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47. Weiner E, Bar J, Fainstein N, et al. e eect of a program to
shorten the decision- to- delivery interval for emergent cesarean
section on maternal and neonatal outcome. Am J Obstet Gynecol.
2014;210(3):224.e1– 6.
48. Balki M, Chakravarty S, Salman A, Wax RS. Eectiveness of using
high- delity simulation to teach the management of general anesthesia for Cesarean delivery. Can J Anaesth. 2014;61(10):922– 34.
Epub 2014 Jul29.
49. Ortner CM, Richebé P, Bollag LA, Ross BK, Landau R. Repeated
simulation- based training for performing general anesthesia for
emergency cesarean delivery:long- term retention and recurring mistakes. Int J Obstet Anesth. 2014;23(4):341– 7. Epub 2014May4.
50. Pratt SD. Focused review:simulation in obstetric anesthesia. Anesth
Analg. 2012;114(1):186– 90. Epub 2011 Oct24.
51. Daniels K, Arafeh J, Clark A, Waller S, Druzin M, Chueh J.
Prospective randomized trial of simulation versus didactic teaching
for obstetrical emergencies. Simul Healthc. 2010;5(1):40– 5.
52. Maslovitz S, Barkai G, Lessing JB, Ziv A, Many A. Recurrent obstetric management mistakes identied by simulation. Obstet Gynecol.
2007;109(6):1295– 300.
53. Guise JM, Lowe NK, Deering S, et al. Mobile in situ obstetric emergency simulation and teamwork training to improve
maternal- fetal safety in hospitals. Jt Comm J Qual Patient Saf.
2010;36(10):443– 53.
54. Sørensen JL, Van der Vleuten C, Lindschou J, etal. “In situ simulation” versus “o site simulation” in obstetric emergencies and their
eect on knowledge, safety attitudes, team performance, stress, and
motivation:study protocol for a randomized controlled trial. Trials.
2013;17(14):220.
55. Sørensen JL, Lottrup P, van der Vleuten C, Andersen KS, Simonsen
M, Emmersen P, Rosthøj S, Ottesen B. Unannounced in situ simulation of obstetric emergencies:sta perceptions and organisational
impact. Postgrad Med J. 2014;90(1069):622– 9. Epub 2014 Sep10.
56. Sweeney J, Maietta R, Olson K. An analysis comparing “Sim
Huddles” to traditional simulation for obstetric emergency preparedness. Nurs Womens Health. 2015;19(1):16– 25.
57. Ryding EL, Wijma B, Wijma K. Posttraumatic stress reactions
aer emergency cesarean section. Acta Obstet Gynecol Scand.
1997;76(9):856– 61.
58. Ryding EL, Wijma K, Wijma B. Predisposing psychological factors
for posttraumatic stress reactions aer emergency cesarean section.
Acta Obstet Gynecol Scand. 1998;77(3):351– 2.
59. Ryding EL, Wijma K, Wijma B. Experiences of emergency cesarean section: a phenomenological study of 53 women. Birth.
1998;25(4):246– 51.
60. am V, Christensson K, Ryding EL. Sense of coherence and symptoms of post- traumatic stress aer emergency caesarean section.
Acta Obstet Gynecol Scand. 2007;86(9):1090– 6.
61. am V, Ryding EL, Christensson K. Experience of support
among mothers with and without post- traumatic stress symptoms following emergency caesarean section. Sex Reprod Healthc.
2010;1(4):175– 80. Epub 2010 Jul23.
62. Reynolds JL. Post- traumatic stress disorder aer childbirth:the phenomenon of traumatic birth. CMAJ. 1997;156(6):831– 5.
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SECTIONB
CARDIACCRISES
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45.
HIGH OR TOTAL SPINAL/ EPIDURAL
Feyce Peralta
CLINICALCASE
addition patients may have symptoms of post- traumatic stress
disorder depending on the events that occurred during the
A 27- year- old laboring patient, G1P0 at 41 weeks estimated
gestational age, admitted for induction of labor, is being
transported from a labor and delivery room to the operating room for cesarean delivery secondary to arrest of dilation. She has a functional labor epidural catheter in place,
which is being dosed in route to the operating room for surgical anesthesia. Afew minutes aer arrival in the operating room the patient complains of diculty breathing and
bilateral hand weakness.
time they were unable to communicate or move. Just as com-
munication is crucial during the event, debrieng aerward
and oering access to counseling can be benecial.
If maternal hemodynamics are signicantly compromised due to a high block level, uteroplacental perfusion
can be compromised, leading to fetal heart rate decelerations and potentially the need for emergency delivery. In
the case of suspected high/ total neuraxial block, fetal heart
tones should be monitored while the patient is stabilized
and preparation made for expedient delivery. In the case
DEFINITION
High spinal/ epidural occurs when a neuraxial block spreads
well above the dermatomal level required for a surgical
of unresolving fetal bradycardia, crash cesarean delivery
should be performed in the usual manner.
INCIDENCE
procedure. is can be acceptable if the patient remains
asymptomatic or only mildly symptomatic (i.e., only upperextremity numbness). However, it can be associated with
respiratory compromise and hemodynamic instability (e.g.,
bradycardia, hypotension) from blockade of the sympathetic system, leading to drastic vasodilation and inhibition
of cardioaccelerator bers. Total spinal or epidural blockade relates to an anesthetic block that causes loss of consciousness and respiratory arrest secondary to central action
at the level of the cervical spine and brainstem. e latter
requires intubation for respiratory support, conversion to
general anesthesia, and supportive measures until the block
recedes. Because there is a ne line between high and total
e true incidence of high or total spinal/ epidural has
been dicult to elucidate because of the rarity of these
events and the variations in the denitions used for these
two complications:high versus total spinal/ epidural.
2,3
e
Serious Complication Repository (SCORE) Project was a
study conducted to establish the incidence of serious complications related to obstetric anesthesia. In this study of
more than 160,000 epidural and combined spinal epidural,
a high neuraxial block (dened as neuraxial block necessitating intubation or conversion to general anesthesia) was
found to be the most frequent serious complication related
to neuraxial anesthesia, occurring in 1:4,336 anesthetics.
4
spinal/ epidural, and the management is similar, related
studies discuss them as one entity.
PATHOPHYSIOLOGY OFDISEASESTATE
COMPLICATIONS
In a 2009 obstetric anesthesia closed claims analysis the most
common anesthetic cause of maternal death/ brain damage in
regional anesthesia claims was high neuraxial block (22%).1 In
It is important to understand the mechanism of disease and
risk factors for high spinal in order to appropriately consider this etiology, recognize the presence of the hemodynamic derangements of high/ total spinal, and immediately
begin treatment.
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MECHANISM
A high or total neuraxial block (spinal or epidural) occurs
aer the injection of local anesthetic in the epidural, subdural, or intrathecal space that spreads higher than intended,
involving at least the cardioaccelerator bers at T1- 4. us,
the local anesthetic may directly block neural conductivity
or otherwise interfere with neuronal function in the cervical spine and brainstem while producing a sympathectomy
below that level. However, the most frequent cause of frank
respiratory arrest during high neuraxial block is brainstem
hypoperfusion secondary to signicant systemic hypotension and decreased cardiac output. In the case of high/ total
spinal aer epidural catheter dosing, this can be due to
unintentional epidural catheter placement into the subdural or intrathecal space or catheter migration to one of these
spaces during labor.
5
RISK
In the SCORE project the most common risk factors for
the development of a high or total spinal/ epidural were
obesity (41%) and the administration of spinal anesthetic
aer a failed epidural anesthetic (27%). Other risk factors
included height <60 inches, epidural aer unintentional
dural puncture, and spinal deformity.
e incidence of unrecognized spinal catheters was
24%. Ninety- four percent (or 1:12,000 labor epidurals) of
the unrecognized spinal catheters that resulted in a high
neuraxial block occurred in the labor suite as opposed to
TABLE45.1 RISK FACTORS FORHIGH NEURAXIALBLOCK
Category Factor Description
Medication Factors Large dose of high concentration local
anesthetic
Isobaric solution (vs. hyperbaric)
Prior drug administration in intrathecal space
(followed by large epidural dose)
Patient Factors Increased abdominal pressure (i.e., obesity,
pregnancy) with resultant increased epidural
fat and volume of epidural venous plexus
Spinal deformity
Height (<60cm)
Technique Factors Epidural after unintentional dural puncture
with large bore needle
Immediate supine position
Higher lumbar position
vasopressors are the mainstays of management of these
patients. While phenylephrine is usually the rst- line vasopressor during pregnancy, in bradycardic and hypotensive
patients epinephrine is the preferred treatment, starting
with small doses (~25– 50 mcg IV) and increasing with each
additional dose every 30– 90 seconds until hemodynamic
stability is achieved. Although it may seem counterintuitive
to supporting hemodynamics, the reverse Trendelenburg
position may help prevent further block spread.
the operating room (95% CI, 1:7,194 to 1:20,842) (See
Table45.1).
ASSESSMENT OFTHE PATIENT
BOX 45.1 SYMPTOMS OFHIGH/ TOTAL NEURAXIAL
BLOCKADE
Nausea/ vomiting
Symptoms typically present immediately following spinal
anesthetic administration, and within minutes aer initial
dosing of an epidural catheter or aer redosing a preexisting
epidural catheter. Common symptoms associated with high
and total spinal are presented in Box45.1.
INITIAL TREATMENTSTEPS
Treatment consists of immediate support of ventilation
and blood pressure. Depending on the extent of the block
rise, oxygen supplementation can be delivered via facemask
or intubation. Administration of intravenous uids and
320 SECTION B. CARDIAC CRISES
Anxiety
Difculty speaking/ swallowing/ coughing
Loss of handgrip
Hypotension
Bradycardia
Paralysis
Respiratory compromise/ respiratoryarrest
Loss of consciousness
Cardiacarrest
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SUBSEQUENT TREATMENTSTEPS
Communication with the patient is paramount, and administration of sedative hypnotics should be considered aer
hemodynamic stability is achieved if the patient expresses
anxiety or dyspnea related to weakness. In this instance the
patient might be unable to move or speak while still maintaining alertness. Patients who will be intubated require
induction medications to ensure amnesia for the event.
Supportive measures should be maintained until the block
has receded to approximately the T2- 4 level to ensure ade-
FOLLOW- UP
Assessment of vital signs, neurologic status, and dermatomal regression of sensory and motor blocks should be done
for patients who experience a high spinal/ epidural block
prior to patient’s discharge to the postpartum oor. is
can be done in the recovery room or the intensive care unit,
depending on the resources available.
Equally important is a follow- up conversation with the
patient to disclose the occurrences that possibly led to these
8
events.
quate cardiac and respiratory dynamics. is should occur
in a period of 30 minutes to 1 hour, but depending on the
contributing factors the time frame could be shorter or lon-
CONCLUSION
ger. If a true high or total neuraxial block occurs, resulting
in neurogenic shock, the provider should be prepared to
start an infusion for chronotropic support until the block
recedes.
High or total neuraxial block is rare, but is associated with
maternal complications if not rapidly treated. Symptoms
include initial nausea and vomiting that are quickly fol-
lowed by hemodynamic instability, particularly bradycar-
dia and hypotension, and oen respiratory compromise.
PREVENTION
The negative aspiration of cerebral spinal fluid and a
Treatment is supportive and denitive resolution depends
only on time. Patients should be counseled aer the fact
regarding likely inciting factors.
negative test dose do not guarantee correct location of
an epidural catheter.1 The aspiration portion is especially true when single- orifice catheters are used, and
after long periods of time with the epidural catheter in
place. The best practice would include a combination
of catheter aspiration + test dose administration via the
catheter at the time of placement. Subsequently, each
time the catheter is accessed, the provider should start
with a small dose of local anesthetic ( +/ - epinephrine)
that acts as a secondary test dose. Once proven negative,
incremental doses of local anesthetics (e.g., 3- 5 mL at a
time) coupled with frequent patient assessments can follow provided a nonemergent situation.
6
In the setting of dysfunctional epidural catheter anal-
CASE- BASED LEARNING DISCUSSION
1. How would you dose the existing epidural catheter for
surgical anesthesia? Which drugs would youuse?
2. In the case presented, what would be part of your
dierential diagnosis?
3. How will you treat this patient? If the symptoms do not
progress, does she require intubation? Will you give her
sedation?
4. How will you counsel her aer the current issue
resolves?
gesia with an existing residual block and an indication for
nonemergent cesarean delivery, replacement of the existing
epidural catheter with a combined- spinal epidural (reduce
REFERENCES
spinal dose by 20% to 30%) or a de novo epidural catheter
titrated to eect have both been suggested as alternatives
to general anesthesia. Single- shot spinal anesthesia should
only be considered aer residual block wears o and aer
waiting at least 30 minutes aer last epidural bolus administrations.7 Labor epidural catheters that appear to be
dysfunctional or when a small bolus dose results an overexaggerated block response should be replaced in a timely
manner during the labor process.
1. Davies JM, Posner KL, Lee LA, Cheney FW, Domino KB. Liability
associated with obstetric anesthesia: a closed claims analysis.
Anesthesiology. 2009;110:131– 9.
2. Hawkins JL, Chang J, Palmer SK, Gibbs CP, Callaghan WM.
Anesthesia- related maternal mortality in the United States:1979-
2002. Obstetrics and Gynecology. 2011;117:69– 74.
3. Paech MJ, Godkin R, Webster S. Complications of obstetric epi-
dural analgesia and anaesthesia: a prospective analysis of 10,995
cases. Int J Obstet Anesth. 1998;7:5– 11.
4. D’Angelo R, Smiley RM, Riley ET, Segal S. Serious complications
related to obstetric anesthesia:the serious complication repository
HIGH OR TOTAL SPINAL/EPIDURAL 321
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project of the Society for Obstetric Anesthesia and Perinatology.
Anesthesiology. 2014;120:1505– 12.
5. Pan PH, Bogard TD, Owen MD. Incidence and characteristics of failures in obstetric neuraxial analgesia and anesthesia: a
retrospective analysis of 19,259 deliveries. Int J Obstet Anesth.
2004;13:227– 33.
6. Gaiser RR. e epidural test dose in obstetric anesthesia: it is not
obsolete. J Clin Anesth. 2003;15:474– 7.
7. Portnoy D, Vadhera RB. Mechanisms and management of an
incomplete epidural block for cesarean section. Anesthesiol Clin
North America. 2003;21:39– 57.
8. Weiss PM, Miranda F. Transparency, apology and disclosure of adverse outcomes. Obstet Gynecol Clin North Am.
2008;35:53– 62,viii.
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46.
PERIPARTUM CARDIOMYOPATHY
Emily J.Baird
CLINICALCASE
PPCM. e prevalence of PPCM is signicantly higher
in developing countries such as Nigeria (1:100)2 and Haiti
A 28- year- old African American female presents 4days postpartum complaining of fatigue, dyspnea, and chest pressure. Physical exam reveals elevated jugular venous pressure,
displaced apical impulse, pulmonary rales, and peripheral
edema. Chest x- ray demonstrates an enlarged cardiac silhouette, pulmonary venous congestion, and interstitial inltrates.
Echocardiogram is signicant for globally decreased contractility with an ejection fraction (EF) of 35% and a le ventricular end- diastolic dimension (LVEDD) of 3.2cm/ m2. Of note,
the patient has no history of cardiac disease and her intrapartum course was uneventful.
(1:300)3 compared to industrialized countries, including
South Africa (1:1,000)4 and the United States (1:,3000).5 e
high incidence in Nigeria may be related to a local Hausa cus-
tom of eating kanwa, a dry lake salt for 40days aer delivery.2
Within the United States, African American women are 3 to
16 times more likely to be diagnosed with PPCM.6 Finally,
the majority of PPCM cases in the United States are associ-
ated with low parity, with 40% of patients diagnosed during
a rst pregnancy and 50% identied within their rst two
pregnancies.7 Elucidation of the pathophysiologic mechanism
of PPCM will hopefully provide further insight into the geo-
graphic and racial variations.
INTRODUCTION
PATHOPHYSIOLOGY OFDISEASEDSTATE
Peripartum cardiomyopathy (PPCM) is an idiopathic form
of heart failure that manifests during the last month of
pregnancy or the rst 5months postpartum. Although the
incidence is relatively low, the maternal impact is high, with
up to 12% of maternal deaths in the United States resulting from sequelae of PPCM.1 Despite research eorts, risk
factors for PPCM are poorly characterized and the pathophysiologic mechanism remains incompletely understood.
Timely diagnosis continues to be a challenge, since many of
the symptoms of PPCM mimic those commonly encountered during the normal peripartum period. Management
of PPCM parallels current heart failure guidelines, with
special consideration to the safety of medications and
interventions during pregnancy and lactation. e clinical
course of PPCM varies between complete recovery to rapid
progression with end- stage heart failure and evendeath.
e pathophysiology of PP CM remains nebulous. Although
numerous potential inciting events have been investigated,
no single factor has been unambiguously identied as the
underlying etiology of PPCM. e most probable causes
of PPCM include inammation, immune- mediated injury,
and/ or genetic contributions. High concentrations of
serum inammatory markers in PPCM patients, includ-
ing tumor necrosis factor- α (TNF- α), C reactive protein
(CRP), interferon- γ (IF- γ), and interleukin- 6 (IL- 6), sug-
gest an underlying inammatory process.
8,9
Furthermore,
myocardial biopsies have found histological evidence
of myocarditis in 9%– 62% of patients with PPCM.10
Although there is certainly an association between inammation and PPCM, it is unclear whether the relationship
is causative or reactive. e maternal immune system is
another potential cause of peripartum cardiac injury. Fetal
EPIDEMIOLOGY
cells introduced into the maternal circulation may interact
with cardiac tissue, triggering a pathologic autoimmune
response directed at the maternal cardiac tissue. Although
Environmental, genetic, cultural, and obstetric factors may
account for the wide variation in the reported incidence of
a maternal immune- mediated injury is certainly plausible,
available data is contradictory and insucient to establish
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Pituitary Gland Placenta
Bromocriptine
sFLT-1
23 kDa Prolactin 16 kDa Prolactin
Cathepsin-D
VEGF
Reactive Oxygen Species
(ROS)
Manganese Sodium Dismutase
Figure46.1 Proposed pathophysiology of PPCM. Decreased concentration of STAT3 causes an increased expression of manganese sodium dismutase
(MnSOD). Decreased MnSOD leads to an increase in reactive oxygen species (ROS), which promotes activation of cathepsin D.Cathepsin D catalyzes
the cleavage of prolactin (PRL) to its 16 kDa form. The antiangiogenic activities of 16 kDa PRL and soluble fms- like tyrosine kinase 1 (sFLT1)
overcome the proangiogenic activities of vascular endothelial growth factor (VEGF), leading to increased endothelial cell apoptosis and cardiomyocyte
dysfunction.
whether an abnormal immunological response is the cause
of PPCM.
10,11
Finally, a susceptible genetic background
superimposed on the physiologic stress of pregnancy may
lead to unmasking of latent idiopathic dilated cardiomyopathy (DCM).
11,12
Previous studies have identied an association with the occurrence of PPCM and a familial history
of DCM.13 Although the etiology remains unclear, recent
evidence suggests PPCM is the result of a common nal
pathway involving enhanced oxidative stress leading to an
imbalance in angiogenic signaling (Figure 46.1).
(MnSOD)
STAT3
Cardiomyocte
14– 17
normal physiologic perturbations during the peripartum
period. Clinical manifestations commonly develop within
the rst 2months following delivery, with less than 10%
of cases occurring in the antepartum period.
18,19
Symptoms,
including dyspnea, orthopnea, palpitations, and chest pressure, are consistent with those experienced in all forms
of heart failure and are not pathognomonic for PPCM.
Other nonspecic symptoms frequently endorsed include
fatigue, malaise, and abdominal discomfort. Physical exam
ndings include signs of both right and le heart failure
such as tachycardia, elevated jugular venous pressure, dis-
DIAGNOSIS OFPPCM
Once the mechanism of disease and risk factors have been
understood, recognizing the clinical presentation is key to
being able to diagnose and treat this serious condition in
placed apical impulse, third heart sound, systolic murmur
of tricuspid or mitral regurgitation, pulmonary rales, and
peripheraledema.
DIAGNOSTIC CRITERIA
the peripartum period.
e diagnosis of PPCM, as previously dened by the
CLINICAL PRESENTATION
e presentation of PPCM can be insidious. Diagnosis is
frequently delayed due to the overlap of symptoms with
National Institutes of Health, is based on four criteria20:
(1) Heart failure develops within a 6- month period spanning from the last month of pregnancy to 5 months postpartum; (2) ere are no other identiable causes for
324 SECTION B. CARDIAC CRISES
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Symptoms of PPCM
• Dyspnea
• Orthopnea
• Palpitations
• Chest pressure
• Fatigue
• Malaise
Normotensive Hypotensive Hypertensive
Signs of PPCM
• JVD
• Pulmonary rales
• Tachypnea
• Tachycardia
• Third heart sound
• New murmur
• Peripheral edema
Clinical History
• Symptoms of heart failure?
• Onset of symptoms within last month of
pregnancy or 5 months postpartum?
• No previous history of cardiac disease?
Yes
Physical Exam
Signs of heart failure?
YesYes
Yes
Echocardiogram
LVEF ≤ 45%
Supportive Studies
• CXR
• ECG
• Labs
Yes
Yes
Yes
No
No
Consider Alternative Diagnosis
LVEF > 45%
Possible Adjunct Studies
• Cardiac MRI
• Myocardial biopsy
• Cardiac catheterization
Yes
Consider Alternative Diagnosis
Yes
Consider Alternative Diagnosis
Consider Alternative Diagnosis
Alternative Diagnosis
• Preeclampsia
• Pulmonary embolism
• Myocardial infarction
• Amniotic fluid embolism
• Severe anemia
Figure46.2 Algorithm for the diagnosis ofPPCM.
the cardiomyopathy; (3) e patient does not have a
prior history of congenital or acquired cardiac disease;
and (4) Echocardiogram ndings demonstrate a dilated
cardiomyopathy with an EF < 45% and/ or M- mode fractional shortening < 30% and a LVEDD > 2.7 cm/ m2.
erefore, PPCM is a diagnosis of exclusion. Other causes
of cardiac dysfunction, including pulmonary embolism,
systemic infection, hypertensive disorders, severe anemia,
and acquired or congenital heart disease, must be ruled out
before the diagnosis of PPCM can be assigned (Figure 46.2).
tachycardia, nonspecic ST- and T- wave changes, le ventricular (LV) hypertrophy, and/ or LV conduction defects.
New- onset atrial and/ or ventricular arrhythmias may be
noted. e ECG is also helpful in excluding conditions in
18,21
the dierential diagnosis such as myocardial infarction and
pulmonary embolism. e CXR may reveal an enlarged
cardiac silhouette, pulmonary venous congestion, and/
or interstitial inltrates. Less commonly, pleural eusions
and/ or pericardial eusion can be identied. Fetal shielding is necessary if the CXR is performed in the antepartum
period. Finally, echocardiogram is essential for the diagno-
SUPPORTING STUDIES
sis of PPCM. e echocardiogram is also useful in identifying other cardiac anomalies commonly occurring with
PPCM including decreased right ventricular systolic funcSupporting studies are necessary to exclude other causes of
symptomology, denitively diagnosis PPCM, and quantify
the extent of heart failure.
10– 12
Evaluation should include electrocardiogram (ECG), chest x- ray (CXR), echocardiogram,
and cardiac protein assays. Other studies that are not routinely
recommended for the diagnosis of PPCM, but may be considered if the diagnosis is unclear, including cardiac magnetic
resolution imaging (MRI), myocardial biopsy, cardiac catheterization, and serum inammatory markers.
No pathognomonic ECG ndings have been identied
for PPCM. e most common ECG changes include sinus
tion, mitral regurgitation, tricuspid regurgitation, mural
thrombus, and pericardial eusion.
Cardiac MRI is increasingly being used to conrm
and complement echocardiogram ndings in PPCM.10
An MRI is particularly useful in identifying intracardiac
thrombus, quantifying cardiac function and structure, and
assessing cardiac volumes. And MRI is especially benecial
in situations where transthoracic ECG is technically suboptimal due to patient factors. Because MRI does not pose the
risk of radiation exposure, serial testing may be performed
safely in most PPCM patients. Gadolinium crosses the
PERIPARTUM CARDIOMYOPATHY 325
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