++
Pregnancy and parturition are considered “high risk” when accompanied
by conditions unfavorable to the well-being of the mother or fetus, or both.
Maternal problems may be related to the pregnancy, that is,
preeclampsia-eclampsia, hypertensive disorders of pregnancy, or antepartum
hemorrhage resulting from placenta previa or abruptio placentae. Diabetes
mellitus; cardiac, chronic renal, and neurologic problems; sickle cell
disease; asthma; obesity; and drug abuse are not related to pregnancy but
often are affected by it. Prematurity (gestation of less than 37 weeks),
postmaturity (42 weeks or longer), intrauterine growth retardation, and
multiple gestation are fetal conditions associated with risk. During labor
and delivery, fetal malpresentation (eg, breech, transverse lie), placental
abruption, compression of the umbilical cord (eg, prolapse, nuchal cord),
precipitous labor, or intrauterine infection (eg, prolonged rupture of
membranes) may increase the risk to the mother or fetus.
++
In general, the anesthetic management of the high-risk parturient is
based on the same maternal and fetal considerations as for the management of
healthy mothers and fetuses. However, there is less room for error because
many of these functions may be compromised before the induction of
anesthesia. For example, significant acidosis is prone to develop in fetuses
of diabetic mothers when delivered by cesarean section with spinal
anesthesia complicated by even brief maternal hypotension.
+++
Preeclampsia-Eclampsia
+++
Pathophysiology and Signs and Symptoms
++
Hypertensive disorders occur in approximately 7% of all pregnancies
and are a major cause of maternal mortality. The most recent diagnostic
criterion for preeclampsia is referred to as “proteinaceous increase in
blood pressure.”96 The presence or absence of edema is no
longer considered on of the required criteria. Rather than a specific blood
pressure elevation, a blood pressure that is consistently 15% above
baseline is now considered diagnostic. The added appearance of convulsions
is diagnostic for eclampsia.96 Preeclampsia-eclampsia is a
disease unique to humans, occurring predominantly in young nulliparous
women. Symptoms usually appear after the 20th week of gestation,
occasionally earlier with a hydatidiform mole.
++
The origin of preeclampsia-eclampsia is unknown, but all patients
manifest placental ischemia. Placental ischemia results in a release of
uterine renin, an increase in a release of uterine renin, an increase in
angiotensin activity, and a widespread arteriolar vasoconstriction causing
hypertension, tissue hypoxia, and endothelial damage (Figure
53–7). Fixation of platelets at sites of endothelial damage results in
coagulopathies, occasionally in disseminated intravascular coagulation.
Enhanced angiotensin-mediated aldosterone secretion leads to an increased
sodium reabsorption and edema. Proteinuria, a sign of preeclampsia, is also
attributed to placental ischemia, which would lead to local tissue
degeneration and a release of thromboplastin with subsequent deposition of
fibrin in constricted glomerular vessels. As a result, increased
permeability to albumin and other plasma proteins occurs. Furthermore, there
is a decreased production of prostaglandin E, a potent vasodilator secreted
in the trophoblast, which normally balances the hypertensive effects of the
rennin–angiotensin system.
++
++
Many of the symptoms associated with preeclampsia, including placental
ischemia, systemic vasoconstriction, and increased platelet aggregation, may
result from an imbalance between the placental production of prostacyclin
and thromboxane. During normal pregnancy, the placental produces equal
amounts of these two, but in a preeclamptic pregnancy, there is seven times
more thromboxane than prostacyclin.97 According to the
latest theory, endothelial cell injury is central to the development of
preeclampsia.98 This injury occurs as a result of reduced placental
perfusion, leading to a production and release of substances (possibly lipid
peroxidases) causing endothelial cell injury. Abnormal endothelial cell
function contributes to an increase in peripheral resistance and other
abnormalities noted in preeclampsia through a release of fibronectin,
endothelin, and other substances.
++
++
In severe preeclampsia-eclampsia, all major organ systems are affected
because of widespread vasospasm. Global cerebral blood flow is not
diminished, but focal hypoperfusion cannot be ruled out. Postmortem
examination has revealed hemorrhagic necrosis in the proximity of thrombosed
precapillaries, suggesting intense vasoconstriction. Edema and small foci of
degeneration have been attributed to hypoxia. Petechial hemorrhages are
common after the onset of convulsions. Symptoms related to the above changes
include headache, vertigo, cortical blindness, hyperreflexia, and
convulsions. Cerebral hemorrhage and edema are the leading causes of death
in preeclampsia-eclampsia, which together account for approximately 50%
of deaths. Heart failure may occur in severe cases as a result of peripheral
vasoconstriction and increased blood viscosity from hemoconcentration.
Decreased blood supply to the liver may lead to periportal necrosis of
variable extent and severity. Subcapsular hemorrhages account for the
epigastric pain encountered in severe cases.
++
In the kidneys, there is swelling of glomerular endothelial cells and
deposition of fibrin, leading to a constriction of the capillary lumina.
Renal blood flow and glomerular filtration rate decrease, resulting in
reduced uric acid clearance and, in severe cases, reduced clearance of urea
and creatinine. Although preeclampsia is accompanied by exaggerated
retention of water and sodium, the shift of fluid and proteins from the
intravascular into the extravascular compartment may result in hypovolemia,
hypoproteinemia, and hemoconcentration, which may be further aggravated by
proteinuria. The risk of uteroplacental hypoperfusion and poor fetal outcome
correlates with the degree of maternal plasma and protein depletion. The
mean plasma volume in women with preeclampsia was found to be 9% less
than normal, and in those with severe disease it was as much as 30–40%
below normal.99
++
Adherence of platelets at sites of endothelial damage may result in
consumption coagulopathy, which develops in approximately 20% of patients
with preeclampsia. Mild thrombocytopenia, with platelet count of
100,000–150,000 per mm, is the most common finding. Prolongation of
prothrombin and partial throboplastin times indicates consumption of
procoagulants. Bleeding time, prolonged in approximately 25% of patients
with normal platelet counts, is no longer considered a reliable test of
clotting.100 The HELLP syndrome is a particular form of
severe preeclampsia characterized by hemolysis,
elevated liver
enzymes, and low
platelets.
++
The goals of the management of the patient with preeclampsia-eclampsia are
to prevent or control convulsions, improve organ perfusion, normalize blood
pressure, and correct clotting abnormalities. The mainstay of anticonvulsant
therapy in the United States is magnesium sulfate. Its efficacy in
preventing seizures has been well substantiated, but its mechanism of action
remains controversial. The patient usually receives a loading dose of 4 g in
a 20% solution, administered over 5 minutes followed by a continuous
infusion of 1–2 g/h.
++
Antihypertensive therapy in preeclampsia is used to lessen the risk of
cerebral hemorrhage in the mother while maintaining, even improving, tissue
perfusion. Plasma volume expansion combined with vasodilation fulfills these
goals.101 Hydralazine is the most commonly used
vasodilator because it increases uteroplacental and renal blood flows.
Nitroprusside is used during laryngoscopy and intubation to prevent
dangerous elevations in blood pressure. Trimethaphan, a ganglion blocking
agent, is useful in hypertensive emergencies when cerebral edema and
increased intracranial pressure are a concern because it does not cause
vasodilation in the brain. Other agents that have been used to control
maternal blood pressure include α-methyldopa, nitroglycerine, and
now more frequently, labetalol.102
++
Consumption coagulopathy may require infusion of fresh whole blood, platelet
concentrates, fresh frozen plasma, and cryoprecipitate. Delivery is
indicated in refractory cases or if the pregnancy is close to term. In
severe cases, aggressive management should continue for at least 24–48
hours after delivery.
+++
Anesthesia Management
++
There are very few contraindications for epidural anesthesia in labor
and delivery. In the presence of severe clotting abnormalities or severe
plasma volume deficit, the risk:benefit ratio favors other forms of
anesthesia.103 In volume-depleted patients positioned with
left uterine displacement, epidural anesthesia does not cause an
unacceptable reduction in blood pressure and leads to a significant
improvement in placental perfusion.104 With the use of
radioactive xenon, it was shown that the intervillous blood flow increased
by approximately 75% after the induction of epidural analgesia (10 mL
bupivacaine 0.25%).105 The total maternal body
clearance of amide local anesthetics is prolonged in preeclampsia, and
repeated administration of these drugs can lead to higher blood
concentrations than in normotensive patients.106
++
For cesarean section delivery, the sensory level of regional anesthesia
must extend to T3-4, making adequate fluid therapy and left uterine
displacement even more vital. Epidural anesthesia has been preferred to
spinal anesthesia in preeclamptic women because of its slower onset of
action and controllability. The rapid onset of spinal anesthesia may be
associated with hypotension, particularly in a volume-depleted patient.
However, in two recent studies, the incidence of hypotension, perioperative
fluid and ephedrine administration, and neonatal conditions were found to be
similar in preeclamptic women who received either epidural or spinal
anesthesia for cesarean delivery.107,108 There is an
increased sensitivity to vasopressors in preeclampsia; therefore, lower
doses of ephedrine are usually required to correct hypotension.
+++
Antepartum Hemorrhage
++
Antepartum hemorrhage occurs most commonly in association with placenta
previa (abnormal implantation on the lower uterine segment and partial to
total occlusion of the internal cervical os) and abruptio placentae.
Placenta previa occurs in 0.11% of all pregnancies, resulting in up to
0.9% incidence of maternal and a 17–26% incidence of perinatal
mortality. It may be associated with abnormal fetal presentation, such as
transverse lie or breech. Placenta previa should be suspected whenever a
patient presents with painless, bright red vaginal bleeding, usually after
the seventh month of pregnancy. The diagnosis is confirmed by
ultrasonography. If the bleeding is not profuse and the fetus is immature,
obstetric management is conservative to prolong the pregnancy. In severe
cases or if the fetus is mature at the onset of the symptoms, prompt
delivery is indicated, usually by cesarean section. An emergency
hysterectomy may be required because of severe hemorrhage, even after the
delivery of the placenta, because of uterine atony. In patients who have
undergone prior uterine surgery, the risk of severe hemorrhage is even
greater owing to a higher incidence of placenta acreta (penetration of
myometrium by placental villi).
++
Abruptio placentae occurs in 0.2–2.4% of pregnant women, usually in
the final 10 weeks of gestation and in association with hypertensive
diseases. Complications include Couvelaire uterus (ie, when extravasated
blood dissects between the myometrial fibers), renal failure, disseminated
intravascular coagulation, and anterior pituitary necrosis (ie, Sheehan
syndrome). The maternal mortality is high (1.8–11.0%), and the perinatal
mortality rate is even higher (excess of 50%). The diagnosis of abruptio
placentae is based on the presence of uterine tenderness, hypertonus, and
vaginal bleeding of dark, clotted blood. Bleeding may be concealed if the
placental margins have remained attached to the uterine wall. Changes in the
maternal blood pressure and pulse rate, indicative of hypovolemia, may occur
if the blood loss is severe. Fetal movements may increase during acute
hypoxia and decrease if hypoxia is gradual. Fetal bradycardia and death may
ensue.
+++
Anesthesia Management
++
Establishment of invasive monitoring (arterial line, central venous
catheter) and blood volume replacement via a 14- or 16-gauge stimulating
needle is usually required. If clotting abnormalities exist, blood
components and fresh frozen plasma, cryoprecipitate, and platelet
concentrates may be required. Epidural anesthesia may be considered, but
general anesthesia is indicated in the presence of uncontrolled hemorrhage
and coagulation abnormalities.109
++
Preterm labor and delivery present a significant challenge to the
anesthesiologist because the mother and the infant may be at risk. The
definition of prematurity was altered to distinguish between the preterm
infant, born before the 37th week of gestation, and the
small-for-gestational-age infant, who may be born at term but whose weight
is more than 2 standard deviations below the mean. Although preterm
deliveries occur in 8–10% of all births, they account for approximately
80% of early neonatal deaths. Severe problems, such as respiratory
distress syndrome, intracranial hemorrhage, hypoglycemia, hypocalcemia, and
hyperbilirubinemia, are prone to develop in preterm infants.
++
Obstetricians frequently try to inhibit preterm labor to enhance fetal
lung maturity. Delaying delivery be even 24–48 hours may be beneficial if
glucocorticoids are administered to the mother to enhance fetal lung
maturity. Various agents have been used to suppress uterine activity
(tocolysis) such as ethanol, magnesium sulfate, prostaglandin inhibitors,
β-sympathomimetics, and calcium channel blockers.
β-Adrenergic drugs, such as ritodrine and terbutaline, are the most
commonly used tocolytics. Their predominant effect is
β2 receptor stimulation, which results in
myometrial inhibition, vasodilation, and bronchodilation. Numerous maternal
complications, that is, hypotension, hypokalemia, hyperglycemia, myocardial
ischemia, pulmonary edema, and death, have been reported.
+++
Anesthesia Management
++
Complications may occur because of interactions with anesthetic drugs
and techniques. With the use of regional anesthesia, peripheral vasodilation
caused by β-adrenergic stimulation increases the risk of hemodynamic
instability in the presence of preexisting tachycardia, hypotension, and
hypokalemia. The premature infant is known to be more vulnerable than the
term newborn to the effects of drugs used in obstetric analgesia and
anesthesia. However, there have been few systemic studies to determine the
maternal and fetal pharmacokinetics and dynamics of drugs throughout
gestation.
++
There are several postulated causes of enhanced drug sensitivity in the
preterm newborn: less protein available for drug binding; higher levels of
bilirubin, which may compete with the drug for protein binding; greater drug
access to the central nervous system because of a poorly developed
blood–brain barrier; greater total body water and lower fat content; and a
decreased ability to metabolize and excrete drugs. However, most drugs used
in anesthesia exhibit low to moderate degrees of binding in the fetal serum:
approximately 50% for bupivacaine, 25% for lidocaine, 52% for
meperidine, and 75% for thiopental.
++
In selection of the anesthetic drugs and techniques for delivery of a
preterm infant, concerns regarding drug effects on the newborn are far less
important than prevention of asphyxia and trauma to the fetus. For labor
vaginal delivery, well-conducted epidural anesthesia is advantageous in
providing good perineal relaxation. Before induction of epidural blockade,
the anesthesiologist should ascertain that the fetus is neither hypoxic nor
acidotic. Asphyxia results in a redistribution of fetal cardiac output,
which increases oxygen delivery to vital organs such as the brain, heart,
and adrenals. Regardless, these changes in the preterm fetus may be better
preserved with bupivacaine or chloroprocaine than with
lidocaine.110,111 Preterm infants with breech presentation
are usually delivered by cesarean section. Regional anesthesia can be
successfully used, with nitroglycerin available for uterine relaxation if
needed.
++
++
Regional analgesia during labor and vaginal delivery has become the
preferred technique of pain relief in selected high-risk patients because it
prevents obtundation of the mother and depression of the fetus and reduces
many of the potential adverse physiologic effects of labor, such as
increased oxygen consumption and hemodynamic alterations. For cesarean
section delivery, regional anesthesia has emerged as a safe and effective
technique in high-risk parturients, partly because of the added ability to
provide prolonged postoperative analgesia.