EMERGENCY MEDICINE

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PRACTICE
EMPRACTICE NET
AN EVIDENCE-BASED APPROACH TO EMERGENCY MEDICINE

Emergencies In The Second December 2004

Volume 6, Number 12

And Third Trimesters: Authors

Ruth Selvidge, MD

Hypertensive Disorders And Department of Emergency Medicine, Boston Medical

Center—Boston, MA.

Antepartum Hemorrhage Robert Dart, MD

Chief of Emergency Services, Quincy Medical Center—
Quincy, MA.
A 20-year-old woman, G1P0, who is 37-weeks pregnant, walks into your ED triage
area complaining of headache. Her BP is 170/100 and vital signs are otherwise Peer Reviewer
normal. As you are approaching her to obtain the history and physical, she collapses Jessica Freedman, MD
and begins having a tonic-clonic seizure. Associate Residency Director, Assistant Professor,
Department of Emergency Medicine, Mount Sinai

E
School of Medicine—New York, NY.
MERGENCY physicians are faced with complications of first-trimester
pregnancies, such as threatened and spontaneous abortions, as well as Andy Jagoda, MD, FACEP
ectopic pregnancy, on a daily basis. Complications of late pregnancy are Vice-Chair of Academic Affairs, Department of
less frequently managed in the ED, and therefore can be more intimidating Emergency Medicine; Residency Program Director,
to emergency physicians. However, the appropriate diagnosis and man- Mount Sinai School of Medicine—New York, NY.
agement of these conditions can significantly impact maternal and fetal
CME Objectives
outcomes. Thus it is important that emergency physicians remain abreast of
the clinical presentation, diagnosis, and management of the most common Upon completing this article, you should be able to:
complications of late pregnancy; namely, preeclampsia/eclampsia, placenta 1. Discuss the role of ultrasound in identifying
and/or excluding placenta previa or abruption
previa, and placental abruption. in patients presenting with second- or third-
trimester vaginal bleeding;
Terminology 2. Describe the management options for
Gestational hypertension is defined as a BP greater than 140/90, without pro- patients presenting with eclampsia or severe
teinuria, which returns to normal after delivery, and is not associated with preeclampsia;
3. Discuss the indications and contraindications to
any of the other features of preeclampsia. expectant management in patients diagnosed
Preeclampsia is defined as a BP greater than 140/90, associated with pro- with preeclampsia, placental abruption, and
teinuria (≥300 mg/24 hr, or persistent 1+ of dipsticks on multiple occasions). placental previa; and
Preeclampsia may be classified as mild or severe. Mild preeclampsia consists 4. List laboratory abnormalities that are frequently
of a DBP >90 but <110 and lacks any of the features of severe preeclampsia. identified in patients with severe preeclampsia.
Severe preeclampsia consists of a DBP ≥110 on 2 occasions, or after treat-
Date of original release: December 17, 2004.
ment with antihypertensive medication, and/or has any of the following
Date of most recent review: December 13, 2004.
features: oliguria, pulmonary edema, thrombocytopenia, severe proteinuria
See “Physician CME Information” on back page.
(≥3.5 gm/24hr, or 2 random UAs with 3+ protein by dipstick), right upper

Editor-in-Chief
Andy Jagoda, MD, FACEP, Vice-
Chair of Academic Affairs,
Department of Emergency
Medicine; Residency Program
Director; Director, International
Studies Program, Mount Sinai
School of Medicine, New York, NY.
Associate Editor
John M. Howell, MD, FACEP, Director
of Academic Affairs, Best Practices,
Inc., Inova Fairfax Hospital, Falls
Church, VA.
Editorial Board
William J. Brady, MD, Associate
Professor and Vice Chair,
Department of Emergency
Medicine, University of Virginia,
Charlottesville, VA.
Judith C. Brillman, MD, Professor,
Department of Emergency
Medicine, The University of
New Mexico Health Sciences
Center School of Medicine,
Albuquerque, NM.
Francis M. Fesmire, MD, FACEP,
Director, Heart-Stroke Center,
Erlanger Medical Center; Assistant
Professor of Medicine, UT College
of Medicine, Chattanooga, TN.
Valerio Gai, MD, Professor and
Chair, Department of Emergency
Medicine, University of Turin, Italy.
Michael J. Gerardi, MD, FAAP,
FACEP, Clinical Assistant
Professor, Medicine, University
of Medicine and Dentistry of
New Jersey; Director, Pediatric
Emergency Medicine, Children’s
Medical Center, Atlantic
Health System; Department of
Emergency Medicine, Morristown
Memorial Hospital.
Michael A. Gibbs, MD, FACEP,
Chief, Department of Emergency
Medicine, Maine Medical Center,
Portland, ME.
Gregory L. Henry, MD, FACEP,
CEO, Medical Practice Risk
Assessment, Inc., Ann Arbor, MI;
Clinical Professor, Department of
Emergency Medicine, University
of Michigan Medical School, Ann
Arbor, MI; Past President, ACEP.
Francis P. Kohrs, MD, MSPH, Lifelong
Medical Care, Berkeley, CA.
Keith A. Marill, MD, Emergency
Attending, Massachusetts
General Hospital; Faculty, Harvard
Affiliated Emergency Medicine
Residency, Boston, MA.
Michael S. Radeos, MD, MPH,
Attending Physician, Department
of Emergency Medicine, Lincoln
Medical and Mental Health Center,
Bronx, NY; Assistant Professor
in Emergency Medicine, Weill
College of Medicine, Cornell
University, New York, NY.
Steven G. Rothrock, MD, FACEP,
FAAP, Associate Professor of
Emergency Medicine, University
of Florida; Orlando Regional
Medical Center; Medical Director
of Orange County Emergency
Medical Service, Orlando, FL.
Robert L. Rogers, MD, FAAEM,
Assistant Professor of Surgery
and Medicine; Program Director,
Combined Emergency Medi-
cine/Internal Medicine Residency,
Department of Surgery/Division of
Emergency Medicine And Depart-
ment of Medicine, The University
of Maryland School of Medicine,
Baltimore, MD.
Alfred Sacchetti, MD, FACEP,
Research Director, Our Lady of
Lourdes Medical Center, Camden,
NJ; Assistant Clinical Professor
of Emergency Medicine, Thomas
Jefferson University, Philadelphia,
PA.
Corey M. Slovis, MD, FACP, FACEP,
Professor of Emergency Medicine
and Chairman, Department of
Emergency Medicine, Vanderbilt
University Medical Center; Medical
Director, Metro Nashville EMS,
Nashville, TN.
Charles Stewart, MD, FACEP, Colorado
Springs, CO.
Thomas E. Terndrup, MD, Professor
and Chair, Department of
Emergency Medicine, University
of Alabama at Birmingham,
Birmingham, AL.
 quadrant (RUQ) abdominal pain, CNS manifestations, with a low-lying placenta, the placenta is in close proximity
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such as headache, scotomata, blurred vision, or changes in to the internal os, but does not touch it.
mental status, and/or HELLP syndrome. HELLP syndrome The terms placenta accreta, increta, or percreta are used
is defined as hemolysis (abnormal peripheral smear, to describe a placenta that remains firmly attached to the
or bilirubin ≥1.2 mg/dL, or LDH ≥600), elevated liver lower uterine segment, and therefore does not deliver nor-
enzymes (aminotransferase ≥2X normal) and low platelets mally. These complications are seen in about 7% of cases
(platelet count <100,000µL).1,2 The above entities must be of placenta previa.8 These women are at increased risk of
distinguished from chronic hypertension, defined by a BP hemorrhage, hysterectomy, blood transfusions, and death.
>140/90 before 20-weeks gestation or prior to pregnancy, Mortality is as high as 10%.9
and/or hypertension which does not resolve postpartum.
Preeclampsia can be superimposed on chronic Critical Appraisal Of The Literature
hypertension, and these patients meet the criteria for
Obtaining Investigational Review Board approval for
both preeclampsia and chronic hypertension. In patients
studies involving pregnant women can be extremely
with chronic hypertension, a diagnosis of superimposed
difficult, resulting in too few randomized clinical tri-
preeclampsia is made when there is an increase in blood
als on these topics. A January 2004 MEDLINE search on
pressure or proteinuria over baseline, and/or evidence of
preeclampsia yielded over 7000 articles; however, this list
new end-organ damage. It is important to be aware that
was comprised of an abundance of retrospective and case-
these definitions are somewhat arbitrary. Preeclampsia is
control studies, with their well-defined weaknesses. Many
an unpredictable disease, and women with mild hyper-
studies had small sample sizes, as well, which makes
tension and minimal proteinuria can have a fulminant
the results even less compelling. An additional problem
course resulting in eclampsia. No studies have been
among preeclampsia papers is that the definitions for
able to identify an accurate method for predicting which
hypertension and preeclampsia are not uniform. Further-
women will progress to the more severe forms of HELLP
more, it is likely that preeclampsia is a syndrome, and
or eclampsia. In the past, edema was an important crite-
therefore arbitrary definitions do not adequately reflect the
rion for diagnosing preeclampsia, but studies reveal that
continuum of changes seen in the disease.3 Some authors
edema is as common in normal pregnancies, and therefore
believe that preeclampsia may represent several different
is not predictive of disease severity. Similarly, in the past
conditions, resulting in a variety of clinical presentations.10
an increase of 30 in the systolic BP or 10 in the diastolic BP
Another issue is raised when reviewing older studies;
would define preeclampsia, but studies have not shown
as the disease has become better understood, clinical
increased morbidity in these women, so the absolute value
definitions have changed, and therefore earlier studies
of blood pressure >140/90 is now the accepted criterion.3
may not reflect today’s definitions.3 For example, earlier
However, the American College of Obstetrics and Gy-
studies may have included women with chronic hyper-
necology (ACOG), as well as the National High Blood
tension among the preeclampsia group, or women with
Pressure Education Working Group, still recommend that
edema and changes in blood pressure that would not meet
women with edema or significant changes in their pre-
today’s criteria for preeclampsia. (See Table 1.)
natal blood pressure be followed closely.4 Finally, women
A number of practice guidelines and systematic
without proteinuria, but with elevated blood pressure and
reviews exist that are relevant to the management of these
evidence of new end-organ damage — in other words, any
conditions. The National High Blood Pressure Education
of the above-mentioned criteria for severe preeclampsia
Program Working Group has published guidelines on the
— should be considered preeclamptic and managed iden-
tically.5
Placental abruption, also called abruptio placentae, is
Table 1. Risk Factors For Preeclampsia.
defined as the premature separation of the placenta from Nulliparity
the uterus. It was first described in 1775 as bleeding into Chronic hypertension
the decidual basalis from abnormal small uterine arterial
Age under 20 or over 35
vessels.6,7 Bleeding from both arterial and venous origins
has been described. The resulting hematoma may be small Multiple pregnancy
and self-limited, resulting in a partial abruption, or it may Pregnancy assisted by reproductive technology
continue to dissect through decidual layers, resulting in Obesity
complete separation of the placenta from the underlying New paternity
uterus, a phenomenon called total abruption.
Preexisting vascular, autoimmune, or renal disease
Placenta previa refers to a placenta that is found to cov-
er, or be in close approximation to, the internal cervical os. Triploidy
There are 4 different degrees of previa. Total placenta previa Excessive weight gain in 3rd trimester
occurs when the internal os is completely covered by the Hydatidiform mole
placenta. Partial placenta previa means the internal os is
Family history of preeclampsia
partly covered by placenta. In marginal placenta previa, the
placental edge is at the margin of the internal os. Finally, History of placental abruption in prior pregnancy

Emergency Medicine Practice 2 EMPractice.net • December 2004

management of hypertension in pregnancy.3 In addition, mains elusive. There seem to be 2 phases to the syndrome:

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The American College of Obstetrics and Gynecology has first, a placental phase, followed by a second, systemic
published guidelines on the diagnosis and management of phase, with effects on multiple organs. The link between
both preeclampsia and eclampsia.4 A systematic review on the 2 phases has not been fully understood.
interventions for suspected placenta previa has been pub- In normal pregnancy, remodeling of the uterine spiral
lished in the Cochrane Database.11 And finally, a system- arteries (the terminal branches of the uterine artery) is
atic review has been published in the Cochrane Database accomplished by invasion of the arterioles by placental
on interventions for treating placental abruption.12 endovascular trophoblasts. The remodeling is completed
by the end of the 2nd trimester and results in a low-resis-
Epidemiology, Etiology, And Pathophysiology tance arteriolar system, which accommodates a 10-fold
increase in uterine blood flow. In preeclampsia many of
Prevalence
the arterioles escape remodeling, thus remaining thick and
About a quarter of all pregnant nulliparous women will
muscular. This leads to increased vascular resistance, and
develop a hypertensive disorder, and 5-10% will meet di-
secondarily decreased blood flow through the preeclamp-
agnostic criteria for preeclampsia.13 Eclampsia appears to
tic arterioles. Therefore these vessels are unable to meet
be decreasing in frequency, involving 1/700 deliveries in
the increasing blood flow demands of the fetus leading to
the 1970s, 1/1150 deliveries in the 1980s, and approximate-
placental ischemia.25 The placental ischemia in turn results
ly 1/2300 deliveries in the 1990s.14 This trend is thought to
in the release of certain vasoactive molecules, which act
be secondary to improving prenatal care, early detection
on the maternal vascular endothelium.26,27 Some authors
and delivery of preeclamptic mothers, and prophylactic
have also implicated oxygen free radicals as a contributing
use of magnesium sulfate. There is also evidence that the
factor in this process.28,29
onset of eclampsia is shifting towards the postpartum
Most authors feel that endothelial activation is the
period.15
final common pathway for the changes seen in preeclamp-
The incidence of placental abruption is about 6 per
sia. Endothelial activation has multiple effects, including:
1000 singleton births.16 It is a significant cause of maternal
release of endothelin and thromboxane, increased sensitiv-
and fetal morbidity and mortality. Perinatal mortality
ity to angiotensin II, and decreased formation of vasodila-
associated with abruption is 119 per 1000, births compared
tors, such as nitric oxide (NO) and prostacyclin. These
to about 8 per 1000 among all births.16 This condition is
changes are thought to be responsible for the preeclamptic
responsible for 12-25% of all perinatal deaths.16,17 Maternal
patient’s increased vascular sensitivity to pressors, which
complications include hemorrhage requiring transfusion,
results in hypertension, as well as the coagulation abnor-
shock, renal failure, disseminated intravascular coagu-
malities common in preeclampsia.30-32
lopathy, couvelaire uterus (also known as uteroplacental
A number of other factors have been proposed as con-
apoplexy) that on occasion requires hysterectomy, chorio-
tributors to the development of this syndrome. Multiple
amnionitis, and, rarely, death.18,19
studies have shown a genetic predisposition to preeclamp-
Neonatal complications include low birth weight or
sia. Women with sisters or mothers who had preeclamp-
small for gestational age,16 preterm birth,20 and prema-
sia have a 4-fold increased risk of severe preeclampsia,33
ture rupture of membranes (PROM).18,19 There is a 9-fold
while increased risk to women with preeclamptic (pa-
adjusted, relative risk of stillbirth with abruption. The rate
ternal) grandmothers has also been demonstrated.34 Still
of stillbirth significantly increases with severe placental
other studies suggest that an infectious etiology acts as a
abruption, defined as abruptions involving greater than
contributing factor.35-38 Finally, some studies suggest that
50% of the placenta.21
an immunologic factor specific to a presumed paternal
Placenta previa occurs in about 4/1000 singleton de-
antigen may play a role in the prevention of the develop-
liveries22 and causes death in about 0.03% of these cases.23
ment of preeclampsia in subsequent pregnancies involving
Serious maternal complications include intra- and postpar-
the same parents. Evidence for this mechanism includes
tum hemorrhage, hysterectomy, placental abruption, and
the fact that preeclampsia is more common in 1st pregnan-
blood transfusion. Pregnancies complicated with placenta
cies, and that it occurs more frequently in multiparous
previa necessitate cesarean delivery and also have been
women with new partners (ie, “new paternity”),39 and less
associated with higher rates of septicemia and thrombo-
frequently in women with a history of prior abortions.40
phlebitis.23,24 Most of the perinatal morbidity and mortal-
ity results from prematurity, since 47% of pregnancies
Risk Factors
with placenta previa must be delivered prior to full-term.
Many studies have documented risk factors for pre-
Placenta previa is occurring with increasing frequency and
eclampsia (Table 1). One of the most significant risk factors
authors speculate that this may be secondary to increasing
is nulliparity. In addition, preeclampsia is more common
rates of cesarean section, which is a prominent risk factor.
in women under the age of 20 or over the age of 35. Chron-
ic hypertension, multiple or IVF pregnancies, obesity,
Pathophysiology
prior history of severe preeclampsia or placental abrup-
Preeclampsia
tion, diabetes, excessive weight gain in pregnancy, and/or
Despite years of research the cause of preeclampsia re-
preexisting vascular, autoimmune, or renal diseases have

December 2004 • EMPractice.net 3 Emergency Medicine Practice

 all been implicated. Hydatiform mole has also been associ-
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ated with preeclampsia. As mentioned above, studies have
also shown increased risk in women with a family history
of preeclampsia and women with new partners.
Placental Abruption
The precise cause of placental abruption is not known,
but as with preeclampsia, a contributing factor is believed
to be the failure of the invading uterine spiral arteries to
transform from muscular arterioles into low-resistance
blood vessels. Placental ischemia is the result, predis-
posing placental blood vessels to rupture or to undergo
thrombosis. These changes can create a hematoma that
leads to placental separation. Likewise, the presence of un-
derlying vascular malformations has also been implicated
as a precipitating factor.41
Although the reason the placenta implants in an
improper position in the case of previas is unknown,
bleeding is thought to occur due to tearing of the placental
attachments during cervical dilation and formation of the
lower uterine segment. Also, the lower uterine segment is
unable to contract and minimize this bleeding.
Risk Factors
A history of previous abruption is the most significant risk
factor for recurrent abruption, increasing the risk by 10-
fold. Pregnancies complicated by hypertensive disorders
— including severe preeclampsia and eclampsia, preterm,
premature rupture of membranes, and polyhydramnios
— lead to increased risk of abruption. Women who smoke
or use cocaine have higher rates of abruption, as do
women with multifetal pregnancies. Placental abruption
is a common complication of trauma, as well. Finally, an
elevated maternal serum alpha fetoprotein (MSAFP) level
Table 2. Differential Diagnosis Of Antepartum Hemorrhage.
Differential Diagnosis Diagnostic Criteria Coagulation Profile
Acute placental abruption Clinical diagnosis and Abnormal in about 30% Normal or demise
pathology, ultrasound
MAY reveal large clot
Chronic abruption or Clinical diagnosis and Usually normal
marginal sinus abruption pathology
Placenta previa Ultrasound Normal
Bloody show of normal Clinical diagnosis mini- Normal
labor mal bleeding & fetal
well-being
Vasa previa Ultrasound with color Normal
Doppler, test for fetal
blood in vaginal blood
Antepartum hemorrhage Diagnosis of exclusion Normal
of unknown origin
Emergency Medicine Practice
is associated with an increased risk of abruption.18,42-46
Recent literature refuted earlier studies that associated
increasing maternal age and black race with an increased
risk of abruption. These factors alone are not significant,
when multivariate analysis is performed and they are
separated from other variables.47,48
Placenta Previa
As with placental abruption, placenta previa is more
common in patients with a history of placenta previa in
prior pregnancies. These patients are thought to be at 10-
fold greater risk. Patients with a history of an extremely
premature delivery (<25 weeks) have a 3-fold increased
risk, and patients with a history of previous perinatal
death, placental abruption, cesarean section, or prior
spontaneous or induced abortions are also at greater risk.
Advanced maternal age and an interpregnancy interval >4
years are additional known risk factors.49,50
Differential Diagnosis
The differential diagnosis for a woman bleeding in late
pregnancy ranges from the common and benign “bloody
show” of active labor, to the rare but dangerous vasa pre-
via, in which the umbilical cord presents below the fetal
presenting part. (See Table 2.) Placental abruption remains
a largely clinical diagnosis, while placenta previa is readily
diagnosed by ultrasound. (See Figures 1-4 on page 5.) The
clinical presentation of placental abruption is wide-rang-
ing, as the amount of vaginal bleeding varies from almost
none to catastrophic. In a small prospective study, Hurd et
al looked at the frequency of certain signs and symptoms
in abruption. They found that vaginal bleeding occurs in
78%, while uterine tenderness and fetal distress occur in-
frequently at presentation, and only about 15% of women
Fetus Presentation
Acute, severe abdominal
with large abruption pain and vaginal bleeding,
or concealed bleeding +/-
shock
Usually viable; at Chronic mild bleeding with
increased risk for no fetal compromise
prematurity
Usually viable; at Painless vaginal bleeding
increased risk for
prematurity
Normal Scant blood mixed with mu-
cus and contractions at term
May be normal, or Vaginal bleeding, usually
distress/demise mother hemodynamically
from bleeding stable
Increased risk of Minimal vaginal bleeding
fetal anomalies and and hemodynamically stable
preterm birth
4 EMPractice.net • December 2004

Figure 1. Low lying placenta.
Figure 3. Partial placenta previa.
with placental abruption present with either hypertonia or
intrauterine fetal demise.51 Sometimes abruptions are mis-
diagnosed as preterm labor, with or without spontaneous
rupture of membranes, and the diagnosis is made when
the fetus becomes distressed, or there is fetal demise.
Disseminated intravascular coagulation is commonly
associated with severe abruption and should lead one to
suspect this diagnosis. Finally, maternal shock can be the
presentation in severe, acute abruptions; in these cases it
is not uncommon for a woman to lose half of her blood
volume. Shock is often accompanied by acute renal failure
and oliguria, usually related to acute tubular necrosis.
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Figure 2. Marginal placenta previa.
Figure 4. Complete placenta previa.
Illustrations by Erin Dart
Renal function will generally improve with adequate fluid
resuscitation.52 Chronic abruption typically presents in a
less dramatic fashion and is usually associated with mild,
chronic vaginal bleeding without fetal distress.
In contrast to abruption, the classic presentation of
placenta previa is painless, bright red vaginal bleeding
occurring at the end of the 2nd trimester. Fortunately, this
“sentinel bleed” is rarely massive and usually stops spon-
taneously, though it often recurs and may become profuse
during labor. Despite the fact that bleeding from previa is
5 Emergency Medicine Practice
 generally painless, women with placenta previa who are in eclamptic patients.54 A small case-control study has
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in active labor may present with acute abdominal pain
from contractions, and vaginal bleeding from the previa.
This may make the distinction from abruption more dif-
ficult.52
Vasa previa, a rare cause of antepartum vaginal
bleeding, must also be considered. Vasa previa is the
velamentous insertion of the cord below the presenting
part of the fetus. When the diagnosis is made antenatally
— before fetal bleeding has occurred — elective cesarean
is performed; but when bleeding has already occurred, an
emergent cesarean is paramount, with access to transfu-
sion for the fetus. Perinatal mortality with vessel rupture
ranges from 75-100%.
Interestingly, in 38-50% of all women with antepar-
tum bleeding, no cause for the bleeding is found. These
women are diagnosed with “antepartum hemorrhage of
unknown origin.” Studies have shown that these women
are at increased risk for fetal anomalies and preterm la-
bor.53
Mild vs Severe Preeclampsia
It should be assumed that pregnant women with protein-
uria and hypertension have preeclampsia, until proven
otherwise. Likewise, a generalized seizure in a pregnant
patient should be considered eclampsia until proven
otherwise. However, determining which women with
preeclampsia at presentation will develop severe compli-
cations, such as HELLP syndrome or eclampsia, is much
more elusive. Researchers have been unable to identify
any single lab test that can determine which women will
develop eclampsia with a high degree of certainty. A
recent study by Small, examining which clinical and lab
features were most helpful in differentiating patients with
preeclampsia from those who develop eclampsia, found
that only oliguria and anuria were statistically different
shown an increased rate of both eclampsia and stillbirth
when acute renal failure was present along with HELLP
syndrome.55 Witlin et al found that only the frequency of
headache and deep tendon reflexes >3+ were significantly
increased among preeclamptic women who developed
eclampsia, compared to those who did not.56
The differential diagnosis of preeclampsia includes
chronic hypertension, but even in these patients, superim-
posed preeclampsia must be seriously considered. Other
etiologies to be considered in the differential diagnosis
will depend on the patient’s symptoms (see Table 3). Right
upper quadrant pain associated with HELLP can some-
times be confused with viral hepatitis, pancreatitis, or gall-
bladder disease, and has even been difficult to distinguish
from appendicitis or kidney stones.57 Acute fatty liver of
pregnancy can also masquerade as HELLP. This entity is
far less common than HELLP syndrome and is typically
associated with marked hypoglycemia, hyperammonemia,
and an increased clotting time.58 Some authors believe it is
actually a variant of HELLP, but this has yet to be proven.
Other rare conditions can mimic preeclampsia, but will
require hospitalization or consultation for work-up. These
include renal diseases, autoimmune diseases, thrombotic
thrombocytopenic purpura (TTP), hemolytic uremic syn-
drome, pheochromocytoma,59 or hydatidiform mole.
Although most pregnant women who seize will be
eclamptic, other etiologies for seizure should be consid-
ered. These are the same etiologies considered for non-
pregnant patients with a first seizure (See Table 4 on page
7). A history of brain tumor, epilepsy, medical problems
predisposing to brain pathology (eg, HIV), head trauma,
travel outside of the US, drug or alcohol use, fever, chills,
and/or headache; these will either clinch the diagnosis, or
direct further work-up.

Table 3. Differential Diagnosis Of Preeclampsia.

Diagnosis Investigation Recommendation
Pheochromocytoma Hospitalize for catecholamine testing
Thrombotic thrombocytopenic purpura DIC is generally not seen Hospitalize for further testing
Hemolytic uremic syndrome Hospitalize for further testing
Acute pancreatitis Lipase elevation +/- imaging Hospitalize
Gallbladder disease Ultrasound and LFTs May be able to discharge if no other signs of
preeclampsia and normal labs
Appendicitis CT scan Surgery consultation
Renal diseases Urine and electrolyte abnormalities Hospitalize for further testing
Chronic hypertension Change in baseline BP or proteinuria May need to hospitalize to rule out super-
imposed preeclampsia or obtain OB/GYN
consultation
Autoimmune diseases Rheumatology screen Hospitalize for further testing
Hydatidiform mole Ultrasound OB/GYN consultation
Acute fatty liver of pregnancy Ultrasound of abdomen or CT scan OB/GYN consultation

Emergency Medicine Practice 6 EMPractice.net • December 2004


Table 4. Differential Diagnosis Of Eclampsia.
Diagnosis Investigation
Epilepsy Usually has prior history
Encephalitis MRI and/or LP
Meningitis LP
Cerebral tumor CT/MRI scan
Cysticercosis CT/MRI scan
Ruptured cerebral aneurysm/ CT/MRI scan
cerebral hemorrhage
Cerebral venous thrombosis CT/MRI scan
Drug- or alcohol-induced seizure Tox screen
Metabolic-related seizure Glucose and electrolytes
Prehospital Care
In women with late-pregnancy vaginal bleeding, abdomi-
nal pain, or seizure, if signs and symptoms of shock are
present, or evidence of significant bleeding has occurred,
then 2 large-bore peripheral intravenous catheters should
be placed, and appropriate fluid resuscitation should be
initiated. The patient should be placed in the left lateral
decubitus position, as the recumbent position can cause
the gravid uterus to compress the vena cava, potentially
inhibiting venous return and leading to hypotension.
Prehospital seizures should be managed with magnesium
(4 gm IV or 10 gm IM) or benzodiazepines. Prehospital
notification is important, as it enables the ED physician to
alert the appropriate specialists, notify the OR, and have
blood available, if needed, for the patient.
ED Evaluation
Initial Evaluation/Triage
Unstable Patient
Patients presenting with signs and symptoms of shock
should proceed to a major resuscitation area, have 2 large-
bore IVs established, and be resuscitated with boluses of
normal saline. Rapid bedside hemoglobin testing should
be performed, if available, and blood sent for type and
cross match. A coagulation profile should also be ordered
to evaluate for possible DIC. The need for blood prod-
ucts will be determined by the degree of hemodynamic
instability, as well as the response to fluid resuscitation.
An emergent bedside ultrasound can be used to assess
for placental previa and fetal viability, and may identify a
placental abruption.
Patients presenting with seizures should also be man-
aged in a resuscitation area. The mainstay of seizure man-
agement will include magnesium and benzodiazepines.
Active airway management may be required for persistent
seizures. Patients with significantly elevated blood pres-
sure, altered mental status, or pulmonary edema should
be managed as hypertensive emergencies. In each case, ob-
stetrical consultation should be obtained on an emergent
basis.
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Table 5. Danger Signs Of Severe
Preeclampsia.
• Headache
• Upper quadrant abdominal pain
• Visual disturbance
• Decreased urine output
• History of convulsion(s)
• Respiratory symptoms that might indicate pulmonary
edema (dyspnea, chest pain, cough)
• Nausea/vomiting
• Blindness
Stable Patient
The site for evaluating patients who are stable, but who
present with symptoms of possible preeclampsia, pla-
cental abruption, or placental previa, is dependent on the
obstetrical capabilities of the evaluating institution. In
many institutions protocols are in place for the evaluation
of stable patients on labor and delivery (L&D). In facili-
ties without an obstetrical ward, the managing clinician
should involve the patient’s obstetrician early on, in order
to determine the scope of the evaluation, as well as the
timing of transfer, if needed.
History of Present Illness
Each patient should be queried as to the presence of any
danger signs of severe preeclampsia, HELLP syndrome,
or impending eclampsia, such as headache, right upper
quadrant (RUQ) tenderness, visual disturbance, convul-
sions, nausea/vomiting, oliguria, or symptoms worrisome
for pulmonary edema (Table 5).
The patient should be queried about the presence or
absence of abdominal pain, which may be a sign of labor
or placental abruption. With placental abruption, pain
may be absent altogether, or range from mild, intermittent
pain to severe, sustained contractions. Pain from abrup-
tion or labor should be localized over the uterus. Pain in
the RUQ is consistent with gallbladder disease, but also
may be seen with HELLP syndrome (from hepatic capsu-
lar distension), and with appendicitis (as the gravid uterus
displaces the appendix to the RUQ). Characterizing the
patient’s pain is useful and may help distinguish typical
labor pains from the sustained hypertonic contractions
sometimes seen with abruption.
The presence and severity of vaginal bleeding should
be noted. Bleeding may be a symptom of placental abrup-
tion or previa; or, with a “bloody show,” it may simply
signify the onset of full-term labor.
Headache, confusion, and visual disturbances may be
warning signs of hypertensive encephalopathy, which can
accompany severe preeclampsia. The presence of seizures
strongly suggests the diagnosis of eclampsia, unless the
patient has a known seizure disorder. With preeclampsia,
the patient may complain of excessive weight gain or
swelling of her face and/or hands. These symptoms, while
7 Emergency Medicine Practice
 not diagnostic, often occur when preeclampsia progresses
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from a milder to a more severe stage.
Gestational age is often a major factor in determin-
ing optimal patient management. The patient should be
queried as to her last menstrual period, as well as any
prior ultrasounds that can be used for pregnancy dating.
It is important to ask the mother if the fetus is still moving
since the presence of fetal movement is usually a sign that
the baby is not yet in distress.60 However, the absence of
fetal movement is not necessarily ominous, since the fetus
could be sleeping or relatively inactive.
One should inquire if preeclampisa, twin pregnancy,
trauma, or polyhydramnios have complicated the current
pregnancy. Also ask if the patient uses cocaine or smokes
cigarettes. The history of past pregnancies can be help-
ful, too, in eliciting risk factors for abruption — such as
history of prior abruption, PROM, or preeclampsia — or
risk factors for previa — such as prior cesarean sections,
abortions, previa, premature labor, and/or still births.
Physical Examination
Vital signs must be monitored to assess for potential
Ten Pitfalls To Avoid
1. “She felt great, her blood pressure was only mildly
elevated, and the dipstick was only +1 protein, so I
discharged her.”
Even mild preeclampsia can have a fulminant course.
The decision to admit or discharge is best made in close
consultation with an obstetrician.
2. “But she had white cells and protein on the dipstick, so I
diagnosed a UTI and discharged her with macrodantin.”
Attributing proteinuria found on a urine dipstick to the
presence of a UTI is another common error. Remember:
proteinuria in the hypertensive patient IS preeclampsia
until proven otherwise and requires hospitalization. A
preeclamptic woman might have a simultaneous urinary
tract infection.
3. “It seemed easier just to give her some diazepam for the
seizure.”
Doctors who failed to use magnesium for seizure or severe
preeclampsia in pregnant women have been pursued in
court. Magnesium is considered the treatment of choice,
and other anticonvulsants should be used only after 2 doses
of magnesium have failed to control the seizures.
4. “I though about abruption, but the ultrasound was
negative.”
Ultrasound frequently fails to identify placental abruption,
and thus a negative ultrasound does not definitively exclude
this diagnosis.
5. “Her pain seemed just like gallstones and was controlled
by pain medication, so I scheduled her for an outpatient
ultrasound.”
Emergency Medicine Practice
shock. Mental status should be evaluated and, if altered,
could be due hypertensive encephalopathy, or second-
ary to: shock from blood loss, intracranial hemorrhage,
or a postictal state. The general appearance of the patient
is helpful in determining the patient’s degree of distress.
Abruption may cause extremely painful contractions. A
pale appearance can signify a blood loss, either internally
or externally. The cardiovascular exam should focus on the
presence or absence of pulmonary edema, while the ab-
dominal exam should assess uterine tonicity and tender-
ness, as well as focal abdominal tenderness. Tenderness
in the RUQ may be seen with HELLP syndrome, as well
as with gallbladder disease. In addition, the gravid uterus
may displace intraabdominal organs; eg, with appendici-
tis, the area of pain and tenderness might be localized to
the RUQ, rather than the RLQ.
The neurologic exam should focus on the presence or
absence of focal neurologic findings (which can be seen
with intracranial hemorrhage), as well as for the presence
of hyperreflexia, which can be seen with preeclampsia.
The skin should be evaluated for the presence and degree
of peripheral edema. Fetal monitoring should be per-
The right upper quadrant pain in severe preeclampsia can
be confused with cholecystitis. A pregnant woman with
epigastric or upper abdominal pain has severe preeclampsia
until proven otherwise. A preeclamptic woman might have
simultaneous gallstones.
6. “I did a quick bimanual and she opened up bleeding.”
Bimanual exam is contraindicated in women in late
pregnancy with vaginal bleeding and no prior ultrasound to
exclude placenta previa.
7. “She only had scant vaginal bleeding, so I didn’t consider
placental abruption. Suddenly she became unstable.”
Placental abruption may present with a small amount of
vaginal bleeding, so always consider it on the differential of
women bleeding late in pregnancy.
8. “I didn’t check a blood type, because she had only had
spotting.”
RhoGAM® is indicated, even with scant vaginal bleeding.
9. “She looked pretty sick and was in DIC, but the Ob/Gyn
said to admit her, and he would see her in the morning. I
thought I could trust him.”
Always insist on having an emergent consultation with
an Ob/Gyn specialist when abruption is suspected. Fetal
distress or demise can occur rapidly.
10. “Why should I have considered eclampsia as the cause of
her seizures? She is not even pregnant anymore.”
Eclampsia is occurring with increased frequency in the
postpartum period and may occur up to 2 weeks post-
delivery. ▲
8 EMPractice.net • December 2004
 are helpful in assessing kidney function. An elevated uric

formed as soon as available to exclude fetal distress, or
evidence of fetal demise.
In patients with vaginal bleeding, a pelvic exam
should be deferred, unless the possibility of a placental
previa has been excluded by a prior ultrasound. Once pre-
via has been excluded, the pelvic exam is helpful to rule
out vaginal or cervical causes for bleeding. Vasa previa is
diagnosed by palpation of the vessels by digital vaginal
examination.61
Diagnostic Studies
Laboratory Studies
A urinalysis should be obtained in third-trimester preg-
nant patients who are hypertensive. A positive result is
suggestive of preeclampsia. In most cases these patients
should be admitted for further evaluation and treatment.
However, a negative urinalysis does not exclude disease.
In a retrospective analysis of 254 women with eclampsia,
Sibai reported that 20% of patients had no proteinuria on
the initial dipstick urinalysis.62 Meyer et al found that, in
hypertensive patients, the presence of urinary protein on
dipstick had a positive predictive value of 92% for predict-
ing > 300 mg urinary protein excretion/24 hr; however,
a negative dipstick has only a 34% negative predictive
value. Thus, a single negative urine dipstick cannot be
used to definitively exclude significant proteinuria.63 This
underscores the fact that a high index of suspicion must
always be maintained in pregnant women with hyperten-
sion.
Other useful lab tests in the diagnosis and manage-
ment of preeclampsia include a CBC, which may demon-
strate anemia or thrombocytopenia. LDH, the reticulocyte
count, and the peripheral blood smear are used to identify
hemolysis. Liver function tests are important in diagnos-
ing HELLP syndrome. Electrolytes, BUN, and creatinine
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acid is considered a marker for severe preeclampsia (Table
6).
For the patient with active bleeding, a CBC and blood
type should be obtained. If an abruption is suspected, a co-
agulation panel consisting of fibrinogen, fibrinogen-fibrin
degradation products, and D-dimer should be considered,
as these results were reported to be abnormal in as many
as 10% of cases.64 However, a recent prospective study
in 25 women with suspected placenta abruption com-
pared to 30 controls did not find a significant difference
in these values between the two groups.65 A recent study
suggests that thrombomodulin, a marker of endothelial
cell damage, is a more sensitive (87%) and specific (76%)
marker for acute placental abruption than the coagulation
profile.66 Larger studies are needed to confirm this finding.
The Kleihauer-Betke test remains critical in an Rh-
negative mother. The test determines the presence and
amount of maternal-fetal blood mixture, which guides the
dosing of Rh immune globulin. It is also useful in detec-
tion of vasa previa with fetal bleeding. The Ogita test is a
quick and useful means of eliciting mixture of maternal
and fetal blood: 1 drop of vaginal blood is added to 5
drops of KOH and shaken for 2 minutes. Next, 10 drops of
a solution of ammonium sulfate and hydrochloric acid are
added, and this mixture is dropped onto filter paper. De-
natured adult hemoglobin stays in the center, while fetal
hemoglobin forms a colored ring at the periphery within
30 seconds.67
Ultrasound
In patients with vaginal bleeding, an ultrasound should
be obtained to exclude placenta previa, as it is reported
to have a sensitivity of 100% in these cases.68 The most
distal placental attachment tends to move away from the
cervical os as the pregnancy progresses over time. Thus,
Continued on page 12

Table 6. Diagnostic Testing In Preeclampsia.

Diagnosis Symptoms
Urinalysis Protein is indication of preeclampsia
CBC: HCT and platelet count Anemia and/or thrombocytopenia seen with HELLP
Blood smear and/or LDH Hemolysis in diagnosing HELLP
LFTs Liver involvement in HELLP
Electrolytes Abnormalities related to kidney failure
BUN/Creatinine Marker of kidney insufficiency
Uric Acid Marker of severe preeclampsia
Ultrasound by Ob/Gyn consultant Evaluate amniotic fluid and fetal well being
CT or MRI or RUQ To exclude subcapsular hematoma in HELLP
Brain CT or MRI To exclude other etiology for seizure in select patients
LP Rule out meningitis
Tox screen Identify other sources for seizure or hypertension

December 2004 • EMPractice.net 9 Emergency Medicine Practice

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Clinical Pathway: Management Of Bleeding In Late Pregnancy

Hypotension/Tachycardia?
NO YES

➤
➤
• Place patient on monitored bed; address airway and breathing problems (Class II)
• Obtain thorough history and physical
• Obtain ultrasound if no prior ultrasound for • High-flow oxygen by facemask (Class III)
previa • Left lateral decubitus position (Class III)
• Consider bloody show, rupture of membranes • Prompt vascular access with large-bore peripheral venous catheters (Class II)
• Reassess vital signs regularly to look for
• Check bedside glucose if mental status is not normal, treat hypoglycemia (Class I)
decompensation
• Check bedside hemoglobin (if available), identify anemia (Class II)
• Fluid resuscitation with normal saline 1 L rapid bolus (Class I)
• Frequently reassess vital signs (Class II)
➤

Decompensation? YES ➤ • Send complete blood count, blood bank specimen for type and cross and Rh testing
and DIC (Class II)

➤
Emergent Obstetric Consultation
➤
Heavy vaginal bleeding?
YES
➤

NO
Prior ultrasound ruling out previa?
YES NO
➤
➤

Placental abruption highly likely Emergent bedside ultrasound

➤

➤
No previa
Patient stabilizes with fluid resuscitation?
➤ Previa
➤

YES
NO Patient stabilizes with fluid resuscitation?
➤

NO
➤

• Consider bedside ultrasound

• Pelvic exam to exclude vasa previa and YES
• Transfuse 2-4 µ PRBCs
assess cervical dilation
• Prepare OR for double set up/rapid delivery
• Continue close monitoring of vital signs
• Correct clotting abnormalities as indicated
• Consider morphine for analgesia
➤

• Await Ob for definitive management:

delivery versus expectant management for
Consult Ob for definitive management:
pregnancy remote from term
delivery vs expectant management for
pregnancy remote from term

The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely
recommended. Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III:
May be acceptable, possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending
upon a patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright ©2004 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any for-
mat without written consent of EB Practice, LLC.

Emergency Medicine Practice 10 EMPractice.net • December 2004

 COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC
Clinical Pathway: Management Of The
Hypertensive Woman In Late Pregnancy
Blood pressure greater than 140/90?
NO

➤
YES Findings suggestive of
hypertensive emergency?
(Seizure, pulmonary edema,
NO changes in mental status)
➤

➤
YES

➤
• Obtain urine for protein
• Check for symptoms of severe preeclampsia: • Place patient on monitored bed in the resuscitation area; address airway and
headache, abdominal pain, visual changes,
breathing problems (Class II)
nausea/vomiting
• Obtain CBC to identify anemia and/or thrombo- • High-flow oxygen by facemask (Class III)
cytopenia, LDH/reticulocyte count and LFTs to • Left lateral decubitus position (Class III)
diagnose HELLP • Prompt vascular access with large-bore peripheral venous catheters (Class II)
• Obtain electrolytes to assess renal function
• Obtain prompt Ob/Gyn consultation
• Obtain uric acid level: marker for severe pre-
eclampsia
• Obtain U/S RUQ for abdominal pain

➤
➤
NO Seizure or postictal?
YES
➤

➤
Diagnosis preeclampsia?
YES • Give magnesium 4 gm IV or 10 gm IM (Class I) with
maintenance infusion 2 gm/hr IV
➤

• Repeat Magnesium 2-4 gm IV over 3-5 min if seizures

Consult Ob/Gyn for definitive DBP >110 on two ➤ continue after 15 min (Class I)
management, ie, delivery • Check bedside glucose if mental status is not normal,
measurements?
and/or transfer for pregnancy treat hypoglycemia (Class I)
remote from term YES • Check bedside hemoglobin (if available), identify
anemia (Class II)
➤

➤ • Frequently reassess vital signs (Class II)

Hydralazine 5 mg IV or • For persistent seizures after 2 doses of magnesium,
10 mg IM (Class II) give diazepam, 5 mg per min up to a max of 20 mg, and
phenytoin 10 - 20 mg /kg no faster than 50 mg/min
➤

Consult Ob/Gyn for definitive management

of delivery

The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely
recommended. Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III:
May be acceptable, possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending
upon a patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright ©2004 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any for-
mat without written consent of EB Practice, LLC.

December 2004 • EMPractice.net 11 Emergency Medicine Practice

 Continued from page 9
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evidence of placenta previa at the time of an initial ultra-
sound is not diagnostic, since the previa often disappears
with time. Absence of placental previa early in pregnancy
excludes this diagnosis for the entire pregnancy.
In the diagnosis of placental abruption, ultrasound
is less sensitive. Massive abruptions are generally easier
to diagnose than the more common, smaller forms. Color
Doppler ultrasound has been used to diagnose vasa pre-
via.
Other Diagnostic Tests
The definitive diagnostic test for confirming placental
abruption is examination of the placenta at pathology after
delivery. In patients with HELLP syndrome and RUQ
pain, if rupture of a subcapsular hematoma is suspected,
then CT of the abdomen is the test of choice. Abnormal
liver function tests do not accurately reflect the presence of
abnormal hepatic imaging findings in these patients.69
In late-pregnancy patients with new onset seizures,
a head CT may be needed to exclude etiologies other
than eclampsia. MRI is an alternative option and has the
advantage of less radiation exposure to the fetus; however,
it is also less readily available. The indications for lumbar
puncture are the same as in the nonpregnant patient: to
rule out meningitis or subarachnoid hemorrhage. Urine
and serum toxicologic screens may elicit other possible
causes of seizure in some patients.
Treatment
Placental Abruption/Previa
Unstable Patient or Fetus
In the unstable patient with signs of hemorrhage, initial
management begins with the essentials: the patient is
placed on a monitored bed, and airway and breathing is-
sues are quickly addressed. High-flow oxygen by face-
mask is initiated, and prompt identification and treatment
of hypovolemic shock is undertaken. Boluses of normal sa-
line should be administered through 2 large-bore periph-
eral intravenous catheters. CBC and blood bank specimens
for type and cross, plus Rh testing, must be sent immedi-
ately. Patients who remain hypotensive should be trans-
fused with packed red blood cells.6,7,52,70 Blood component
therapy is guided by clinical exam, CBC, and coagulation
profiles.70,71 Fulminant maternal DIC often occurs within
1-2 hours of complete abruption, and delivery is the only
way to reverse it. Coagulation studies should be followed
serially. Patients in significant pain may be treated with
low doses of morphine while following their hemodynam-
ic status. Obstetrical coverage should be emergently con-
sulted. Patients who remain unstable despite resuscitation,
or who exhibit significant persistent fetal distress, should
be transported rapidly to the OR for a double set-up exam
and/or possible delivery.72,73
Stable Patient and Fetus
Full-term Pregnancy
In the stable patient with suspected abruption or previa,
Emergency Medicine Practice
further diagnostic testing, such as ultrasound, may help
guide management. In suspected placental abruption with
imminent delivery, vaginal delivery is preferred, if mother
and fetus can tolerate it. The delivery should preferably
take place in a setting with cesarean and hysterectomy
capabilities, in the event that an intervention becomes
necessary for maternal hemorrhage. Cesarean section is
indicated if vaginal labor fails to progress, or if mother or
fetus become unstable.
When abruption occurs in the presence of fetal de-
mise, vaginal delivery is preferred since there is less risk
to the mother. In full-term patients with placenta previa,
cesarean section is indicated.
Preterm Pregnancy
Multiple studies have demonstrated that expectant
management in stable preterm pregnancies with placental
abruption is safe and effective.72,74-77 In addition, a retro-
spective study by Towers, et al, evaluated the safety of
tocolysis in preterm patients with abruption and placenta
previa. They found no untoward events related to this
treatment.74 However, there have been no prospective
randomized trials to confirm these findings.
A small amount of preterm bleeding in placenta pre-
via is generally managed by close surveillance in the hos-
pital, although a number of small studies have suggested
that these patients may be safely discharged to home.
Wing et al reported no difference in maternal or perinatal
morbidity in a randomized controlled trial of inpatient
versus outpatient management of placenta previa. The Co-
chrane Database review of all RCT on the subject of home
versus hospitalization for stable women with placenta
previa found that there are insufficient data to recommend
a change to the clinical practice of routine hospitalization.11
Larger studies will be needed to confirm whether it is safe
for some women to be managed as outpatients.
Preeclampsia Management
Delivery
Definitive treatment of preeclampsia/eclampsia is de-
livery of the fetus. All other treatments are temporizing
measures only. Expeditious delivery in full-term pregnan-
cies (≥38 weeks gestation) is indicated. Management of
preeclampsia in preterm gestations is more variable. All
preeclamptic, preterm women should be considered for
transfer to a tertiary facility with obstetric and neonatal ca-
pabilities. Delivery is recommended for most women with
preeclampsia at 32-38 weeks gestation. Women who are at
<32 weeks gestation and who have mild preeclampsia are
usually treated conservatively. When severe preeclamp-
sia is present in these women, however, management
becomes controversial. Studies comparing expectant
management to rapid delivery suggest that expectant
management may be appropriate in some cases. However,
these studies are quite small and lack standardized defini-
tions of severe preeclampsia. In addition, the indications
for delivery varied from study to study. In 1994, Sibai et
al randomized 95 patients with severe preeclampsia at 28
to 32 weeks gestation to either aggressive management
12 EMPractice.net • December 2004
(delivery 48 hours after betamethasone administration) or
expectant management. Women with HELLP syndrome or
eclampsia were excluded. In the expectant management
group, fewer neonatal complications occurred compared
to the aggressively managed group.78 A second study of
58 women randomized to conservative versus aggressive
management found no increase in maternal complications,
but a significant increase in gestational age at delivery in
the conservatively managed group. However, 20 women
in this study could not be randomized, because they de-
veloped complications necessitating delivery.79
In all cases, preterm, preeclamptic women should
be admitted and corticosteroids administered to acceler-
ate fetal lung development.3,78,80 Either maternal or fetal
decompensation would be an indication for immediate
delivery.78,81
With respect to route of delivery, a large retrospective
study showed no advantage to cesarean over vaginal de-
livery. Labor is generally initiated via standard methods.82
Seizure Management/Prophylaxis
While the actual mechanism by which magnesium con-
trols seizures in preeclampsia is not clearly defined, Wat-
son et al found that magnesium increases the release of en-
dothelial prostacyclin, a potent vasodilator that is deficient
in preeclampsia. This led to the hypothesis that cerebral
ischemia may be the cause of seizures in preeclampsia and
suggests that vasodilation of cerebral arteries, which leads
to improved perfusion, may result in fewer seizures.83
In severe preeclampsia, the superiority of magne-
sium to other anticonvulsants in preventing seizures is
well documented. A large multicenter randomized trial in
1995 compared magnesium sulfate to both diazepam and
phenytoin in eclamptic women. A lower risk of recurrent
seizure with magnesium sulfate versus either agent was
demonstrated. When compared to phenytoin, magnesium
was also found to lower the risk for maternal intubation,
pneumonia, and ICU admission. The neonatal intubation
risk was also lower in the magnesium group.84 However, a
decrease in maternal mortality was not demonstrated. An-
other large randomized trial of almost 2000 women with
severe preeclampsia by Lucas in 1995 found that mag-
nesium was superior to phenytoin in eclamptic seizure
prophylaxis.85 A randomized controlled trial of IV magne-
sium versus placebo in 1998 showed lower progression to
Table 7. Anticonvulsant Dosage For Eclampsia Or Preeclampsia.
Agent Loading Dose
Magnesium sulfate • 4 -6 gm over 20 min IV (20% solu-
tion)
• If convulsions persist after 15 min,
give 2-4 gm IV over 3-5 min
Phenytoin • 10-20 mg/kg to a maximum rate of
50 mg/min
Diazepam • 5 mg/min up to a max of 20 mg
December 2004 • EMPractice.net
eclampsia with magnesium treatment.86
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In mild preeclampsia, the advantages of magnesium
treatment are less compelling. A double blind placebo
controlled trial of 222 women with mild preeclampsia,
randomized to receive magnesium sulfate or placebo IV,
showed no decrease in progression of disease or the rate
of overall complications in the magnesium-treated group,
compared to placebo. There was an overall low rate of
development of eclampsia in both groups, possibly as a re-
sult of close clinical surveillance.87 Despite these findings,
current practice is to administer magnesium to all women
with preeclampsia, as there currently is no reliable way to
identify those who will progress to severe preeclampsia.
In women with preeclampsia, magnesium is typi-
cally infused during labor and delivery, and for at least 24
hours postpartum. Patients receiving magnesium should
be monitored hourly for signs/symptoms of magnesium
toxicity. These include loss of reflexes, respiratory depres-
sion, and decreased urine output. Magnesium is renally
excreted. Therefore, patients with renal compromise
should have magnesium levels checked every 4 hours. The
treatment goal is to keep the serum magnesium levels in
the 5-8 mg/dL range. In the event of magnesium toxicity,
the infusion should be discontinued. Treatment with 10
ml of 10% Ca gluconate IVP will often reverse symptoms
of magnesium toxicity. In women who continue seizing
after two boluses of magnesium, benzodiazepam, and/or
phenytoin may be necessary.88 (See Table 7 for dosing.)
Antihypertensive treatment is generally recommend-
ed for preeclamptic women with a diastolic blood pressure
>110mm. Though several randomized studies have shown
no improvement in perinatal morbidity/mortality, rate of
maternal complications or progression of preeclampsia to
severe preeclampsia, with antihypertensive treatment,57,89-
93
the complication rates in these studies were low, and
the number of enrolled patients was small. It is generally
thought that antihypertensive treatment is indicated,
based upon the benefit of treatment found with large,
randomized studies of hypertension among the general
population.94
Management of Preeclamptic Hypertension
Hydralazine has long been used as first-line treatment in
preeclamptic hypertension. Despite many years of use of
this medication, no long-term, adverse effects to exposed
Maintenance IM Dosing (Parkland IM Protocol)
• 2 gm/hr IV • 10 gm deep IM with 3-inch
needle, divided in each buttock,
mixed with 1 ml 2% Lido, then 5
gm IM Q 4hr
13 Emergency Medicine Practice
 fetuses have been reported. Other antihypertensive agents
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are currently being tested, but no large study has found an
agent superior to hydralazine for preeclamptic hyperten-
sion. The goal in treatment is to stabilize the BP at about
160/100, NOT to try to normalize the BP, since there are
no studies showing benefits to treating mild hypertension
in pregnant women (DBP <100). In addition, hypoten-
sion is to be avoided in a state where there is already
decreased perfusion to the placenta.57,95 Labetalol appears
to be particularly effective in controlling the occurrence of
serious ventricular arrhythmias in hypertensive crises in
preeclampsia.96 (See Table 8 for dosing guidelines.)
Corticosteroids
A Cochrane database review of 18 randomized controlled
trials concluded that a single dose of corticosteroids is
recommended for preeclamptic patients at <34 weeks
gestation.97 In addition to the benefit of corticosteroids in
hastening lung maturity in premature fetuses, some stud-
ies suggest that corticosteroids may exert a direct positive
impact in treating preeclampsia. In a retrospective study,
O’Brien et al demonstrated significant improvement in
platelet count, AST, and LDH in patients treated with cor-
ticosteroids.98 In addition, a small prospective randomized
study of patients with HELLP syndrome demonstrated
improvement in lab abnormalities, blood pressure control,
and urine output in corticosteroid-treated patients versus
controls.99 However, improvement in overall morbidity
and mortality was not demonstrated. Corticosteroid thera-
py has also been proven beneficial in patients with HELLP
syndrome. Patients who were given corticosteroids to ac-
celerate fetal lung development were also shown to have
improvement in their coagulation profiles. This improve-
ment in coagulation profiles allowed significantly more
women to be given regional (epidural) anesthesia versus
general anesthesia.100
Isler et al compared dexamethasone IV to betametha-
sone IM and found improved blood pressure control,
significantly decreased AST level and improved urinary
output with IV dexamethasone.101 All of these studies are
either small, lack randomization, or both, so larger ran-
domized studies will be needed to confirm these results.
Intravenous Fluids
Preeclamptic patients are prone to fluid overload, so intra-
Table 8. Antihypertensive Treatment Of Preeclampsia.
NHBPEP Guidelines For BP Treatment In Preeclampsia.
First line: Hydralazine 5 mg IV or 10 mg IM, may repeat if needed every 20 min to max 20 mg IV or 30 mg IM
Second line: Labetalol 20 mg IV bolus, if BP not controlled after 10 min, give 40 mg IV; if BP still not controlled, give 80
mg every 10 min for 2 more doses (maximum 220 mg)
Third line: Nifedipine 10 mg orally, may repeat in 30 min as needed (short-acting nifedipine has not been approved,
due to risk of inducing profound hypotension)
Sodium Nitroprusside Used in rare cases of hypertension not responding to drugs above, or clinical encephalopathy.
Start at rate of 0.25 mcg/kg/min to a max dose of 5 mcg/kg/min. Fetal cyanide poisoning may
occur if used >4 hr.
Emergency Medicine Practice
venous fluids should be used cautiously in these patients,
while urine output should be closely monitored. The ideal
degree of hydration recommended for these patients has
not been established. Obviously, fluids may be appropriate
in women who are dehydrated or hypovolemic for other
reasons.5 In any case, urine output must be measured care-
fully with a Foley catheter.
Intubation
Indications for intubation are the same as for the nonpreg-
nant patient. Hypertension can be significantly worsened
during laryngoscopy and intubation of the preeclamptic or
eclamptic woman, but pretreatment with hydralazine or
labetalol may block this response. Airway edema may be
present; therefore, these patients should be considered a
difficult airway, with the appropriate precautions taken.3
Invasive Hemodynamic Monitoring
Swan-Ganz catheters are sometimes used in patients with
severe preeclampsia who have either pulmonary edema
or persistent oliguria unresponsive to fluid challenge. A
small, retrospective study of the use of pulmonary artery
catheterization found it to be subjectively useful in 93/100
cases where a determination of maternal fluid status
altered or determined the appropriate management of the
patient. However, complications related to the use of this
procedure occurred in 4% of patients,102 and overall mater-
nal outcome was not improved.103
Controversies/Cutting Edge
Preeclampsia
Much research has focused on discovering early biochemi-
cal markers of preeclampsia, in the hopes of finding pre-
ventative strategies that could reduce the complications
of the disease. Unfortunately, most of these studies are
disappointing, in that no single test has been found to be
both sensitive and specific. Small studies using a urinary
assay of creatinine and kallikrein show promise, but larger
studies are needed to examine this more closely. Research-
ers believe that using a combination of these markers will
eventually be effective in predicting future disease. This
method would screen for several different aspects of the
disease process and potentially increase the sensitivity and
specificity of the screening. There may also be a role for
14 EMPractice.net • December 2004
screening later in the pregnancy when most of these mark-
ers become more robust screening methods.104
Another topic gaining attention recently is finding a
role for outpatient management of preeclampsia that is
mild and/or remote from term. In the future, a potential
“low-risk” group may be identifiable, but at this point
hospitalization is still recommended for a thorough assess-
ment of mother and fetus.
Finally, the timing of delivery in those patients who
are remote from term when they develop preeclampsia
remains controversial. This is described more thoroughly
in the Disposition section that follows.
Placenta Previa
A recent Cochrane review of 2 new interventions for
suspected placenta previa — home versus hospitalization,
and cervical cerclage — found that there are insufficient
data to recommend changing current clinical practice.105
However, 1 of 2 recent studies using cervical cerclage for
placenta previa showed possible benefit. Small studies
have also shown some possible benefit to tocolytic therapy
in selected patients with placenta previa. The group
that might benefit most has yet to be defined by further
study.106
Placental Abruption
Similarly, a recent Cochrane review of interventions for
treating placental abruption found no studies meeting
inclusion criteria of reporting meaningful outcomes. They
recommend: “The clinical management of placental abrup-
tion has to rely on knowledge other than that obtained
through randomized clinical trials.” Thus, future clinical
Key Points For Second- And Third-Trimester Emergencies
• Think about placental abruption in women with severe,
painful contractions, even in the absence of vaginal
bleeding. Abruptions can have concealed retroperitoneal
bleeding.
• Ultrasound is not a sensitive or specific test for abruption,
so a negative exam does not exclude the diagnosis.
• In young women presenting in shock late in pregnancy,
abruption is high on the differential.
• Never perform a pelvic exam on a patient bleeding in
late pregnancy, if she has not had a prior ultrasound
documenting normal position of the placenta. A digital
exam could stimulate hemorrhaging from a previa.
• Consider placenta previa in a woman with painful
contractions and heavy, bright-red bleeding. She might
have placenta previa and be in active labor.
• Usually the first “sentinel bleed” of placenta previa stops
spontaneously.
December 2004 • EMPractice.net
trials need to be performed, in order to identify the opti-
COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC
mal management strategy for this entity.107
Disposition
Discharge
A select group of pregnant or postpartum women with
mild increases in blood pressure may be discharged home
with close follow-up. These patients should have BP <
140/90 and should have no proteinuria, no signs or symp-
toms of severe preeclampsia (headache, blurred vision,
right upper quadrant or epigastric pain), and no abnormal
labs (platelet count, renal function, liver enzymes). Follow-
up exam with their obstetrician is recommended within
1-3 days.3,4
Consult/Hospitalization
Hospitalization is recommended for pregnant or postpar-
tum women with new-onset BP ≥140/90 and/or signifi-
cant proteinuria (≥300 mg/24 hr or 1+ on dipstick). The
same is true for women with signs or symptoms of HELLP
syndrome or severe preeclampsia. Chronic hypertensive
women with increasing BP or proteinuria, or with new
symptoms of severe preeclampsia, should also be hospital-
ized to exclude superimposed preeclampsia.4
Transfer
Consider transferring patients with preterm preeclamp-
sia to a facility equipped to handle preterm infants. Also
consider transferring patients with diagnoses of severe
preeclampsia or eclampsia to facilities with in-house ob-
stetric services.▲
• Treat hypovolemia in antenatal bleeding aggressively
with 2 large-bore peripheral intravenous catheters
running normal saline. Transfuse if you don’t get a rapid
response.
• Stable patients with preterm pregnancies and antenatal
bleeding should be transferred to institutions with NICU
capabilities.
• If the umbilical cord is palpated in the vagina below
the fetal presenting part, continue upward traction on
the fetus while the mom is taken to the OR for cesarean
delivery.
• Vaginal delivery is the preferred method of delivery with
abruption and fetal demise.
• No etiology is ever identified in close to half of all women
with antepartum bleeding.
• There have been multiple malpractice cases against ED
physicians who failed to check Rh status with antenatal
bleeding and/or failed to administer RhoGAM® to Rh-
negative mothers. ▲
15 Emergency Medicine Practice
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located to hospitalization vs hospitalization and labetalol)
92. Sibai BM, Mabie WC, Shamsa F et al. A comparison of no ver-
sus methyldopa or labetalol in chronic hypertension during
pregnancy. Am J Obstet Gynecol 1990;162:960-967. (Random-
ized study of 300 women allocated to methyldopa versus
labetalol)
93. Sibai BM, Barton JR, Aki S, et al. A randomized prospective
study of nifedipine and bed rest versus bed rest alone in the
management of preeclampsia remote from term. Am J Obstet
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nifedipine versus bed rest)
94. Collins R, Peto R, MacMahon S, at al. Blood Pressure, stroke
and coronary heart disease. Part 2. Short-term reductions in
blood pressure: overview of randomized drug trials in their
epidemiological context. Lancet 1990;335:827-838. (Review)
95. Henriksen T. Hypertension in pregnancy: use of antihyper-
tensive drugs. Acta Obstet Gynecol Scand 1997;76(2):96-106.
(Review)
96. Bhorat IE, Naidoo DP, Rout CC. Malignant ventricular arryth-
mias in eclampsia: a comparison of labetalol with dihydrala-
zine. Am J Obstet Gynecol 1993;168(4):1292-1296. (Random-
ized trial in 40 eclamptic subjects)
97. Crowley P. Prophylactic corticosteroids for preterm birth.
Cochrane Database Syst Rev 2000;(2):CD000065. (Includes data
from 18 RCTs or semi-RCTs and >3700 babies)
98. O’Brien JM, Milligan DA, Barton JR. Impact of high-dose
corticosteroid therapy for patients with HELLP (hemolysis,
elevated liver enzymes, and low platelet count) syndrome.
Am J Obstet Gynecol 2000;183(4):921-924. (Retrospective
study of 37 women with HELLP)
99. Magann EF, Perry KG, Meydrech EF, et al. Postpartum cortico-
steroids: accelerated recovery from the syndrome of hemoly-
sis, elevated liver enzymes, and low platelets (HELLP). Am J
Obstet Gynecol 1994;171(4):1154-1158. (Prospective random-
ized study of 40 women)
100. O’Brien JM, Shumate SA, Satchwell SL, et al. Maternal benefit
of corticosteroid therapy in patients with HELLP (hemolysis,
elevated liver enzymes, and low platelet count) syndrome:
impact on the rate of regional anesthesia. Am J Obstet Gynecol
2002;186(3):475-479. (Retrospective analysis of 69 patients
with HELLP)
101. Isler CM, Barrilleaux SP, Magann EF. A prospective random-
ized trial comparing the efficacy of dexamethasone and
betamethasone for the treatment of antepartum HELLP
(hemolysis, elevated liver enzymes, and low platelet count)
syndrome. Am J Obstet Gynecol 2001;184(7):1332-1339. (Pro-
spective randomized trial of 40 patients)
102. Gilbert WM, Towner DR, Field NT, et al. The safety and util-
ity of pulmonary artery catheterization in severe preeclamp-
sia and eclampsia. Am J Obstet Gynecol 2000;182(6):1397-1403.
(Retrospective chart review 1995-1997 of 115 patients)
103. Clark SL, Cotton DB. Clinical indications for pulmonary ar-
tery catheterization in the patient with severe preeclampsia.
Am J Obstet Gynecol 1988;158(3):453-458. (Expert opinion/re-
view)
104. Farag K, Hassan I, Ledger WL. Prediction of preeclampsia:
can it be achieved? Obstet Gynecol Surv 2004 Jun;59(6):464-
482; quiz 485. (Review)
105. Nielson JP. Interventions for suspected placenta praevia.
Cochrane Database Syst Rev 2003;(2):CD001998. (Cochrane
18 EMPractice.net • December 2004
 review) 85. The percentage of patients with placental abruption

COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC
106. Royal College of Obstetricians and Gynaecologists, Clinical presenting with either uterine hypertonia or intra-
Green Top Guidelines. Placenta Praevia: Diagnosis and Man-
uterine fetal demise is:
agement (27) -- Jan 2001. Available at: http://www.rcog.org.
uk/guidelines.asp?PageID=106&GuidelineID=17. Accessed a. 1%
December 15, 2004. (Guidelines) b. 15%
107. Nielson JP. Interventions for treating placental abruption. c. 30%
Cochrane Database Syst Rev 2003;(1):CD003247. (Cochrane d. 50%
review)

86. Ultrasound is much more sensitive in detecting

placental abruption then placental previa.
Physician CME Questions a. True
b. False
79. The absence of proteinuria on dipstick definitively
excludes the diagnosis of preeclampsia. 87. In suspected placental abruption with imminent
a. True delivery, vaginal delivery is contraindicated:
b. False a. True
b. False
80. The first-line medication for management of
eclamptic seizures is: 88. The primary reason to consider expectant manage-
a. Dilantin ment in confirmed placental previa is to:
b. Phenobarbital a. Avoid cesarean section
c. Magnesium b. Minimize blood loss
d. Tegretol c. Accelerate lung maturity in a preterm fetus
e. Valproic Acid d. Prevent Rh sensitization

81. The IV antihypertensive most often used in the set- 89. The diastolic blood pressure threshold for initiation
ting of hypertensive urgency with preeclampsia is: of antihypertensive treatment in preeclampsia is:
a. Esmolol a. 80
b. Labetalol b. 90
c. Hydralazine c. 100
d. Nipride d. 110
e. Nifedipine
90. The primary role for the use of corticosteroids in the
82. For gestational hypertension, all of the following are treatment of preeclampsia is to:
true except: a. Hasten fetal lung development
a. The BP is >140/90 b. Prevent hemolysis
b. Proteinuria is present c. Prevent seizures
c. No other features of preeclampsia are present d. Prevent encephalopathy
d. Blood pressure returns to normal after delivery
91. Risk factors for preeclampsia include all of the fol-
83. All of the following are components of HELLP syn- lowing except:
drome except: a. Multiparity
a. Hemolysis b. Maternal age > 35
b. Elevated lactate c. Hydatidiform mole
c. Elevated liver enzymes d. Chronic hypertension
d. Low platelets
92. Vaginal bleeding occurs in approximately what
84. The prevalence of preeclampsia in pregnant, nul- percentage of patients with placental abruption:
liparous women is: a. 10%
a. 0.5 – 1% b. 20%
b. 1-2% c. 50%
c. 5-10% d. 75%
d. 15-20%
93. Ultrasound is the definitive diagnostic test for pla-
cental abruption:
a. True
b. False

December 2004 • EMPractice.net 19 Emergency Medicine Practice

 94. The initial dose of magnesium used to prevent sei- Physician CME Information
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zures with preeclampsia is: This CME enduring material is sponsored by Mount Sinai School of Medicine
a. 1-2 gm and has been planned and implemented in accordance with the Essentials
and Standards of the Accreditation Council for Continuing Medical Education.
b. 2-4 gm
Credit may be obtained by reading each issue and completing the printed
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Target Audience: This enduring material is designed for emergency medicine
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This test concludes the July through December 2004
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• Non-randomized or retrospective sociation and representatives from the gency Medicine Practice six-month testing period, complete the post-test and
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