIFFERENTIAL DIAGNOSIS OFAMNIOTIC FLUID
EMBOLISM
Nonobstetric
ATPRESENTATION
Percent Exhibiting
Feature
(n=60)*
Percent Exhibiting Feature
as First Symptom or Sign
(n=60)*
• Myocardial infarction
• Pulmonary embolism
• Aspiration
• Sepsis
• Anaphylaxis
• Venous air embolism
Maternal hemorrhage 65% 2%
Hypotension 63% 8%
Shortness of breath 62% 20%
Coagulopathy 62% 0%
Premonitory symptoms
(i.e., restlessness,
agitation, numbness,
tingling)
Acute fetal compromise 43% 20%
47% 30%
Obstetric
Cardiac arrest 40% 8%
• Placental abruption
• Eclampsia
• Magnesium toxicity
• Uterine rupture or laceration
• Uterineatony
Dysrhythmias 27% 5%
Seizure 15% 7%
* Some women had multiple features; therefore, the totals are greater than100%.
SOURCE:Data from Knight M, Tuffnell D, Brocklehurst P, etal. Incidence and risk factors for
amniotic- uid embolism. Obstet Gynecol. 2010; 115:910– 17.
to guide volume resuscitation and to select appropriate
Anesthetic
• High neuraxial blockade (“total spinal”)
• Local anesthetic systemic toxicity
• Medicationerror
and acute pulmonary edema.
14,15
Continued progression
with obstetric hemorrhage and disseminated intravascular
coagulopathy is prototypical. Laboratory evaluation may
reveal anemia, thrombocytopenia, prolonged prothrombin
time or activated partial thromboplastin time (aPTT) or
both, and decreased brinogen levels.
MANAGEMENT OFPATIENT
6,16
Maternal resuscitation should focus on three priorities:(1)maintenance of oxygenation, (2)hemodynamic sup-
vasopressor therapy. In the event of maternal cardiopulmonary arrest, the American Heart Association recommends
that delivery of the fetus should occur within 5 minutes
to increase the probability of good outcomes for both the
mother and her neonate.17 Intact neonatal survival is related
to the time interval from the onset of maternal compromise
to delivery.
6
Other management strategies described for AFE
include: the use of cardiopulmonary bypass, extracorporeal membrane oxygenation, continuous hemoltration,
and exchange transfusions.
2,12,18
e usage of inhaled nitric
oxide, prostacyclin, right ventricular assist devices, and
vasopressor and inotropic infusions such as vasopressin,
epinephrine dobutamine, and milrinone may be benecial
in the management of early right- sided heart failure.
19,20
e use of extracorporeal membrane oxygenation and
intra- aortic balloon counterpulsation has been reported for
management of le- sided heart failure.
21
port, and (3)correction of coagulopathy. Upon recognition
of AFE, 100% oxygen should be delivered. Management
may include intubation, initiation of large- bore intravenous
access, invasive access (i.e., arterial line and central venous
pressure catheter), and activation of a massive transfusion
protocol. Transesophageal echocardiography may be useful
FOLLOW- UP
Given the consumptive coagulopathy and the need for
massive transfusion and potentially continued pharmacologic hemodynamic support, these patients should be
PERIPARTUM EMBOLISM 333
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monitored in an intensive care unit with serial laboratory evaluations. Maternal mortality rates are high following AFE, and many women who survive have residual
cognitive sequelae.
CASE- BASED DISCUSSION
1. e patient begins feeling short of breath and becomes
endometrium can be caused by the separation of the placenta from the uterine wall, accelerating the coagulation
cascade. Furthermore, pregnancy is a hypercoagulable state,
associated with enhanced platelet turnover, an increase in
prothrombotic coagulation factors, and brinolysis.
25,26
During pregnancy the incidence of all three factors is
increased compared with the nonpregnant population,
placing parturients at higher risk ofVTE.
hypoxemic and hypotensive shortly aer delivery. What
are likely diagnoses at this time? Are there any exams
you would perform to help narrow your diagnosis?
2. e patient becomes unresponsive, and cardiovascular
collapse occurs. What are your next steps in
management of this patient?
3. Cardiopulmonary resuscitation is initiated. What
additional monitoring and access would you obtain?
RISK FACTORS
e two most important risk factors for VTE are a previous
history of thromboembolism and diagnosis of thrombo-
22,24,27
philia.
lization, smoking, obesity, and cesarean delivery.
Other risk factors include antenatal immobi-
22– 24,28
Risk
factors for the nonpregnant population also apply to pregnant patients.
What laboratory evaluations would you obtain? If the
patient appeared to be in right heart failure, how would
your medical management dier?
4. You notice during resuscitation that there is oozing
around the IV sites and surgeon notes continued
oozing. What is the diagnosis? What laboratory
abnormalities do you expect to see in early versus late
disseminated intravascular coagulation (DIC)? What
blood products would you administer?
5. Aer initial resuscitation in a massive AFE, the patient
DEEP VEIN THROMBOSIS
ASSESSMENT (PRESENTING SIGNS AND
SYMPTOMS)
e signs and symptoms of DVT are nonspecic and oen
mimic normal symptoms of pregnancy, specically lower
leg edema and pain. Uneven or unilateral lower extremity
symptoms should prompt evaluation.
regains hemodynamic stability. Will you attempt
extubation? Will you send her to the postanesthesia
MANAGEMENT
care unit (PACU)?
Compression ultrasonography of proximal veins is the initial
recommended diagnostic test in the setting of new- onset symp-
THROMBOEMBOLISM
CASE
37YO G1P0 at 34 weeks presents to the emergency room with
unilateral leg swelling, shortness of breath, and chestpain.
toms.29 If the test is negative, and involvement of the iliac vessels
is not suspected, only routine surveillance is recommended. In
the setting of high clinical suspicion with equivocal or negative results, the clinician may opt for magnetic resonance imaging or presumptive anticoagulation.29 e - dimer test is not
currently recommended for diagnosis of DVT in pregnancy,
as baseline values in pregnancy are signicantly higher than
MECHANISM
in nonpregnant women.29 If a DVT is identied, therapeutic
anticoagulation should be initiated.
Venous thromboembolic events (VTE) include both deep
venous thrombosis (DVT) and pulmonary thromboembolism (PTE). e incidence of pregnancy- related thromboembolic events is 1.0 to 1.7 events per 1,000 pregnancies.
e pathogenesis of VTE is described by Virchow’s
triad:(1)venous stasis, (2)vascular damage, and (3)hypercoagulability. Venocaval compression by the enlarging uterus leads to venous stasis. Vascular damage to the
334 SECTION B. CARDIAC CRISES
PULMONARY THROMBOEMBOLISM
22– 24
ASSESSMENT (PRESENTING SIGNS AND
SYMPTOMS)
Presenting signs and symptoms for PTE are shown in
Table 47.2. Physical examination of the patient commonly
P
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335
TABLE47.2 PHYSICAL FINDINGS INPULMONARY EMBOLISM
Finding Patients Affected (%)
Tachypnea 85
Tachycardia 40
Fever 45
Accentuated second heart sound 50
Localized rales 60
Thrombophlebitis 40
Supraventricular dysrhythmia 15
SOURCE:Modied from Spence TH. Pulmonary embolization syndrome. In:Civetta JM, Taylor
RW, Kirby RR, eds. Critical Care. Philadelphia:JB Lippincott; 1988:1091– 102.
PTE, compression ultrasonography should be performed to
evaluate for DVT. If results are negative, further imaging is
necessary. In the absence of signs or symptoms of DVT, a chest
radiograph should be performed as a screening tool to exclude
alternative diagnoses and guide further imaging. If the chest
radiograph is normal, ventilation- perfusion (V/ Q) scanning
or computed tomography pulmonary angiography (CTA)
should be performed.33 If the chest radiograph is abnormal,
computed tomography CTA is preferred, as V/ Q scanning
would likely be nondiagnostic.
TREATMENT FORTHROMBOEMBOLISM
If the V/ Q scan or CTA is positive, therapeutic anticoagulation should be initiated.29 Anticoagulation is usually initi-
reveals tachypnea, crackles, decreased breath sounds, and tachycardia. Evidence of a DVT generally accompanies the pulmonary or cardiovascular ndings.
30,31
Central venous monitoring
may reveal an increased (>8mmHg) central venous pressure,
a low to normal (<15mmHg) pulmonary artery occlusion
pressure, and an increased mean pulmonary artery pressure.32
Although pulmonary shunt is a common feature of PTE, the
diagnosis of PTE cannot be excluded on the basis of a normal
PaO2.31 Pulmonary vascular resistance is oen increased, and
patients should be monitored for right ventricular failure if the
mean pulmonary artery pressure exceeds 35 to 45mmHg.32
Le ventricular failure may also occur secondary to poor le
ventricular lling and arterial hypoxemia.
ated with either low molecular weight heparin (LMWH)
or unfractionated heparin (UFH). e American College
of Chest Physicians recommends LMWH for prophylactic and therapeutic anticoagulation for pregnant women
instead of UFH.34 e LMWH has an enhanced ratio of
antithrombotic (anti– factor Xa) to anticoagulant (anti–
factor IIa) activity than UFH and does not aect aPTT
measurement.35 When LMWH is used for therapeutic anticoagulation, dosing can be adjusted based on anti– factor
Xa activity; the desired peak level is 0.6 to 1.0 U/ mL measured 4 hours aer injection.
29
As the patient nears delivery, UFH therapy may be used
to initiate, or maintain anticoagulation. Unfractionated
heparin binds to antithrombin III and potentiates inac-
MANAGEMENT
An algorithm for the management of suspected PTE is shown
in Figure 47.1.33 Initial steps include supplemental oxygen and
hemodynamic support if necessary. If a patient has suspected
tivation of other coagulation factors, including thrombin (IIa), factors Xa, XIIa, XIa, and IXa, and kallikrein.
Unfractionated heparin is administered as a subcutaneous
injection for both prophylactic and therapeutic therapy;
however, intravenous therapy may be necessary in the
Figure47.1 Diagnostic algorithm for workup of suspected
pulmonary embolism during pregnancy. PE, pulmonary
embolism; DVT, deep vein thrombosis; CXR, chest
radiograph; CUS, compression ultrasonography; CTA,
computed tomography pulmonary angiography; V/
Q scan, ventilation- perfusion scan. SOURCE:Adapted
from Leung AN, Bull TM, Jaeschke R, etal. An ofcial American
Thoracic Society/ Society of Thoracic Radiology clinical practice
guideline:evaluation of suspected pulmonary embolism in
pregnancy. American Journal Respiratory and Critical Care
Medicine. 2011;184:1200– 8.
PERIPARTUM EMBOLISM 335
Suspected PE
DVT symptoms
Present Absent
CUS CXR
ositive
Treat
Negative
No
treatment
CTPA V/Q scan
PositivePositiveNegative
Treat
NormalAbnormal
Negativ
No
treatment
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