FORCEPS DELIVERY

Design of Forceps
These instruments basically consist of two crossing branches. Each branch has four components: blade, shank, lock,
and handle. Each blade has two curves. The cephalic curve conforms to the shape of the fetal head, and the pelvic
curve corresponds more or less to the axis of the birth canal (Fig. 231). Some varieties are fenestrated or
pseudofenestrated to permit a firmer hold on the fetal head.

Simpson forceps. Note the ample pelvic curve in the single blade above and the cephalic curve evident in the
articulated blades below. The fenestrated blade and the wide shank in front of the English-style lock characterize
the Simpson forceps.
The blades are connected to the handles by the shanks, which are either parallel as in Simpson forceps, or crossing as
in TuckerMcLane forceps. The common method of articulation, the English lock, consists of a socket located on the
shank at the junction with the handle, into which fits a socket similarly located on the opposite shank A sliding lock is
used in some forceps, such as Kielland forceps ( TuckerMcLane forceps. The blade is solid and the shank is narrow

Kielland forceps. The characteristic features are the sliding lock, minimal pelvic curvature, and light weight
Indications for Forceps
maternal indications include heart disease, pulmonary injury or compromise, intrapartum infection, certain neurological
conditions, exhaustion, or prolonged second-stage labor. The latter is defined by the American College of
Obstetricians and Gynecologists (2002) as more than 3 hours with, and more than 2 hours without, regional analgesia
in the nulliparous woman. In the parous woman, a prolonged second stage is defined as more than 2 hours with, and
more than 1 hour without, regional analgesia. Fetal indications for operative vaginal delivery with either forceps or
vacuum include prolapse of the umbilical cord, with the other requisites for instrument delivery present; premature
separation of the placenta; or a nonreassuring fetal heart rate pattern.
Prerequisites for Forceps Application
There are at least six prerequisites for successful application of forceps:
1.

2.

The head must be engaged. Extensive caput succedaneum formation and molding sometimes make
determination of the station of the fetal head difficult. When difficulties of station assignment occur, it is
important to realize that a "low-forceps" procedure may actually be a more difficult midforceps operation.
The fetus must present as a vertex or by the face with the chin anterior.

3.

The position of the fetal head must be precisely known.

4.

The cervix must be completely dilated.

5.

The membranes must be ruptured.

6.

There should be no suspected cephalicpelvic disproportion.

VACUUM EXTRACTION
Indications and Prerequisites

Generally, the indications and prerequisites for the use of the vacuum extractor for delivery are the same as for
forceps delivery (American College of Obstetricians and Gynecologists, 2000). The tendency to attempt vacuum
deliveries at stations higher than is usually attempted with forceps is worrisome (Broekhuizen and colleagues, 1987).
In a recent review of vacuum extraction, Koscica and Gimovsky (2002) concluded that CONTRAINDICATIONS TO
VACUUM EXTRACTION INCLUDE operator inexperience, inability to assess fetal position, high station, and suspicion
of cephalopelvic disproportion. Relative contraindications for delivery using vacuum extraction include face or other
nonvertex presentations, fetal coagulopathy, known macrosomia, and recent scalp blood sampling. Generally, vacuum
extraction is reserved for fetuses 34 weeks or older.
COMPARISON OF VACUUM EXTRACTION WITH FORCEPS
There have been numerous studies comparing vacuum extraction with forceps deliveries. Vacca and associates (1983)
cup vacuum extraction with forceps delivery. They reported a higher frequency of maternal trauma and blood loss in
the forceps group, but an increase in the incidence of neonatal jaundice in the vacuum group. Bofill and colleagues
(1996b) randomized 637 women to forceps versus vacuum extraction with the Mityvac M-cup. There were significantly
more third- and fourth-degree lacerations (29 versus 12 percent) in the forceps-delivered group. Conversely, the
incidence of shoulder dystocia and cephalohematomas was doubled in the vacuum group. Other investigators have
found decreased maternal trauma and similar neonatal morbidity in infants delivered by vacuum compared with
forceps (Berkus, 1985; Broekhuizen, 1987; Dell, 1985; Williams, 1991, and all their colleagues). Infants delivered with
forceps have more marks and bruising from the instrument (Johnson and associates, 2004). Although retinal
hemorrhage occasionally is seen with vacuum usage, it has no apparent long-term effects. Johanson and Menon
(2000b) analyzed 10 randomized trials and confirmed that vacuum extraction was associated with less maternal but
more fetal
BREECH PRESENTATION AND DELIVERY: INTRODUCTION
Specifically, the annual rate of breech presentation at delivery in nearly 150,000 infants delivered at Parkland
Hospital in the 10-year period ending in 2002 was 3.6 percent.
Delivery of the Aftercoming Head
The fetal head may be extracted with forceps or by one of the following maneuvers.
1.

Mauriceau Maneuver

2.

Prague Maneuver

If this is impossible, the fetus still may be delivered using the modified Prague maneuver, which, as practiced today,
consists of two fingers of one hand grasping the shoulders of the back-down fetus from below while the other hand
draws the feet up over the maternal abdomen
3.

Forceps to Aftercoming Head

Specialized forceps can be used to deliver the aftercoming head. Piper forceps, shown in or divergent Laufe forceps
may be applied electively or when the Mauriceau maneuver cannot be accomplished easily. The blades of the forceps
should not be applied to the aftercoming head until it has been brought into the pelvis by gentle traction, combined
with suprapubic pressure, and is engaged. Suspension of the body of the fetus in a towel effectively holds the fetus
and helps keep the arms out of the way.
CERVICAL CHANGES

The cervical modifications during phase 1 of parturition principally involve changes in the connective tissue. These
are accompanied by the invasion by inflammatory cells to the extent that the process has been likened to a state of
inflammation. Two complementary changes occur to its connective tissues as the cervix softens. The first change
relates to the state of the bundles of collagen fibers that act during most of gestation to provide rigid support. Late
in gestation there is an increase in collagen breakdown and a rearrangement of the collagen fiber bundles. This
process causes a decrease in the number and size of collagen bundles within the cervix. During this same period, there
are changes in the relative amounts of the various glycosaminoglycans, particularly hyaluronic acid, a compound
associated with the capacity of the cervix to retain water. The second change relates to the striking increase in the
amount of hyaluronic acid in the cervix, with a concomitant increase in water. In addition, there is a decrease in
dermatan sulfate, which is needed for collagen fiber cross-linking (Cabrol and associates, 1985). Other cervical
changes associated with softening include an increased production of cytokines that causes infiltration of leukocytes,
which also degrade collagen. The result of these changes is cervical thinning, softening, and relaxation, which allow the
cervix to initiate dilatation.
The exact mechanisms that lead to cervical ripening are still being defined, but several candidates have already been
used clinically. Prostaglandins E2 (PGE2) and F2 (PGF2) applied directly to the cervix will induce these same
maturational softening changes. Specifically, they cause modification of collagen and alterations in the relative
concentration of the glycosaminoglycans . This property is useful clinically, and prostaglandin preparations placed
intravaginally adjacent to the cervix effect cervical softening or "ripening" to facilitate the induction of labor. In
some species, but not humans, these events are induced by falling levels of progesterone. However, even in
humans, progesterone antagonists will cause cervical softening. As discussed later, humans may have developed unique
mechanisms to cause a localized decrease in progesterone action in the cervix and myometrium.
MYOMETRIAL CHANGES
Most relate to its state of contractility. These changes are manifest by a transition from a contractile state
characterized predominantly by occasional painless contractions to one in which more frequent contractions develop.
This shift probably results from alterations in the expression of key proteins that control myometrial contractility.
These have been termed the contraction-associated proteins (CAPs). During phase 1 there is a striking increase in
myometrial oxytocin receptors. There are increased numbers and surface areas of myometrial cell gap junction
proteins such as connexin-43. Together these changes result in increased uterine irritability and responsiveness to
uterotonins.
UTERINE CONTRACTIONS CHARACTERISTIC OF LABOR
The cause of the pain is not known definitely, but several possibilities have been suggested:
1.
2.

Hypoxia of the contracted myometrium (as in angina pectoris).

Compression of nerve ganglia in the cervix and lower uterus by the interlocking muscle bundles.

3.

Stretching of the cervix during dilatation.

4.

Stretching of the peritoneum overlying the fundus.

Compression of nerve ganglia in the cervix and lower uterine segment by the contracting myometrium is an especially
attractive hypothesis. Paracervical infiltration with a local anesthetic usually produces appreciable relief of pain
during subsequent contractions Uterine contractions are involuntary and, for the most part, independent of
extrauterine control. Neural blockage from epidural analgesia does not diminish their frequency or intensity.
Mechanical stretching of the cervix enhances uterine activity in several species, including humans. This phenomenon
has been referred to as the Ferguson reflex (Ferguson, 1941). The exact mechanism by which mechanical dilatation of

the cervix causes increased myometrial contractility is not clear. Release of oxytocin was suggested as the cause, but
this is not proven. Manipulation of the cervix and "stripping" the fetal membranes is associated with an increase in the
levels of prostaglandin F2 metabolite (PGFM) in blood which could also increase contractions.
The interval between contractions diminishes gradually from about 10 minutes at the onset of the first stage of labor
to as little as 1 minute or less in the second stage.
HYPERTENSIVE DISORDERS IN PREGNANCY: INTRODUCTION
Hypertensive disorders complicating pregnancy are common and form one of the deadly triad, along with hemorrhage
and infection, that contribute greatly to maternal morbidity and mortality. In 2001, according to the National Center
for Health Statistics, gestational hypertension was identified in 150,000 women, or 3.7 percent of pregnancies
(Martin and colleagues, 2002). Importantly, Berg and colleagues (2003) reported that almost 16 percent of 3201
pregnancy-related deaths in the United States from 1991 to 1997 were from complications of pregnancyrelated hypertension
Table 341. Diagnosis of Hypertensive Disorders Complicating Pregnancy

Gestational hypertension
BP 140/90 mm Hg for first time during pregnancy
No proteinuria
BP returns to normal < 12 weeks' postpartum
Final diagnosis made only postpartum
May have other signs or symptoms of preeclampsia, for example, epigastric discomfort or thrombocytopenia
Preeclampsia

Minimum criteria
BP 140/90 mm Hg after 20 weeks' gestation
Proteinuria 300 mg/24 hours or 1+ dipstick

Increased certainty of preeclampsia

BP 160/110 mg Hg
Proteinuria 2.0 g/24 hours or 2+ dipstick
Serum creatinine > 1.2 mg/dL unless known to be previously elevated
Platelets < 100,000/mm3
Microangiopathic hemolysis (increased LDH)
Elevated ALT or AST
Persistent headache or other cerebral or visual disturbance
Persistent epigastric pain
Eclampsia
Seizures that cannot be attributed to other causes in a woman with preeclampsia
Superimposed Preeclampsia (on chronic hypertension)
New-onset proteinuria 300 mg/24 hours in hypertensive women but no proteinuria before 20 weeks' gestation

A sudden increase in proteinuria or blood pressure or platelet count < 100,000/mm 3 in women with hypertension and
proteinuria before 20 weeks' gestation
Chronic Hypertension
BP 140/90 mm Hg before pregnancy or diagnosed before 20 weeks' gestation not attributable to gestational
trophoblastic disease

or
Hypertension first diagnosed after 20 weeks' gestation and persistent after 12 weeks' postpartum

ALT = alanine aminotransferase; AST = aspartate aminotransferase; BP = blood pressure; LDH = lactate dehydrogenase.
Adapted from National High Blood Pressure Education Program Working Group Report on High Blood Pressure in
Pregnancy (2000).
PREECLAMPSIA
This condition is best described as a pregnancy-specific syndrome of reduced organ perfusion secondary to
vasospasm and endothelial activation. Proteinuria is an important sign of preeclampsia, and Chesley (1985) rightfully
concluded that the diagnosis is questionable in its absence.
Thus, the minimum criteria for the diagnosis of preeclampsia are hypertension plus minimal proteinuria. The more
severe the hypertension or proteinuria, the more certain is the diagnosis of preeclampsia

Epigastric or right upper quadrant pain is thought to result from hepatocellular necrosis, ischemia, and edema that
stretches the Glisson capsule. This characteristic pain is frequently accompanied by elevated serum hepatic
transaminase levels and usually is a sign to terminate the pregnancy. The pain presages hepatic infarction and
hemorrhage or catastrophic rupture of a subcapsular hematoma. Fortunately, hepatic rupture is rare.
Thrombocytopenia is characteristic of worsening preeclampsia, and it probably is caused by platelet activation and
aggregation as well as microangiopathic hemolysis induced by severe vasospasm. Evidence of gross hemolysis such as
hemoglobinemia, hemoglobinuria, or hyperbilirubinemia is indicative of severe disease.
Other factors indicative of severe hypertension include cardiac dysfunction with pulmonary edema as well as obvious
fetal growth restriction
ECLAMPSIA
This condition is somewhat preventable, and its incidence has decreased in the United States because most women
now receive adequate prenatal care. For example, in the 15th edition of Williams Obstetrics (1976), for the prior 25year period, the incidence of eclampsia at Parkland Hospital was 1 in 700 deliveries. For the 4-year period from 1983
to 1986, it decreased to 1 in 1150 deliveries, and for the 3-year period ending in 1999, it was approximately 1 in 1750
deliveries (Alexander and associates, 2004). In the National Vital Statistics Report, Ventura and colleagues (2000)
estimated that the incidence of eclampsia in the United States in 1998 was about 1 in 3250. In the United Kingdom in
1992, Douglas and Redman (1994) reported that the incidence of eclampsia was 1 in 2000.

ETIOLOGY
Any satisfactory theory concerning the etiology and pathophysiology of preeclampsia must account for the
observation that hypertensive disorders due to pregnancy are very much more likely to develop in women who:
1.
2.

Are exposed to chorionic villi for the first time.

Are exposed to a superabundance of chorionic villi, as with twins or hydatidiform mole.

3.

Have preexisting vascular disease.

4.

Are genetically predisposed to hypertension developing during pregnancy

According to Sibai (2003), currently plausible potential causes include the following:
1.
2.

Abnormal trophoblastic invasion of uterine vessels.

Immunological intolerance between maternal and fetoplacental tissues.

3.

Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy.

4.

Dietary deficiencies.

5.

Genetic influences.

Abnormal Trophoblastic Invasion

In normal implantation, the uterine spiral arteries undergo extensive remodeling as they are invaded by endovascular
trophoblasts. In preeclampsia, however, there is incomplete trophoblastic invasion. In this case, decidual vessels, but
not myometrial vessels, become lined with endovascular trophoblasts. Meekins and co-workers (1994) described a
continuum in the number of spiral arteries with endovascular trophoblasts in placentas of normal women and in those
with preeclampsia. Madazli and colleagues (2000) showed that the magnitude of defective trophoblastic invasion of
the spiral arteries correlated with the severity of the hypertensive disorder.
Using electron microscopy, De Wolf and co-workers (1980) examined arteries taken from the uteroplacental
implantation site. They observed that early preeclamptic changes included endothelial damage, insudation of plasma
constituents into vessel walls, proliferation of myointimal cells, and medial necrosis. They found that lipid accumulates
first in myointimal cells and then in macrophages. such lipid-laden cells and associated findings have been termed
atherosis (Hertig, 1945). Typically, the vessels affected by atherosis develop aneurysmal dilatation and are frequently
found in association with spiral arterioles that have failed to undergo normal adaptation (Khong, 1991). Obstruction of
the spiral arteriolar lumen by atherosis may impair placental blood flow. It is thought that these changes cause
placental perfusion to be pathologically diminished, which eventually leads to the preeclampsia syndrome (Lain and
Roberts, 2002; Redman and Sargent, 2003).

Immunological Factors

There is circumstantial evidence to support the theory that preeclampsia is immune mediated. Certainly the
microscopic changes at the maternalplacental interface are suggestive of acute graft rejection (Labarrere, 1988).
There are also inferential data. For example, the risk of preeclampsia is appreciably enhanced in circumstances where

formation of blocking antibodies to placental antigenic sites might be impaired. This may arise in situations in which
effective immunization by a previous pregnancy is lacking, as in first pregnancies; or in which the number of antigenic
sites provided by the placenta is unusually great compared with the amount of antibody, as with multiple fetuses
(Beer, 1978). "Immunization" from a prior abortion does not seem to occur. The immunization concept was supported
by their observations that preeclampsia developed less often in multiparas who had a prior term pregnancy. Other
studies have shown that multiparous women impregnated by a new consort have an increased risk of preeclampsia
(Mostello and co-workers, 2002; Trupin and colleagues, 1996).
Dekker and Sibai (1998) have reviewed the possible role of immune maladaptation in the pathophysiology of
preeclampsia. Beginning in the early second trimester, women destined to develop preeclampsia have a significantly
lower proportion of helper T cells (Th1) compared with that of women who remain normotensive (Bardeguez and
associates, 1991). This Th1/Th2 imbalance, with Th2 dominance, may be mediated by adenosine, which is found in higher
serum levels in preeclamptic compared with normotensive women (Yoneyama and co-workers, 2002). These helper T
lymphocytes secrete specific cytokines that promote implantation, and their dysfunction may favor preeclampsia
(Hayashi and associates, 2004; Whitecar and colleagues, 2001).
In women with anticardiolipin antibodies, placental abnormalities and preeclampsia develop more commonly (see Chap.
54, Pathophysiology of Antiphospholipid Antibodies in Pregnancy). This, however, was recently challenged by Branch
and associates (2001). According to Katano and colleagues (1996), antibodies associated with 2-glycoprotein I appear
most relevant. Immune complexes and anti-endothelial cell antibodies may also be involved (Taylor and Roberts, 1999).

The Vasculopathy and the Inflammatory Changes

In many ways, inflammatory changes are a continuation of the placental cause(s) discussed above. In response to
placental factors released by ischemic changes, or any other inciting cause, a cascade of events is set in motion
(Redman and Sargent, 2003). The decidua also contains an abundance of cells that, when activated, can release
noxious agents (Staff and colleagues, 1999). These then serve as mediators to provoke endothelial cell injury.
Redman and colleagues (1999) have proposed that the endothelial cell dysfunction associated with preeclampsia can
result from a "generalized perturbation of the normal, generalized maternal intravascular inflammatory adaptation to
pregnancy" (Fig. 343). In this hypothesis, preeclampsia is considered a disease due to an extreme state of activated
leukocytes in the maternal circulation (Faas and colleagues, 2000; Gervasi and co-workers, 2001). Briefly, cytokines
such as tumor necrosis factor- (TNF-) and the interleukins may contribute to the oxidative stress associated with
preeclampsia. Oxidative stress is characterized by reactive oxygen species and free radicals that lead to formation
of self-propagating lipid peroxides (Manten and associates, 2005). These in turn generate highly toxic radicals that
injure endothelial cells, modify their nitric oxide production, and interfere with prostaglandin balance.

Nutritional Factors

A number of dietary deficiencies or excesses over the centuries have been blamed as the cause of eclampsia. Dietary
taboos that have included meat, protein, purines, fat, dairy products, salt, and other elements have been advocated at
times. Observations and theories led to studies of dietary deprivation of various sorts that many times were models
of absurdity. In more recent times, sanity and a scientific approach have prevailed. For example, blood pressure in
nonpregnant individuals is affected by a number of dietary influences, including minerals and vitamins. Some studies
have shown a relationship between dietary deficiencies and the incidence of preeclampsia. This was followed by
studies of supplementation with various elements such as zinc, calcium, and magnesium to prevent preeclampsia.
Other studies, such as the one by John and co-workers (2002), showed that in the general population a diet high in
fruits and vegetables that have antioxidant activity is associated with decreased blood pressure. This is related to
the case-control study by Zhang and associates (2002) cited above, in which the incidence of preeclampsia was
doubled in women whose daily intake of ascorbic acid was less than 85 mg.

As previously discussed, obesity is a potent risk factor for preeclampsia (see also Chap. 43, Preeclampsia). Evidence
has accrued that obesity in nonpregnant individuals causes endothelial activation and a systemic inflammatory
response associated with atherosclerosis (Ross, 1999). In the study of pregnant women by Wolf and colleagues (2001),
C-reactive protein, an inflammatory marker, was shown to be increased in obesity, which in turn was associated with
preeclampsia.

Genetic Factors

The predisposition to hereditary hypertension undoubtedly is linked to preeclampsia (Ness and colleagues, 2003), and
the tendency for preeclampsiaeclampsia is inherited. Chesley and Cooper (1986) studied sisters, daughters,
granddaughters, and daughters-in-law of eclamptic women and concluded that preeclampsiaeclampsia is highly
heritable. The single-gene model, with a frequency of 0.25, best explained their observations.
PATHOGENESIS
Vasospasm
The concept of vasospasm was advanced by Volhard (1918) based on direct observations of small blood vessels in the
nail beds, ocular fundi, and bulbar conjunctivae. It was also surmised from histological changes seen in various
affected organs (Hinselmann, 1924; Landesman and co-workers, 1954). Vascular constriction causes resistance and
subsequent hypertension. At the same time, endothelial cell damage causes interstitial leakage through which blood
constituents, including platelets and fibrinogen, are deposited subendothelially. Wang and colleagues (2002) have also
demonstrated disruption of endothelial junctional proteins. Suzuki and co-workers (2003) demonstrated
ultrastructural changes in the subendothelial region of resistance arteries in preeclamptic women. With diminished
blood flow because of maldistribution, ischemia of the surrounding tissues would lead to necrosis, hemorrhage, and
other end-organ disturbances characteristic of the syndrome. Ironically, vasospasm may be worse in women with
preeclampsia than in those with the HELLP syndrome (Fischer and colleagues, 2000).
Endothelial Cell Activation
Over the past two decades, endothelial cell activation has become the centerpiece in the contemporary understanding
of the pathogenesis of preeclampsia (see Fig. 343). In this scheme, unknown factor(s), likely from the placenta, are
secreted into the maternal circulation and provoke activation and dysfunction of the vascular endothelium. The clinical
syndrome of preeclampsia is thought to result from these widespread endothelial cell changes (Hayman and
associates, 2000; Roberts, 2000; Walker, 2000).
Intact endothelium has anticoagulant properties, and it also blunts the response of vascular smooth muscle to agonists
by releasing nitric oxide. Damaged or activated endothelial cells secrete substances that promote coagulation and
increase the sensitivity to vasopressors. Further evidence of endothelial activation includes the characteristic
changes in glomerular capillary endothelial morphology, increased capillary permeability, and elevated blood
concentrations of substances associated with such activation. These latter substances are transferrable, and serum
from women with preeclampsia stimulates cultured endothelial cells to produce greater amounts of prostacyclin than
serum from normal pregnant women.
Increased Pressor Responses
Normally, pregnant women develop refractoriness to infused vasopressors (Abdul-Karim and Assali, 1961). Women with
early preeclampsia, however, have increased vascular reactivity to infused norepinephrine and angiotensin II (Raab and
co-workers, 1956; Talledo and associates, 1968). Moreover, increased sensitivity to angiotensin II clearly precedes
the onset of gestational hypertension (Fig. 344).

PATHOPHYSIOLOGY

Cardiovascular System
Severe disturbances of normal cardiovascular function are common with preeclampsia or eclampsia. These are related
to (1) increased cardiac afterload caused by hypertension; (2) cardiac preload, which is substantively affected by
pathologically diminished hypervolemia of pregnancy or is iatrogenically increased by intravenous crystalloid or oncotic
solutions; and (3) endothelial activation with extravasation into the extracellular space, especially the lung (see Chap.
42, Etiology). In addition, left ventricular mass is increased relative to normal pregnancy (Borghi and colleagues,
2000).
Hemodynamic Changes
Blood Volume It has been known for over 75 years that hemoconcentration is a hallmark of eclampsia

Blood and Coagulation

Hematological abnormalities develop in some women with preeclampsia. Among these are thrombocytopenia, which at
times may become so severe as to be life threatening. In addition, the levels of some plasma clotting factors may be
decreased, and erythrocytes may display bizarre shapes and undergo rapid hemolysis.
Thrombocytopenia results from platelet activation, aggregation, and consumption that is accompanied by increased
mean platelet volume and decreased life span (Harlow and colleagues, 2002). Levels of platelet-activating factor are
increased (Rowland and co-workers, 2000). Platelet production is increased, and thrombopoietin, a cytokine that
promotes platelet proliferation from megakaryocytes, is increased in preeclampsia with thrombocytopenia (Frolich and
associates, 1998). Paradoxically, in most studies, platelet aggregation is decreased compared with the normal increase
seen in pregnancy (Baker and Cunningham, 1999). This likely is due to platelet "exhaustion" following in vivo activation.
Although the cause(s) is unknown, immunological processes or simply platelet deposition at sites of endothelial damage
may be implicated (Pritchard and colleagues, 1976). Platelet-bound and circulating plateletbindable immunoglobulins
are increased, which suggest platelet surface alterations (Samuels and colleagues, 1987).
Uric Acid Elevated serum uric acid levels due to decreased renal urate excretion are frequently found in women with
preeclampsia
Glucocorticoids In attempts to enhance fetal lung maturation, glucocorticoids have been administered to women with
severe hypertension who are remote from term.
There has been only one randomized clinical trial of corticosteroids given to hypertensive women for fetal lung
maturation (Amorim and associates, 1999). This trial included 218 women with severe preeclampsia between 26 and 34
weeks who were randomly assigned to be given betamethasone or placebo. Neonatal complications, including
respiratory distress, intraventricular hemorrhage, and death, were decreased significantly when betamethasone was
given compared with placebo. But two maternal deaths and 18 stillbirths occurred
ECLAMPSIA Preeclampsia complicated by generalized tonicclonic convulsions is termed eclampsia. Fatal coma without
convulsions has also been called eclampsia
Major complications included placental abruption (10 percent), neurological deficits (7 percent), aspiration pneumonia
(7 percent), pulmonary edema (5 percent), cardiopulmonary arrest (4 percent), acute renal failure (4 percent), and
maternal death (1 percent).
PHARMACOLOGY AND TOXICOLOGY OF MAGNESIUM SULFATE

Magnesium sulfate USP is MgSO4 7H2O and not MgSO4. Parenterally administered magnesium is cleared almost totally
by renal excretion, and magnesium intoxication is avoided by ensuring that urine output is adequate, the patellar or
biceps reflex is present, and there is no respiratory depression. Eclamptic convulsions are almost always prevented by
plasma magnesium levels maintained at 4 to 7 mEq/L (4.8 to 8.4 mg/dL, or 2.0 to 3.5 mmol/L).
Patellar reflexes disappear when the plasma magnesium level reaches 10 mEq/L (about 12 mg/dL) presumably
because of a curariform action. This sign serves to warn of impending magnesium toxicity, because a further increase
leads to respiratory depression. When plasma levels rise above 10 mEq/L, respiratory depression develops, and at
12 mEq/L or more, respiratory paralysis and arrest follow. Somjen and co-workers (1966) induced in themselves, by
intravenous infusion, marked hypermagnesemia, achieving plasma levels up to 15 mEq/L.
UTERINE EFFECTS Magnesium ions in relatively high concentration depress myometrial contractility both in vivo and
in vitro.High concentrations of extracellular magnesium have been reported not only to inhibit calcium entry into
myometrial cells but to also lead to high intracellular magnesium levels.
This latter effect has been reported to inhibit calcium entry into the cellpresumably by blocking calcium channels
(Mizuki and associates, 1993). These mechanisms for inhibition of uterine contractility appear to be dose
dependent, because serum magnesium levels of at least 8 to 10 mEq/L are necessary to inhibit uterine
contractions (Watt-Morse and associates, 1995). This likely explains why there is no uterine effect clinically when
magnesium sulfate is given for treatment or prophylaxis of eclampsia.