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Abstract
Physiological
Changes associated with Pregnancy
Cardiovascular
System
Hemodynamic
changes
Blood
Pressure
Respiratory
System
Lung
Volumes and Mechanics
Ventilation
Gastrointestinal
System
Endocrine
System
Renal System
Hepatic System
Teratology
and Teratogenicity
Drug Effects
Anesthetic Agents
Antibiotic Agents
 Abstract
Problems created by maternal and fetal trauma during pregnancy such as
road traffic accidents, pelvic fractures
and other severe trauma, both blunt and
penetrating, are discussed.
Assessment of maternal injuries and
fetal well-being prior to surgery is
reviewed.
Implications of the
physiological changes in pregnancy along
with the principle of teratology and other
adverse fetal affects associated with
commonly used analgesics, antibiotics and
some anesthetic agents are shown. Finally, the prevention of preterm birth which is a
major complication of trauma and/or
incidental surgery in a pregnant woman is
reviewed.
The pregnant trauma victim presents a unique challenge to the health
care team.
Two patients are being treated, and
expertise of care is needed for both. Physiological changes in pregnancy, along with concomitant
anatomic changes, are factors which may
alter injury response and necessitate
modified resuscitation techniques and
therapy.
Even societal trends for the
pregnant woman to continue active
employment and participation in most
activities may predispose her to an
increased risk of trauma from gait
instability secondary to pelvic
ligamentous laxity and/or increased
abdominal protuberance. Physicians must be knowledgeable about these changes to
ensure that appropriate and timely care is
rendered to the injured gravida.
Key Words: Pregnancy,
trauma, diagnosis, obstetric management,
anaesthetic considerations.
Short running title: "Two
lives at risk"
Physiological
Changes associated with Pregnancy
Cardiovascular System
Alterations in circulating blood volume and other blood factors accompany
the progressive growth of the foetus,
placenta, and uterus(1).
These cardiovascular changes begin
early during pregnancy and are probably
hormonally produced.
Both the plasma volume and the red
cell volume begin to increase between the
sixth and 12th weeks of pregnancy,
resulting at term in an increased plasma
volume of 40% to 50%, and a total blood
volume increase of 25% to 40%.
Since red blood cell volume only
increases by approximately 20%, there is a
"physiologic" decline in the red
blood cell count, hemoglobin, and
hematocrit.
The fibrinogen content increases
throughout pregnancy both in absolute
amounts and in relative concentrations,
the latter from between 250 and 350 mg/dL
to 450 mg/dL.
There is also a marked increase in
activity of several clotting factors,
rendering the blood hypercoagulable and
predisposing the pregnant woman to
thromboembolic phenomena.
The fibrinolytic system is usually reduced with the dilutional anemia
that often ensues, and administration of
iron and folic acid supplement restores
hemoglobin to relatively normal levels.
As stated, blood volume first
expands at 12 weeks' gestation, increases
rapidly during the second trimester, and
then increases more slowly during the
third trimester. This physiologic
hypervolemia may mask volume loss, giving
the clinician an unfounded sense of
security about the patient's hemodynamic
stability.
Hemodynamic Changes
Cardiac output begins to rise during the first trimester of pregnancy and
rapidly reaches a maximal increase of
about 30%, usually by 30 to 34 weeks.
The rise is produced by a 15%
increase in heart rate and a 35% increase
in stroke volume.
Investigational work performed on
women in the supine position indicated
that the cardiac output appeared to
decline by the 30th to 35th week, but this
is apparently produced by the supine
hypotensive syndrome:
the encroachment on the abdominal
great vessels by the enlarged uterus.
Cardiac output
when measured in the lateral decubitus
position during the last few weeks of
pregnancy has been shown to equal that
seen in the second trimester.
Maximum reduction of cardiac output
occurs in the supine position with less of
a decrease when the mother is sitting or
semi-recumbent.
During
early labor, cardiac output increases a
further 15% in response to catecholamine
secretions associated with the pain.
Augmented venous return also occurs
with each contraction when 300 to 500 mL
of blood is expelled into the circulation.
In the second and third stages of
labor, cardiac output is 45% and 80%
respectively above pre-labor values, and
returns to normal approximately two weeks
postpartum.
This immediate postpartum increase
in blood volume represents a major hazard
to patients at risk from circulatory
overload.
Blood
Pressure
There
is a decrease in peripheral vascular
resistance in midtrimester, yielding a mild
drop in systolic pressure and a more
significant drop in diastolic pressure.
An increase in blood pressure over
first trimester levels is not normal.
Respiratory System
Endotracheal
intubation in the parturient can be
difficult because of obesity, breast
enlargement, tongue size, and the presence
of a "bull neck."
Visualization of the cords may be
extremely difficult.
Laryngeal edema may involve the vocal
cords, allowing passage of only a
small-diameter endotracheal tube.
The respiratory tract is vascular
during pregnancy, and even minor trauma
inflicted during an attempt to secure the
airway can result in profuse bleeding from
the nose or pharynx.
Though general anesthesia is
frequently induced under emergency
conditions, most intubation problems can be
anticipated by a quick, thorough examination
of the airway. Lifting the shoulders with a wedge of some type (towels),
followed by putting adequate support under
the head to place it in the "sniffing
position," usually prevents the breasts
from obstructing the laryngoscope handle
during intubation.
A selection of laryngoscope blades
and a variety of sizes of endotracheal tubes
are necessary at all times.
Lung Volumes and Mechanics
Although
there is a trend toward change in all lung
volumes very early in pregnancy, the most
marked deviations occur in the second half
of gestation(2).
At term, the pregnant uterus measures
about 40 cm which thereby elevates the
diaphragm, producing a compensatory increase
in the antero-posterior and transverse
diameters of the chest.
Total lung capacity and vital
capacity usually do not alter.
Functional residual capacity (FRC) is
decreased, which can decrease oxygenation
because of the changed relationship to
closing volume.
Closing volume is the lung volume at
which the "end" airways close
during expiration.
This produces perfused but
non-ventilated alveoli.
If enough alveoli do not contribute
to gas exchange, shunting of deoxygenated
blood results in hypoxemia.
In young, healthy women, closing
volume is considerably less than functional
reserve capacity, although it steadily
increases with age.
Any factor that decreases functional
reserve capacity (obesity, general
anesthesia, or the supine, lithotomy, or
Trendelenburg positions), or that increases
closing volumes (advancing age, lung
disease), can result in airway closure
occurring during normal tidal ventilation.
Airway
resistance decreases during pregnancy due to
progesterone's relaxant effect on the
bronchial smooth muscle.
Maximum breathing capacity and
diffusing capacity remain unchanged.
Chest wall compliance, but not lung
compliance, decreases but returns to normal
immediately after delivery; this suggests
the change was related to increased
intra-abdominal mass.
Ventilation
Significant
hyperventilation occurs during pregnancy and
labor, beginning as early as eight to ten
weeks' gestation, probably in response to
hormonal influences.
Progesterone stimulates the central
respiratory centre, and high circulatory
levels of this hormone most likely account
for the hyperventilation in pregnancy.
A chronic respiratory alkalosis may
develop, secondary to this physiologic
hyperventilation(3).
Estrogen may further sensitize the
respiratory center's response to carbon
dioxide.
Minute volume usually has increased
by about 50% at term, mostly due to tidal
volume changes and not to respiratory rate.
Alveolar ventilation is about 70%
above non-pregnant levels.
In the first trimester, when
ventilation is only slightly increased, many
women complain of dyspnea.
Oxygen
consumption increases by 20% during
pregnancy and increases by as much as 100%
during labor.
This change reflects the needs of the
enlarging fetus, placenta and uterus as well
as the increased work demand on all organ
systems during labour.
Arterial
blood gases often reflect a mild respiratory
alkalosis, with PaCO2 levels in the range of
32 to 34 mmHg by the end of the first
trimester.
Arterial oxygen concentration (PaO2)
has been reported at various times as being
slightly elevated; from 102 to 104 mmHg, or
it may be normal or slightly subnormal
during pregnancy.
Metabolic acidosis can occur readily
during difficult labors or subsequent to
trauma because lactic acid and pyruvate may
accumulate in the face of diminished
buffering capacity and increased oxygen
consumption.
Gastrointestinal
System
During the course of pregnancy, the stomach
and intestines are gradually pushed upward
by the enlarging uterus.
Eventually the stomach assumes a
horizontal position with the polaris
displaced upward and posteriorly, thus
slowing the evacuation of gastric contents.
It has also been noted that gastric
retention of a watery meal is prolonged
from the 34th week onward.
Pain, anxiety, and administration of
narcotics and belladonna alkaloids may
further delay gastric emptying.
In labor, gastric motility is
further inhibited by fear and/or pain, and
the intragastric pressure is even more
elevated at term due to the mechanical
effects of the gravid uterus.
Bumm et al(4) found that the pressure
gradient across the lower esophageal
sphincter was only 7.3 cm H2O in pregnant
women symptomatic for heartburn, compared
with 27.6 cm H2O in those free from this
symptom and 22.7 cm H2O in non-pregnant
controls.
Pressure from the gravid uterus
causes compression of the stomach and
alters the angle of the gastroesophageal
junction.
The sphincter's ability to tighten
or constrict is impaired and makes reflux
more likely.
Gastric acidity is increased during
pregnancy and gastrin is produced in
greater amounts than during the
non-pregnant state.
Endocrine
System
Normal endocrine changes during pregnancy
usually do not produce problems for the
anesthesiologist(5).
During labor, stress and pain
results in significant increases in plasma
cortisol levels which can be prevented by
epidural anesthesia.
Endocrine disease is rare during
pregnancy, as fertility is often decreased
in association with these conditions. Thyroid disease is rare in pregnancy and may be difficult to
diagnose as symptoms are variable, and in
normal pregnancy the basic metabolic rate
and thyroid gland size increase, although
the patient will often have normal thyroid
function with unchanged levels of free
thyroxine and triiodothyronine.
Renal
System
The ureters dilate and renal pelves widen
by the end of the first trimester of
pregnancy.
Outside urinary blockade may be
produced by engorged vessels and the
enlarging uterus causing this obstruction.
By the 16th week of gestation, renal
blood flow and glomerular filtration rate
increase above non-pregnant levels by 60%
and 50%, respectively(6).
This rise accompanies the increases
in blood volume and cardiac output.
When the pregnancy reaches term,
renal blood flow drops slightly.
During normal pregnancy, the
increase in glomerular filtration rate (GFR)
causes more sodium and water to be
reabsorbed.
Glucosuria occurs because the
augmented GFR exceeds the tubular
reabsorption capacity of glucose.
Urinary protein excretion increases
from non-pregnant values of less than 150
mg/day to 300 to 400 mg/day, most likely as
a result of the increased GFR.
As a consequence of the increases in renal
blood flow and GFR, the creatinine, serum
urea nitrogen, and uric acid levels are one
half to two thirds of non-pregnant values.
Evaluation of the parturient must
take this into account, as laboratory data
that at other times would be within normal
limits may signify renal insufficiency
during pregnancy.
Hepatic
System
Hepatic blood flow remains unchanged but
function may be altered.
Bilirubin, serum glutamic
oxaloacetic transaminase, serum glutamic
pyruvic transaminase, lactic dehydrogenase,
alkaline phosphatase and sedimentation rate
levels may increase.
Serum cholinesterase activity decreases
early in pregnancy and remains low until
delivery.
The levels may remain low throughout
during the first postpartum week after
gradually returning to normal during the
puerperium.
Proposed etiologies for this change
include hemodilution, hepatic dysfunction,
hypoalbuminemia and elevated estrogen
levels.
It is important to establish whether
decreased cholinesterase levels result in
prolonged pharmacologic effects of drugs
metabolized by this enzyme.
One study compared the duration of
paralysis following succinylcholine
administration in 25 patients undergoing
Cesarean section and an equal number of
non-pregnant women(7). Although cholinesterase levels were lower in the pregnant
women, the
time to reach 90% recovery of twitch height
was the same in both groups.
These investigators and others have
concluded that unless gross overdosage of
succinylcholine occurs, prolongation of
effect should not be a problem during
pregnancy. However, in another study of 941 pregnant women, it was
reported that a higher percentage of women
had enzyme values below the critical level
which represented a high risk from
succinylcholine(8).
This study excluded women with
genotypes likely to render them sensitive
to succinylcholine when not pregnant.
It is obviously prudent to control
succinylcholine dosage carefully in the
parturient and to monitor neuromuscular
function with a nerve stimulator.
Pregnant or postpartum women with
genetically determined atypical or
decreased enzyme levels may be at
significant risk from prolonged
succinylcholine effect or toxic reaction
from other drugs metabolized by
cholinesterase.
Teratology
and Teratogenicity
Shepherd and Lemire(9) many years ago
discussed the following principle of
teratology of which all physicians caring
for pregnant patients should be aware:
"The period of development when
exposure to a teratogen occurs, controls to
a great extent the conceptus' sensitivity
to teratogenesis."
Discussion of the potential adverse fetal
affect to the wide array of drugs commonly
administered to surgical patients is beyond
the scope of this review.
Discussion here is limited to
commonly used analgesics, antibiotics, and
anesthetic agents and alterations in
arterial blood gas concentration.
Care should be taken and the
standard texts(10) utilized to confirm the
safety of all medications prescribed to
pregnant women.
However, it must be realized that
even those agents thought to be safe have
generally been studied in a relatively
small number of patients, and hence caution
is warranted when any therapeutic agent is
administered to a pregnant patient.
Drug
Effects
Anesthetic
Agents
The knowledge that many anesthetic agents
interfere with cell division(11) at
concentrations encountered in clinical
practice has raised concern that these
agents may be teratogenic, particularly
because
most drugs used during surgical anesthesia (except
skeletal-muscle relaxants) are transferred
rapidly across the placenta.
At present unfortunately, there is
no clear view of the actual teratogenic
affect of surgery or anesthesia on the
developing human embryo or fetus.
Because no adequate prospective
studies have been done involving humans, we
must rely on data from animal and
retrospective human studies.
Interpretation of animal studies is
difficult because of extreme variability in
drug-induced teratogenic effects among
various species, best exemplified by the
fact that the most notorious human
teratogen, thalidomide, produces few
congenital defects in rats and mice.
Furthermore, proof that a given
agent is teratogenic in humans requires
exposure of large numbers of persons to the
agent in question.
The teratogenicity of many inhalational
anesthetics including halothane, nitrous
oxide, methoxyflurane, diethyl ether,
cyclopropane and fluroxene has been studied
in a number of animal models, primarily the
chick and the rat.
Most authors have reported that
these agents cause a high incidence of both
intrauterine death and congenital
anomalies; however a few have been unable
to show any adverse effects.
In many of the reports showing
adverse outcomes, animals were subjected to
prolonged exposure to the anesthetic in
question, often at concentrations
considerably higher than those encountered
in clinical practice.
Stanaway(11) has concluded that
short exposure, even to high concentrations
of these inhalational agents, has little or
no proven adverse effects on reproduction.
Attempts have been made to assess the
reproductive toxicity of inhalational
anesthetics through epidemiologic
investigation of operating room personnel
who were chronically exposed to trace
concentrations of these agents.
A number of investigators have
suggested that there is an association
between chronic anesthetic gas exposure for
both congenital anomalies and spontaneous
abortions, but their findings have been
disputed by others(12).
Unfortunately,
the designs of many of these studies are
flawed and the data often difficult to
interpret.
However, in one careful study in
which bias in data collection was minimized
through use of registry information rather
than patient interviews or mailed
questionnaires (as done in most previous
studies), no increase in congenital
anomalies was seen in the offspring of
operating room personnel exposed to small
concentrations of anesthetic gases during
pregnancy.
Even if one accepts the hypothesis
that chronic exposure to low levels of
inhalational anesthetics during pregnancy
is harmful, the relevance to the gravid
surgical patient undergoing a brief, single
exposure remains dubious.
There are a few studies that have
critically evaluated the incidence of birth
defects in the infants of women who have
required general or regional anesthesia for
surgery during pregnancy.
However, investigations to date have
disclosed there is no evidence of an increase
in the rate of congenital
malformation(13-15).
Analgesic agents are frequently prescribed
for surgical patients, and two of the most
commonly used, meperidine and morphine,
appear to be safe when administered for
short periods.
Long-term narcotic use in pregnant
addicts has been associated with fetal
growth retardation, premature delivery, and
neonatal withdrawal syndrome(10).
Administration for anesthetic needs
in surgery is unlikely to produce such
effects.
Narcotics may be used when needed. However,
the use of codeine is of greater concern,
as several studies have suggested that this
drug is associated with an increased risk
of congenital anomalies(10).
Prescription of codeine should be
avoided, particularly during the first
trimester.
Neonatal respiratory depression may
be caused by any of the above narcotic
analgesics when used immediately before
delivery.
Controversy remains regarding the safety of
acetylsalicylic acid (aspirin) during
pregnancy.
Although several large retrospective
studies have shown an increased rate of
malformations in infants of mothers who
have consumed salicylates during gestation,
other studies, including the Collaborative
Perinatal Project, have failed to identify
such an association(11).
In utero constriction of the ductus
arteriosus and persistent pulmonary
hypertension of the newborn could
theoretically result from the prostaglandin
synthetase-inhibiting properties of aspirin
and other nonsteroidal anti-inflammatory
agents.
This complication has been reported with use of naproxen(10);
however, current data suggest that this is
not an important hazard for brief periods
of aspirin exposure.
Use of aspirin during the week
before delivery has been reported to affect
hemostasis in the neonate and increase the
incidence of intracranial hemorrhage in
premature infants(10,11).
Since surgical disease may be
associated with an increased risk of
premature delivery, aspirin should be used
with great caution in the gravid surgical
patient.
Acetaminophen provides an apparently
safe alternative when a mild analgesic or
an antipyretic is required(10).
Antibiotic
Agents
Antimicrobial prophylaxis, a common
perioperative practice, has been shown to
reduce the incidence of infection after
various surgical procedures.
Fortunately, the antibiotic agents
most commonly used in this setting, the
cephalosporins, have not been reported to
have significant adverse fetal effects.
The penicillins and erythromycin
appear to be equally safe, although the
estolate salt of the latter should be
avoided because of the potential
hepatotoxicity(10).
Although all the aminoglycosides
share a potential for fetal ototoxicity and
nephrotoxicity, such complications would be
expected to be a rare consequence of the
few doses required for prophylaxis.
Although rarely used for
prophylaxis, a number of antimicrobial
agents should be specifically avoided
during pregnancy unless there is no
appropriate alternative.
The tetracyclines are deposited in
fetal tissues undergoing calcification and
may result in permanent discoloration of
the teeth.
Intravenous tetracycline has also
been associated with acute fatty liver of
pregnancy and maternal death.
The sulfonamides do not appear to
pose a significant teratogenic risk;
however, because these drugs compete with
bilirubin for binding to albumin, they may
increase unbound plasma bilirubin levels
and cause neonatal kernicterus. Therefore, sulfonamides should not be used near term or when
there is a risk of premature delivery.
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