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OBSTETRICS
PHYSIOLOGIC CHANGES IN
PREGNANT WOMEN
Cardiovascular System Changes
• Changes in the cardiovascular system during
pregnancy can be summarized as
• (I) an increase in intravascular fluid volume,
• (2) an increase in cardiac output,
• (3) a decrease in systemic vascular resistance
INTRAVASCULAR FLUID VOLUME
Maternal intravascular fluid volume increases in the first
trimester, and at term the plasma volume is increased
about 45% and the erythrocyte volume about 20%.
This disproportionate increase in plasma volume accounts for
the relative anemia of pregnancy. The increased intravascular
fluid volume offsets the 300 to 500 mL blood loss
that accompanies vaginal delivery and the average 800 to
1000 mL blood loss that accompanies cesarean section.
The total plasma protein concentration is decreased as a
result of the dilutional effect of the increased intravascular
fluid volume.
CARDIAC OUTPUT
Cardiac output increases about 10% by the 10th week of
gestation and increases 40% to 50% by the third trimester.
This augmentation of cardiac output is due to an increased
stroke volume (25% to 30%) and heart rate (15% to 25%).
The onset of labor is associated with further increases in
cardiac output, with the largest increase occurring immediately
after delivery, when cardiac output is increased by
as much as 80%. This presents a unique postpartum risk
for patients with cardiac disease, such as fixed valvular
stenosis. A regional anesthetic is capable of attenuating
the release of catecholamines during painful labor and the
resultant maternal tachycardia and systemic hypertension.
Cardiac output substantially returns toward prepregnant
values by 2 weeks postpartum.
SYSTEMIC VASCULAR RESISTANCE
Systolic blood pressure decreases by as much as 15%
during an uncomplicated pregnancy. Although there is an
increase in cardiac output and plasma volume, systemic
blood pressure does not increase because of a decrease in
systemic vascular resistance (mean arterial pressure may
decrease slightly). Furthermore, there is no change in central
venous pressure during pregnancy despite the increased
plasma volume because venous capacitance increases.
Femoral venous pressure increases about 15%, presumably
reflecting compression of the inferior vena cava by the
gravid uterus.
AORTOCAVAL COMPRESSION
(SUPINE HYPOTENSION SYNDROME)
Decreases in maternal blood pressure because of aortocaval
compression by the gravid utems are associated with
the supine position. Significant aortoiliac artery compression
occurs in 15% to 20% of pregnant women and vena
cava compression in all such women. Vena cava compression
may contribute to lower extremity venous stasis and
thereby result in ankle edema and varices. Diaphoresis,
nausea, vomiting, and changes in cerebration may accompany
this hypotension. These symptoms are termed the
"supine hypotension syndrome."
Mechanism and Compensatory Responses
The mechanism of supine hypotension
syndrome is decreased venous return as a
result of compression of the inferior vena cava
by the gravid uterus when the pregnant
woman assumes the supine position. The
resulting decrease in venous return leads to a
decrease in cardiac output and a decline in
systemic blood pressure.
compensatory responses that prevent hypotension despite
aortocaval compression:
One compensatory mechanism is increased venous pressure
below the level of compression of the inferior vena cava,
which serves to divert venous blood from the lower half of
the body via the paravertebral venous plexuses to the
azygos vein. Flow from the azygos vein enters the superior
vena cava and venous return is maintained. Dilation of the
epidural veins may make penetration of a vein more likely
during attempted lumbar epidural anesthesia and thus
could lead to accidental intravascular injection of the local
anesthetic solution. This would result in a bolus delivery of
local anesthetic to the heart with potentially profound
consequences on the central nervous and cardiovascular
systems.
Another compensatory response that prevents hypotension
with aortocaval compression is a reflex increase in
peripheral sympathetic nervous system activity. This results
in increased systemic vascular resistance and permits
systemic blood pressure to be maintained despite decreased
cardiac output. It is important to recognize that compensatory
increases in systemic vascular resistance are impaired
by regional anesthetic techniques. Indeed, arterial
hypotension is more common and profound during regional
anesthesia administered to pregnant as compared with
nonpregnant women.
In addition to compression of the inferior
vena cava, the gravid uterus can compress the
lower abdominal aorta . Such compression
leads to arterial hypotension in the lower
extremities, but maternal symptoms or
decreases in systemic blood pressure as
measured in the arms do not occur.
RISKS:
The significance of aortocaval compression is the associated decrease in
uterine and placental blood flow. Even with a healthy uteroplacental unit,
prolonged maternal hypotension (approximately 90 to 100 mm Hg systolic
blood pressure for an average patient) for longer than 10 to 15 minutes will
most likely significantly decrease uterine blood flow and lead to
progressive fetal acidosis. Venous compression by the gravid uterus diverts
some blood returning from the lower extremities through the internal
vertebral venous plexus to the azygos and epidural veins, thereby
increasing the likelihood of epidural venous puncture with epidural or
spinal techniques. Supine positioning is avoided in pregnant women during
anesthetic administration in the second and third trimesters. Anesthetic
techniques that interfere with increased sympathetic nervous system tone
will further compromise the compensatory mechanisms for vena cava
compression induced by supine positioning and potentially cause profound
hypotension
Treatment
Displacing the gravid uterus can minimize the incidence
of supine hypotension syndrome, which is important for
patients undergoing regional or general anesthesia because
their compensatory increases in systemic vascular
resistance will be impaired. Displacement of the gravid
uterus can be achieved by placing the pregnant woman in
the lateral position or by moving the gravid uterus to the
left and off the inferior vena cava or aorta. Displacement
of the uterus to the left can be accomplished manually or
by elevation of the right hip 10 to 15 cm with a blanket
or wedge .
Pulmonary System Changes
• The most significant changes in the pulmonary
system during pregnancy include alterations in
• (l) the upper airway,
• (2) minute ventilation,
• (3) lung volumes,
• (4) arterial oxygenation
UPPER AIRWAY
Capillary engorgement of the mucosal lining of the upper
respiratory tract accompanies pregnancy, emphasizing
the need for careful instrumentation of the upper airway
during suctioning, placement of airways (avoid nasal
instrumentation if possible), and direct laryngoscopy. It
may be prudent to select a smaller cuffed tracheal tube
(6.5 to 7.0 mm internal diameter) because the vocal cords and
arytenoids are often edematous.
Weight gain associated with pregnancy, particularly in women of short
stature or with coexisting obesity, can result in difficulty inserting the
laryngoscope because of a short neck and large breasts.
MINUTE VENTILATION
Minute ventilation is increased about 50% above
prepregnant
levels during the first trimester and is maintained for
the remainder of the pregnancy. This increased minute
ventilation is achieved primarily by an increased tidal
volume,
with small increases in the respiratory rate (see 1able 322).
Increased circulating levels of progesterone are presumed
to be the stimulus for increased minute ventilation.
Resting maternal Paco2 decreases from 40 to about
32 mm Hg during the first trimester as a reflection of the
increased minute ventilation. Arterial pH, however,
remains near normal because of increased renal excretion
of bicarbonate ions. The pain associated with labor and
delivery results in further hyperventilation, which can be
attenuated by adequate analgesia, such as lumbar
epidural analgesia.
LUNG VOLUMES
Lung volumes, in contrast to the early appearance of
increased minute ventilation, do not begin to change until
about the third month of pregnancy.
With increasing enlargement of the uterus, the
diaphragm
is forced cephalad, which is primarily responsible for the
20% decrease in functional residual capacity (FRC)
present at term. As a result, FRC can be less than closing
capacity for many small airways and may give rise to
atelectasis in the supine position. Vital capacity is not
significantly changed.
The combination of increased minute ventilation
and
decreased FRC results in an increase in the rate
at which
changes in the alveolar concentration of inhaled
anestheticcan be achieved. This affects
induction of anesthesia, emergence
from anesthesia, and changes in depth of
anesthesia.
ARTERIAL OXYGENATION
Early in gestation, maternal Pao2 while breathing room
air is normally above 100 mm Hg because of the presence
of hyperventilation. Later, Pao2 becomes normal or even
slightly decreased, most likely reflecting airway closure.
During induction of general anesthesia in a pregnant patient,
Pao2 decreases more rapidly than in a nonpregnant patient
because of decreased oxygen reserve (decreased FRC)
and increased oxygen uptake (increased metabolic rate).
For these reasons, the administration of supplemental
oxygen during a regional anesthetic or "preoxygenation"
(breathe oxygen for 3 minutes, four to five deep breaths,
or eight maximal breaths over a I-minute period) before
any anticipated period of apnea (such as induction of
general anesthesia) is recommended.
Nervous System Changes
Anesthetic requirements (minimum alveolar concentration
[MAC]) for volatile anesthetics decrease during pregnancy
as demonstrated in humans and animals.s The sedative
effects produced by progesterone may be partially responsible.
The important clinical implication of decreased
MAC is that alveolar concentrations of inhaled drugs that
would not produce unconsciousness in nonpregnant
patients may approximate anesthetizing concentrations in
pregnant women. This degree of central nervous system
depression can impair protective upper airway reflexes
and subject pregnant women to pulmonary aspiration.
Furthermore, the decreased FRC increases the rate at which
potential excessive alveolar concentrations of anesthetics
can be achieved.
Engorgement of epidural veins as intra-abdominal pressure
increases with progressive enlargement of the uterus
results in a decrease in the size of the epidural space and
decreased volume of cerebrospinal fluid (CSF) in the
subarachnoid space. The decreased volume of these spaces
facilitates the spread of local anesthetics. The observation
of increased spread of local anesthetic solutions
placed in the epidural space as early as the first trimester
suggests a role for biochemical as well as mechanical
changes. Indeed, data from pregnant women demonstrate
increased peripheral nerve sensitivity to lidocaine. These
mechanical and biochemical changes are consistent with
the decrease in dose requirements of local anesthetics
necessary for epidural or spinal anesthesia in pregnant
women at term gestation.
Renal Changes
Renal blood flow and the glomerular filtration
rate are
increased about 50% to 60% by the third month
of
pregnancy. Therefore, the normal upper limits in
blood urea nitrogen and serum creatinine
concentrations are
decreased about 50% in pregnant women.
Hepatic Changes
Plasma protein concentrations are reduced during pregnancy
because of dilution, similar to the physiologic anemia
of pregnancy. Decreased serum albumin levels can result
in higher free blood levels of highly protein-bound drugs.
Slightly elevated liver function test results do not necessarily
indicate hepatic disease. Plasma cholinesterase
(pseudocholinesterase) activity is decreased about 25%
from the 10th week of gestation to as long as 6 weeks
postpartum. This decreased activity is unlikely to be associated
with significant prolongation of the neuromuscular
blocking effects of succinylcholine or mivacurium. As
part of the hypercoagulable state of pregnancy, plasma
concentrations of coagulation factors, including fibrinogen,
are increased.
Gastrointestinal Changes
Gastrointestinal changes during pregnancy make pregnant
women vulnerable to regurgitation of gastric contents
and to the development of acid pneumonitis should
pulmonary aspiration occur. Displacement of the pylorus
cephalad by the enlarged uterus retards gastric emptying,
and progesterone decreases gastrointestinal motility. As a
result, gastric fluid volume tends to be increased even in
the fasting state. In addition, gastrin, which is secreted by
the placenta, stimulates gastric hydrogen ion secretion
such that the pH of gastric fluid is predictably low in
pregnant women. The enlarging uterus changes the angle
of the gastroesophageal junction and thereby leads to
relative incompetence of the physiologic sphincter
mechanism. For this reason, gastric fluid reflux into the
esophagus with subsequent esophagitis (heartburn) is
common in pregnant women.
RISK OF ASPIRATION
Regardless of the time interval since the ingestion of food,
women in labor must be treated as having a full stomach.
Pain, anxiety, and drugs (especially opioids) administered
during labor can all slow gastric emptying beyond an
already prolonged transit time.
The increased risk for pulmonary aspiration of gastric
contents is the reason for recommending placement of a
cuffed tube in the trachea of pregnant women rendered
unconscious by anesthesia. The recognition that the pH
of inhaled gastric fluid is important in the production and
severity of acid pneumonitis is the basis for the administration
of antacids to pregnant women before induction
of anesthesia. To obviate the hazards of inhalation of
particulate antacids that can increase pulmonary damage,
the use of a nonparticulate antacid such as sodium citrate
is recommended.
H2 receptor antagonists usually increase gastric fluid pH in pregnant women without
producing
adverse effects and are recommended by some. 1-12receptor
antagonists, unlike antacids, do not alter the pl-l of gastric
fluid already present in the stomach. Combinations of an
1-12receptor antagonist and sodium citrate may be more
useful than an antacid alone for producing a persistent
increase in gastric fluid pH.
Metoclopramide can be useful for decreasing the gastric
fluid volume of pregnant women in active labor who
require general anesthesia and are considered to be at high
risk for increased gastric fluid volume (apprehension,
systemic opioid analgesia, recent solid food ingestion).
The gastric hypomotility associated with opioid administration,
however, may be resistant to treatment with
metoclopramide.
PHYSIOLOGY OF THE
UTEROPLACENTAL CIRCULATION
The placenta is a union of maternal and fetal tissue for
the purpose of physiologic exchange. Maternal blood is
delivered to the placenta by the uterine arteries, and fetal
blood arrives via two umbilical arteries. Nutrient-rich and
waste-free blood is delivered to the fetus through a single
umbilical vein.
Uterine Blood Flow
Uterine blood flow increases to about 700 mUmin (about
10% of cardiac output) at term gestation, with about 80%
of the uterine blood flow perfusing the intervillous space
(placenta) and 20% the myometrium. The uterine vasculature
is not autoregulated and remains essentially maximally
dilated under normal conditions during pregnancy.
Though capable of marked vasoconstriction in response
to a-adrenergic drugs, pregnancy is associated with reduced
uterine artery response and sensitivity to vasoconstrictors.
Uterine blood flow decreases because of decreased
uterine perfusion pressure as a result of systemic hypotension
(shock; general, epidural, or spinal anesthesia). Uterine
blood flow also decreases with aortocaval compression or
increased uterine venous pressure as a result of vena cava
compression (supine position) or uterine contractions
(particularly uterine hyperstimulation as may occur with
oxytocin administration or abruption). Epidural or spinal
anesthesia does not alter uterine blood flow as long as
maternal hypotension is avoided.
ephedrine
has been considered the drug of choice for the
treatment of hypotension caused by the
administration of regional
anesthesia to pregnant women.
Increased uterine vascular resistance with decreases in
uterine blood flow can also result from maternal stress or
pain that stimulates the endogenous release of
catecholamines. This response suggests that a regional
or general anesthetic may be protective to the fetus
in certain instances. Uterine contractions also decrease
uterine blood flow secondary to increased uterine venous
pressure.
PLacentaL Exchange
Placental exchange of substances occurs principally by
diffusion from the maternal circulation to the fetus and
vice versa. Diffusion of a substance across the placenta to
the fetus depends on maternal-to-fetal concentration
gradients, maternal protein binding, molecular weight,
lipid solubility, and the degree of ionization of that
substance. Minimizing the maternal blood concentration
of a drug is the most important method of limiting the
amount that ultimately reaches the fetus.
The high molecular weight and poor lipid solubility of
nondepolarizing neuromuscular blocking drugs result in
limited ability of these drugs to cross the placenta.
Succinylcholine has a low molecular weight but is highly
ionized and therefore does not readily cross the placenta.
Thus, during administration of a general anesthetic for
cesarean section, the fetus/neonate is not paralyzed.
Placental
transfer of barbiturates, local anesthetics, and opioids is
facilitated by the relatively low molecular weights of these
substances. Drugs that readily cross the blood-brain barrier
also cross the placenta.
FETAL UPTAKE
Fetal uptake of a substance that crosses the placenta is
facilitated by the lower pH (0.1 unit) of fetal than maternal
blood. The lower fetal pH means that weakly basic drugs
(local anesthetics, opioids) that cross the placenta in the
nonionized form will become ionized in the fetal circulation.
Because an ionized drug cannot readily cross the
placenta back to the maternal circulation, this drug will
accumulate in the fetal blood against a concentration
gradient. This phenomenon is known as ion trapping and
may explain the higher concentrations of lidocaine found
in the fetus when acidosis secondary to fetal distress is
present . Furthermore, conversion of lidocaine
to the ionized fraction maintains the concentration gradient
from the mother to the fetus for continued passage of
nonionized lidocaine to the fetus. Despite decreased enzyme
activity in comparison to adults, neonatal enzyme systems
are adequately developed to metabolize most drugs, with
the possible exception of mepivacaine.
UNIQUE CHARACTERISTICS OF THE FETAL
CIRCULATION
The unique characteristics of the fetal circulation influence
the distribution of drugs in the fetus and protect the vital
organs of the fetus from exposure to high concentrations
of drugs initially present in umbilical venous blood. For
example, about 75% of umbilical venous blood passes
through the liver such that significant portions of drugscan be
metabolized before reaching the fetal arterial
circulation for delivery to the heart and brain. Moreover,
drugs in the portion of umbilical venous blood that
enters the inferior vena cava via the ductus venosus will
be diluted by drug-free blood returning from the lower
extremities and pelvic viscera of the fetus.
ANESTHESIA FOR CESAREAN DELIVERY
Although the majority of cesarean deliveries are performed
with regional anesthesia, sometimes the severity of the fetal
condition (severe fetal heart rate deceleration) necessitates
the use of general anesthesia for its rapidity, and at
other times it is required when regional anesthesia is
contraindicated. Regardless, in preparation for cesarean
delivery, all pregnant women should receive an oral antacid
(nonparticulate such as sodium citrate) to reduce gastric
fluid pH. In addition, some anesthesiologists routinely
administer a drug to accelerate gastric emptying (metoclopramide)
or an H2 receptor antagonist (ranitidine), or
both, to reduce gastric acid production.
Spinal Anesthesia
For a pregnant woman without an epidural catheter, spinal
anesthesia is the most common regional anesthetic technique
used for cesarean delivery (Table 32-6). The block
is technically easier than an epidural anesthetic, more rapid
in onset, and more reliable in providing surgical anesthesia
from the mid thoracic level to the sacrum.The
incidence of post-dural puncture headache has become
low with the introduction of noncutting, "pencil-point"
spinal needles. However, maternal hypotension is more
likely and more profound with spinal anesthesia than with
epidural anesthesia because the onset of sympathectomy
is more rapid. Prehydration, avoidance of aortocaval
compression, and aggressive use of ephedrine (even as a
prophylactic) may minimize the risk for hypotension.
Spinal anesthesia can be safely used in patients with
preeclampsia.
Lumbar Epidural Anesthesia
Epidural anesthesia is an excellent choice for surgical
anesthesia when an indwelling, functioning epidural catheter
has been placed for labor analgesia. It is also ideal for
patients who cannot tolerate the sudden onset of sympathectomy
or in some patients with cardiac disease. The
volume and concentration of local anesthetic drugs used
for surgical anesthesia are larger than those used for labor
analgesia; however, the technique of catheter placement,
test dosing, and potential complications are similar. Typically,
the anesthesiologist attempts to provide sensory
anesthesia from the T4 level to the sacrum. This level of
anesthesia may not always alleviate the visceral pain associated
with peritoneal manipulation, and adjuvant drugs
may be necessary (see Table 32-5).
Local Anesthesia
Although cesarean delivery can be performed by local
infiltration, it is accompanied by considerable discomfort
and risks the possibility of local anesthetic overdose;
moreover, most obstetricians have not been trained to do
this. However, in rare circumstances of acute fetal distress,
when a regional block is inadequate, and when induction
of general anesthesia is considered dangerous (morbid
obesity), local infiltration can be helpful to at least deliver
the baby. General anesthesia can then be induced after
securing the patient's airway with appropriate techniques,
which may include awake fiberoptic tracheal innlbation.
General Anesthesia
General anesthesia is used in obstetric practice for cesarean
section, typically when regional anesthesia is contraindicated
(coagulopathy, certain cardiac lesions, hemorrhage)
or for emergencies (placental abruption, uterine rupture,
fetal bradycardia, prolapsed umbilical cord) because of its
rapid and predictable action (Table 32-7).
After rapid-sequence induction of anesthesia and placement
of a cuffed tracheal tube facilitated by the administration
of succinylcholine or a nondepolarizing neuromuscular
blocking drug, anesthesia is maintained by
inhalation of nitrous oxide and a volatile anesthetic, often
in combination with sedative-hypnotics or opioids (or both).
Nondepolarizing neuromuscular blocking drugs are
subsequently administered to facilitate surgery.
INDUCTION DRUGS
Thiopental
Thiopental (4 to 6 mg/kg IV) is the most commonly used
drug for induction of general anesthesia in obstetrics
because it renders the patient unconscious within 30
seconds of administration. This dose of thiopental has no
significant clinical impact on neonatal well-being. Neonatal
depression may, however, occur with higher doses of
thiopental, and cardiorespiratory supportive techniques
are necessary until the neonate can excrete the drug (may
take up to 48 hours).
Ketamine
Ketamine produces a rapid onset of anesthesia and, unlike
thiopental, increases systemic blood pressure, heart rate,
and cardiac output by central stimulation of the sympathetic
nervous system. Increased uterine tone and decreased
uterine blood flow can accompany excessively large doses
of ketamine. In contrast to thiopental, low doses of ketamine
(0.25 mglkg IV) have profound analgesic effects.
The undesirable psychotomimetic side effects (hallucinations,
bad dreams) associated with ketamine administrations
can be lessened by coadministration of benzodiazepines .
Many anesthesiologists consider ketamine the appropriate
drug for induction of anesthesia in a pregnant woman who
is actively hemorrhaging, has uncertain blood volume,
and is at risk for profound hypotension in response to
intravenous thiopental.
Etomidate
Etomidate, like thiopental, has a rapid onset of action
because
of its high lipid solubility, and redistribution results in a
relatively short duration of action. Although etomidate
has minimal effects on the cardiovascular system, unlike
thiopental and ketamine, it is painful on injection, induces
extrapyramidal motor activity, and thus is rarely used
in obstetrics.
PropofoI
The need to have syringes of induction drugs ready to
administer for rapid response to urgent situations requiring
induction of general anesthesia (fetal distress) detracts
from the value of preservative-free propofol in the obstetric
suite. For an elective cesarean section, this highly lipid soluble
drug results in rapid onset of action similar to thiopental and rapid and
complete recovery with less
residual sedative effect than is the case with thiopental.
Nevertheless, propofol has not been demonstrated to be
superior to thiopental in maternal or neonata] outcome.
Furthermore, propofol has been associated with maternal
bradycardia when administered with succinylcholine for
induction of general anesthesia for cesarean section.
MAINTENANCE OF ANESTHESIA
Maintenance of anesthesia for cesarean section often
includes the inhalation of 50% nitrous oxide in combination
with a low concentration of volatile anesthetic. A
volatile anesthetic is an important component of general
anesthesia for cesarean section because the incidence of
maternal recall of intraoperative events without these drugs
is unacceptably high. During a typical general anesthetic
for cesarean delivery, opioids are administered after the
baby is delivered to avoid the concern of placental
transfer to the neonate.
Placental transfer of volatile anesthetics is rapid because
they are nonionized, highly lipid-soluble substances of
low molecular weight. Fetal concentrations depend on
the concentration and duration of anesthetic administered
to the mother. If excessive concentrations of volatile
anesthetics are administered for prolonged periods,
neonatal effects of these drugs, as evidenced by flaccidity,
cardiorespiratory depression, and decreased tone, may be
anticipated. It is important to recognize that if neonatal
depression is due to transfer of anesthetic drugs, the infant
is merely lightly anesthetized and should respond easily
to simple treatment measures such as assisted ventilation
of the lungs to facilitate excretion of the inhalation anesthetic.
Rapid improvement of the infant should be expected,
and if it does not occur, it is important to search for other
causes of depression.
There may be confusion regarding the presence of fetal
distress, the use of general anesthesia, and subsequent
delivery of a depressed neonate. A depressed fetus is
likely to be associated with a depressed neonate, and
general anesthesia is selected because it is the most
rapidly acting anesthetic technique to allow cesarean
delivery. For a healthy fetus, the interval from
induction to delivery is not as important to neonatal
outcome as the interval from uterine incision to
delivery, when uterine blood flow may be
compromised and fetal asphyxia may occur. A long
time from induction to delivery may result in a lightly
anesthetized neonate, but not an asphyxiated neonate.
NEUROMUSCULAR BLOCKING DRUGS
Succinylcholine remains the neuromuscular blocking drug
of choice for obstetric anesthesia because of its rapid
onset and short duration of action. This depolarizing
neuromuscular blocking drug is normally hydrolyzed in
maternal blood by the enzyme pseudocholinesterase and
does not generally interfere with fetal neuromuscular
activity. If the hydrolytic enzyme is present either in
lowconcentration or in a genetically determined
atypical form,
prolonged maternal or neonatal respiratory depression
secondary to muscular paralysis can occur
Nondepolarizing neuromuscular blocking drugs are
titrated to response with the use of a peripheral nerve
stimulator. Under normal circumstances, the poorly
lipidsoluble,
highly ionized, non depolarizing neuromuscular
blocking drugs do not cross the placenta in amounts
signifIcant
enough to cause neonatal skeletal muscle weakness.
This placental impermeability is only relative, however,
and when large doses are given over long periods, as for
the treatment of maternal tetanus or status epilepticus,
neonatal neuromuscular blockade can occur.
The diagnosis of neonatal depression secondary to drug-induced
neuromuscular blockade may be made on the basis of the maternal
history (prolonged administration of neuromuscular blocking drugs,
history of atypical pseudocholinesterase), the response of the
mother to neuromuscular blocking drugs, and physical examination
of the newborn. A paralyzed neonate will have normal
cardiovascular function and good color, but no spontaneous
ventilatory movements or reflex responses, and skeletal muscle
flaccidity is present. The anesthesiologist can test the neonate with
a peripheral nerve stimulator and demonstrate the classic signs of
neuromuscular blockade. Treatment consists of respiratory support
until the neonate excretes the drug (may take up to 48 hours).
Antagonism of nondepolarizing neuromuscular blocking drugs with
cholinesterase inhibitors (neostigmine, edrophonium) may be
attempted, but adequate respiratory support is the mainstay of
treatment.