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patient is associated with the risk of maternal bleeding and abruptio
concentration of 0.4 U/ml to 0.7 U/ml. Optimally, LMWH pro-
placentae,96,97,98,99 and thus should be used cautiously after con-
phylaxis for patients at risk for thromboembolic disease should
sultation with a hematologist. Surgical embolectomy is associated
continue throughout delivery and into the postpartum period. As
with a high mortality rate and therefore should be a last measure in
with UFH, the pharmacokinetics of LMWH are altered during
pregnancy.93 those patients showing rapid clinical deterioration.

Pulmonary thromboembolism
Anesthetic management
The successful management of a patient with PTE requires prompt
There are reports of epidural hematoma after anticoagulation and
diagnosis and rapid institution of appropriate therapy (see
neuraxial blockade100 and after anticoagulation without neuraxial
Table 4.9). The first hour after a PTE is the most critical, and
blockade.101 Due to the serious consequences of an epidural
approximately 10% of all affected patients die during that period.
hematoma, the anesthesiologist should carefully assess the risks
Initial supportive management of PTE consists of maintaining
versus the benefits of performing regional anesthesia in a patient
oxygenation, ventilation, and hemodynamic status. Hypoxemia
with coagulopathy.
should be treated with supplemental O2 but this may not be

Chapter 4

A regional block should be avoided for either labor analgesia or Hypoxemia invariably occurs in clinically significant air embo-
C/S in patients with an abnormal aPTT. Heparin should be dis- lism primarily due to increased V/Q mismatching. Hypercarbia
continued and aPTT should be normal before elective C/S. In can also occur due to an increased alveolar dead space. In
laboring women heparin should be discontinued with the onset humans, large volumes (more than 3 ml/kg) of air may obstruct
of active labor, and i.v. opioid analgesia can be considered in the pulmonary artery and can be fatal, while smaller amounts
place of epidural analgesia until the aPTT is normal. Protamine may result in a V/Q mismatch, hypoxemia, dysrhythmias, and
may be administered in selected patients who require emergency hypotension. Venous air embolism produces a compensatory
C/S. Protamine is unpredictable in reversing the anti-Xa activity increase in minute volume during spontaneous ventilation
caused by LMWH. and may cause a reflex gasp, probably mediated by pulmonary
The American Society of Regional Anesthesia and Pain stretch receptors.
Medicine (ASRA) has provided guidelines to improve safety of The open uterine vessels during C/S allow easy access of air
regional anesthesia/analgesia in anticoagulated patients (see into the venous circulation. The risk of VAE (as suggested by
Table 1.7 in Chapter 1).102 Doppler studies) during C/S, further increases with exterioriza-
Neuraxial blockade is contraindicated in patients receiving tion of the uterus. Furthermore, left uterine displacement, use of
concomitant fibrinolytic therapy, because of the risk of epidural the Trendelenburg position, and hemorrhage all increase the
hematoma. All patients who receive regional anesthesia after pressure gradient and thus increase the risk of VAE during C/S.
anticoagulation or fibrinolytic therapy should be followed for Some investigators have suggested that the incidence of VAE, is
signs and symptoms of a developing epidural hematoma “ reduced to 1% when patients are placed in a five-degree reverse
Trendelenburg position during C/S.104 However, others have
these include severe persistent backache; neurological deficit,
failed to demonstrate this benefit.105
including decreased lower limb movement; tenderness over the
spinous process; and unexplained fever. Magnetic resonance In paradoxical air embolism (arterial air embolus via a patent
imaging or CT scan can be useful if the diagnosis of epidural foramen ovale or through microvascular intrapulmonary shunts)
a small volume of air, as little as 0.025 ml in an animal model,106
hematoma is in doubt. Early spinal cord decompression reduces
the risk of permanent neurological deficits in cases of epidural entering the coronary or cerebral circulation can lead to severe
hematoma. cardiovascular and neurological sequelae. Rarely, during the
If C/S is needed in a patient with abnormal coagulation, GA is antepartum period, air can be forced through the vagina and
administered. The risk of GA in the anticoagulated patient travel through the cervical canal to pass beneath the fetal mem-
includes airway bleeding. There should be a gentle approach to branes and enter the circulation via subplacental sinuses result-
ing in severe VAE.107
laryngoscopy, tracheal intubation, placement of nasopharyngeal
and oral airways, and placement of gastric tubes.

Clinical presentation
Venous air embolism Depending on its severity, VAE may go unrecognized or may
present with cardiopulmonary dysfunction (Figure 4.4). Chest
pain and/or dyspnea can occur in approximately 50% of cases
Venous air embolism is a common occurrence during C/S103 and and SaO2 may fall in 25% of cases. Other physical findings include
vaginal delivery.104 The incidence of VAE during C/S, as detected hypotension, alteration in heart rate (tachycardia and bradycar-
dia), and signs of elevated right-sided pressures. In addition,
by precordial Doppler monitoring, has been reported to be
10“60%.104,105 Venous air embolism accounts for approximately wheezing and rales due to acute bronchospasm and pulmonary
edema may occur. Massive air embolism can present as a sudden,
1% of all maternal deaths in the United States.
dramatic, and devastating event with hypotension, hypoxemia,
and even cardiac arrest.108
For VAE to occur there must be vascular access and a gradient
between the incisional area and the right side of the heart.
Subatmospheric venous pressure allows air to be entrained into The clinical diagnosis of VAE may be difficult because it often
the venous circulation. A gradient as small as 5 cmH2O may result mimics other acute cardiopulmonary and cerebrovascular
in entrainment of large amounts of air. The pressure gradient events. Thus, diagnosis of VAE requires a high level of clinical
increases with the height of the venous site above the level of suspicion. Venous air embolism should be suspected when
the heart. patients complain of chest pain and/or dyspnea, or develop
The volume and rate of air entrainment and the site of hypotension, low SaO2, and dysrhythmias.
embolization determine the outcome from VAE. Other factors Electrocardiographic changes during VAE include bradycardia
that modify outcome include body position, depth of ventila- or tachycardia, premature ventricular contractions, heart block,
tion, and central venous pressure. Pulmonary edema can and ST-segment depression. A decrease in SaO2 and EtCO2 reflect
develop following VAE, secondary to increased capillary perme- the abnormal V/Q relationship and increased physiological dead
ability and/or an increase in hydrostatic pulmonary pressure. space that can result from clinically significant VAE. A rise in

1 Cardiovascular and respiratory disorders

Table 4.10 Management of venous air embolism during











cesarean birth

Flood surgical field with saline
Cardio echo
Position patient 58 head-down and left lateral
and Doppler
Discontinue nitrous oxide
Administer 100% oxygen
Support circulation with intravenous volume expansion and
vasopressor drugs
FETN2 Aspirate air through a multiorifice CVP line

FETCO2 demonstrate an air fluid level in the pulmonary vessels and is
artery pressure
pathognomonic for VAE.110 Central venous and pulmonary artery
pressures increase and CO decreases with VAE. Abrupt elevations
Volume of air infused

PaCO2 in pulmonary artery pressure (PAP) accompanied by a fall in
EtCO2 are indicative of VAE. However, the sensitivity of PAP
with respect to VAE is similar to that of the EtCO2. Aspiration of
(tc)PCO2 air from the right atrium via the central venous catheter also
indicates the occurrence of VAE and may be therapeutic.
Arterial blood-gas analysis will often show hypoxemia and
CVP hypercarbia.

The management of VAE includes prevention of further air
entrainment by flooding the surgical field with saline and posi-
BP tioning the patient in the left lateral position with five-degree
head-down tilt (see Table 4.10). This maneuver places the heart
in a dependent position, minimizing the possibility of developing
an airlock and improving venous return. Nitrous oxide should be
esophageal discontinued and 100% O2 administered. In addition, cardiopul-
stethoscope monary support includes the use of volume expanders and vaso-
pressors. A large multiorifice central venous catheter with the tip
placed in the right atrium allows aspiration of air and thus pre-
vents or breaks an airlock. In patients with delayed emergence
from anesthesia, CT scan or MRI should be considered to exclude
Figure 4.4 Sensitivity of the detection parameters for venous air embolism the presence of intracerebral air.
with increasing air volume (from Black, S. & Cucchiara, R. F. Tumor surgery. In
Cucchiara, R. F. & Michenfelder, J. D. (eds.,) Clinical Neuroanesthesia. New York:
Amniotic fluid embolism
Churchill Livingstone, 1990, p. 285).

Amniotic fluid embolism (AFE) is a rare but catastrophic compli-
cation of pregnancy, which presents with sudden hypoxemia,
end-tidal concentration of nitrogen, as detected by ˜˜RASCAL™™ hypotension, and coagulopathy. The syndrome of AFE was first
monitors, is specific for air embolism, as is a transient ˜˜mill described in 1926 by Meyer, who reported the presence of con-
wheel™™ murmur, heard during continuous monitoring with an stituents of amniotic fluid in the pulmonary vasculature of a
esophageal or precordial stethoscope. This murmur is described young woman who suffered fatal cardiopulmonary collapse dur-
as a rhythmic churning sound produced by movement of air bub- ing pregnancy.
bles in the RV and is heard throughout the cardiac cycle.
In high-risk patients, such as patients with intracardiac shunts
and hypovolemia, precordial Doppler monitoring is recom-
mended. Precordial, low-frequency Doppler is a highly sensitive The reported incidence varies from 1 in 8000 to 1 in 80 000 preg-
and readily available method that detects air bubbles as small nant women. The overall mortality of clinically recognized AFE is
as 0.1 ml.109 Transesophageal echocardiography (TEE) is most reported to be 37“86% with cardiopulmonary collapse occurring
sensitive in detecting air embolism; however, it requires expen- in most cases. Approximately 25“50% of patients with AFE die
within the first hour of clinical presentation.111,112
sive equipment and interpretation skills. The CXR can

Chapter 4

Anaphylaxis Sepsis Amniotic fluid embolism
Table 4.11 Pathophysiology of amniotic fluid embolism
(immunoglobin E) (endotoxin) (various fetal elements)
 Mechanical obstruction of pulmonary vasculature by particulate
“ fetal squamous epithelium
Endogenous mediator release
“ mucin
“ lanugo hair
 Pulmonary edema due to:
“ alveolar capillary leak Clinical manifestations
“ microvascular embolic insult
Figure 4.5 Proposed pathological relation between embolism, septic shock, and
 Left ventricular dysfunction secondary to: anaphylactic shock (from Clark, S. L., Hankins, G. D. V., Dudley, D. A. et al. Amniotic
“ arterial hypoxia fluid embolism: analysis of the national registry. Am. J. Obstet. Gynecol. 1995;
“ decreased coronary blood flow 172: 1158“69).
“ circulatory myocardial depressants
 Release of vasoactive substances eliciting a hemodynamic response: Release of amniotic fluid
containing substances
“ pulmonary hypertension
(arachidonic acid metabolites?)
 Anaphylactic shock

Amniotic fluid access to the maternal circulation is essential to
Hypoxia, hypotension,
the pathogenesis of AFE. The disruption of the integrity of fetal
Phase I pulmonary hypertension, cor pulmonale,
membranes, open uterine or cervical veins, and a concomitant left ventricular injury
pressure gradient between the amnion and the uterine and cervi-
cal veins sufficient to drive the amniotic fluid into the maternal
circulation, facilitate amniotic fluid access to the maternal circu-
lation. However, it must be emphasized that there is no correla-
Left ventricular failure,
tion between the presence of amniotic fluid in the circulation and
Phase II adult respiratory distress syndrome,
the onset of clinical symptoms.113 In a review of cases reported to
consumptive coagulopathy
the national registry for AFE, the presence of meconium in the
amniotic fluid was associated with a poor prognosis, with no Figure 4.6 Proposed pathophysiology of amniotic fluid embolism (from
neurologically intact survivors.112 In this report, out of 46 cases Clark, S. L. Amniotic fluid embolism. Crit. Care. Clin. 1991; 7: 877“82).
of AFE, 30 occurred during labor and 13 occurred after C/S or
vaginal delivery. No correlation between hypertonic contractions maternal endogenous mediators, which results in a clinical
and the occurrence of amniotic fluid embolism was found, so the response similar to both anaphylaxis and septic shock, which
authors concluded that uterine hyperstimulation was a result suggests a common pathophysiologic mechanism for all of
rather than a cause of amniotic fluid embolism. these conditions (see Figure 4.5).
There are various proposed mechanisms that produce the clin- The coagulopathy associated with AFE is also incompletely
ical picture of AFE (see Table 4.11). Pulmonary edema is a com- understood. Some in vitro studies have shown that amniotic fluid
mon (70%) presentation in humans with AFE, but is absent in has a thromboplastin-like quality, which decreases whole blood
primates. Left heart failure is a major physiologic aberration in clotting time, induces platelet aggregation, is associated with the
AFE, but may be preceded by right heart failure. A report of TEE release of platelet factor III and activation of complement and
factor X-activating factor.115,116 In addition, uterine atony caused
initiated within 15 minutes of the onset of symptoms of a fatal
AFE confirmed the occurrence of acute, massive right heart fail- by the myometrial depressant effect of amniotic fluid may result in
ure and severe pulmonary artery hypertension.114 The specula- massive hemorrhage and contribute to a coagulopathy.
tion that mechanical obstruction is fundamental to the The clinical course of AFE may be attributable to the metabo-
lites of arachidonic acid117 since the concentration of these meta-
pathogenesis of AFE has been discounted by autopsy studies
that have shown a poor correlation between the amount of parti- bolites in amniotic fluid increases during labor. The summation
culate matter and clinical findings. Clark and colleagues sug- of many of these findings led Clark to propose a biphasic model
gested that the syndrome of AFE is not consistent with an for pathogenesis of AFE that reconciles human and animal
data.111 The model describes the release of amniotic fluid con-
embolic event, and the term ˜˜amniotic fluid embolism™™ should
be discarded. This syndrome seems to occur after maternal intra- taining vasoactive substances leading to an initial Phase I
vascular exposure to fetal tissue during normal labor, vaginal response, which lasts for 15“30 minutes and involves hypoxemia,
delivery, or C/S and should be designated in a more descriptive dyspnea, pulmonary hypertension, cor pulmonale, and LV injury.
manner as anaphylactoid syndrome of pregnancy.111 Clark and A secondary Phase II response includes LV failure, ARDS, and
colleagues state that amniotic fluid triggers the release of consumptive coagulopathy (see Figure 4.6).

1 Cardiovascular and respiratory disorders

Clinical presentation The presence of anucleate squamous epithelial cells in the
pulmonary microvascular circulation is supportive of AFE.
Most AFE syndromes have been reported during labor. However,
However, this is no longer considered pathognomonic.
this syndrome has occurred during first and second trimester
abortions,118 and as late as 48 hours postpartum.119
The clinical presentation of AFE is generally dramatic, with abrupt
onset of hypoxemia (O2 desaturation), dyspnea, and hypotension
Aggressive cardiopulmonary resuscitation (CPR) is imperative
with rapid progression to cardiopulmonary arrest. Pulmonary
due to the catastrophic nature of AFE. Supplemental O2 should
edema has been observed in 24“70% of cases.119 In 40% of cases,
be provided to treat hypoxemia. If this is insufficient, high con-
pulmonary edema is followed by varying degrees of consumptive
centrations of O2 with continuous positive airway pressure
coagulopathy, although coagulopathy may be the presenting man-
(CPAP) increase functional residual capacity. However, mechan-
ifestation in 10“15% of patients. Central nervous system hypoxia
ical ventilation is usually necessary because of inadequate mater-
may lead to alterations in mental status with seizures developing in
nal PaO2 and hemodynamic instability. If pulmonary edema
10“20% of cases. Amniotic fluid embolism may be complicated by
ensues, use of PEEP should be considered.
myocardial ischemia and infarction, renal failure, liver damage, and
It is important to maintain left uterine displacement to avoid
neurologic deficits. Superimposed renal failure worsens the prog-
aortocaval compression by the gravid uterus during CPR. If
nosis. Occlusion of retinal arterioles by amniotic fluid emboli may
there is no response to advanced CPR within five minutes, C/S
occur. These dramatic features may be heralded by nonspecific
should be performed to optimize the outcome for both mother
symptoms of shivering, anxiety, coughing, vomiting, a sensation of
and baby.
bad taste in the mouth, and a sense of impending doom.119
Hypotension following AFE should initially be treated with
rapid volume administration so as to optimize cardiac preload.
In cases of persistent hypotension, fluid administration should be
titrated to central venous pressure measurements. Placement of a
The initial diagnosis is based on the clinical presentation. The pulmonary artery catheter is helpful in fluid management and
definitive diagnosis is made at autopsy with the finding of fetal drug therapy in those patients who develop pulmonary edema.
debris in the maternal pulmonary vasculature, generally in the Coagulopathy associated with AFE may be severe but is usually
arterioles and capillaries, but occasionally in the large vessels as self-limiting. Administration of blood components (fresh-frozen
well. Routine hematoxylin-eosin staining may be insufficient to plasma, platelets, packed red blood cells) is often successful.
demonstrate the fetal elements, and special stains such as acid Esposito and colleagues reported the successful use of cardiopul-
mucopolysaccharide may be required. monary bypass and pulmonary artery embolectomy for treat-
A number of noninvasive methods for the antemortem diag- ment of postpartum shock caused by AFE.122 Amniotic fluid
nosis of AFE have been suggested, including the use of an anti- embolism causing intense pulmonary vasoconstriction can be
body to human keratin, determination of zinc coproporphyrin diagnosed with TEE and treated with cardiopulmonary bypass.
levels in maternal plasma,120 and the use of monoclonal antibod- Continuous arteriovenous hemofiltration has been used in a
ies to an amniotic fluid-specific antigen.121 The sensitivity, spe- patient who developed AFE complicated by renal failure after
cificity, and positive and negative predictive values of these C/S.123 Patients who receive regional anesthesia before the onset
methods of diagnosis remain poorly defined. In addition, there of AFE should be monitored for the development of an epidural
may be no time to perform these tests, due to the catastrophic hematoma. Neurologic function should be assessed frequently, as
nature of this syndrome. Electrocardiographic changes include allowed by the physical condition of the patient. The indwelling
nonspecific ST-segment and T-wave changes, atrial or ventricular epidural catheter should preferably be removed as soon as possible
rhythm disturbances, RV abnormalities, such as right bundle but only after correction of the coagulopathy.124
branch block, right atrial strain, and right axis deviation.
Changes on CXR include infiltrates, pleural infusion, atelectasis,
Miscellaneous emboli
or elevation of a hemidiaphragm owing to pneumoconstriction.
Arterial blood-gas measurements may show hypoxemia with a
Fat embolism
mixed metabolic acidosis and respiratory alkalosis. Coagulation
Pulmonary fat embolism is a pathological entity characterized by
abnormalities include decreased fibrinogen and elevated levels of
occlusion of pulmonary blood vessels with fat globules that are
fibrin degradation products (FDP), prolonged PT, aPTT, and
too large to pass through the capillary bed. The reported inci-
thrombocytopenia. Ventilation perfusion scans may be useful to
dence of posttraumatic fat embolism syndrome (FES) in the lit-
estimate the probability of embolism based on the size of perfu-
erature ranges from 19“29%,125,126 with a mortality rate of
sion defect and the presence or absence of matching ventilation
10“20%.127 The prognosis in patients with cerebral manifesta-
scan and CXR abnormalities.
tions of fat embolism is very poor.
Patients surviving to receive invasive hemodynamic monitor-
Entry of fat globules into the circulation occurs following skel-
ing generally demonstrate LV dysfunction accompanied by mod-
etal trauma, particularly involving the lower extremity long
erate or severe elevations in PAOP, PAP, and PVR and depressed
bones.128 Fat is detected in pulmonary arterial samples of up to
LV stroke work index.

Chapter 4

70% of patients with long-bone and pelvic fractures. Other causes desaturation, respiratory distress, and cardiovascular collapse.
of fat embolism include burns, subcutaneous adipose tissue Consumptive coagulopathy and ARDS are the most common com-
injury, and acute pancreatitis, sickle-cell crisis during pregnancy, plications observed in patients who survive acute AFE. The AFE

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