December 2004Volume 6, Number 12

Authors

Ruth Selvidge, MDDepartment of Emergency Medicine, Boston Medical Center—Boston, MA.

Robert Dart, MDChief of Emergency Services, Quincy Medical Center—Quincy, MA.

Peer Reviewer

Jessica Freedman, MDAssociate Residency Director, Assistant Professor, Department of Emergency Medicine, Mount Sinai School of Medicine—New York, NY.

Andy Jagoda, MD, FACEPVice-Chair of Academic Affairs, Department of Emergency Medicine; Residency Program Director, Mount Sinai School of Medicine—New York, NY.

CME Objectives

Upon completing this article, you should be able to:Discuss the role of ultrasound in identifying and/or excluding placenta previa or abruption in patients presenting with second- or third-trimester vaginal bleeding;Describe the management options for patients presenting with eclampsia or severe preeclampsia;Discuss the indications and contraindications to expectant management in patients diagnosed with preeclampsia, placental abruption, and placental previa; andList laboratory abnormalities that are frequently identified in patients with severe preeclampsia.

Date of original release: December 17, 2004. Date of most recent review: December 13, 2004. See “Physician CME Information” on back page.

1.

2.

3.

4.

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.

EMERGENCY MEDICINE PRACTICE A N E V I D E N C E - B A S E D A P P R O A C H T O E M E R G E N C Y M E D I C I N E

EMPRACTICE.NET

Emergencies In The Second And Third Trimesters:Hypertensive Disorders And Antepartum HemorrhageA 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 normal. As you are approaching her to obtain the history and physical, she collapses and begins having a tonic-clonic seizure.

EMERGENCY physicians are faced with complications of first-trimester pregnancies, such as threatened and spontaneous abortions, as well as

ectopic pregnancy, on a daily basis. Complications of late pregnancy are less frequently managed in the ED, and therefore can be more intimidating to emergency physicians. However, the appropriate diagnosis and man-agement of these conditions can significantly impact maternal and fetal outcomes. Thus it is important that emergency physicians remain abreast of the clinical presentation, diagnosis, and management of the most common complications of late pregnancy; namely, preeclampsia/eclampsia, placenta previa, and placental abruption.

TerminologyGestational hypertension is defined as a BP greater than 140/90, without pro-teinuria, which returns to normal after delivery, and is not associated with any of the other features of preeclampsia. Preeclampsia is defined as a BP greater than 140/90, associated with pro-teinuria (≥300 mg/24 hr, or persistent 1+ of dipsticks on multiple occasions). Preeclampsia may be classified as mild or severe. Mild preeclampsia consists of a DBP >90 but <110 and lacks any of the features of severe preeclampsia. Severe preeclampsia consists of a DBP ≥110 on 2 occasions, or after treat-ment with antihypertensive medication, and/or has any of the following features: oliguria, pulmonary edema, thrombocytopenia, severe proteinuria (≥3.5 gm/24hr, or 2 random UAs with 3+ protein by dipstick), right upper

CO

PY

RIG

HTE

D M

ATE

RIA

L—D

O N

OT

PH

OTO

CO

PY

OR

DIS

TRIB

UTE

ELE

CTR

ON

ICA

LLY

WIT

HO

UT

WR

ITTE

N C

ON

SEN

T O

F EB

PR

AC

TIC

E, L

LC

Emergency Medicine Practice 2 EMPractice.net • December 2004

quadrant (RUQ) abdominal pain, CNS manifestations, such as headache, scotomata, blurred vision, or changes in mental status, and/or HELLP syndrome. HELLP syndrome is defined as hemolysis (abnormal peripheral smear, or bilirubin ≥1.2 mg/dL, or LDH ≥600), elevated liver enzymes (aminotransferase ≥2X normal) and low platelets (platelet count <100,000µL).1,2 The above entities must be distinguished from chronic hypertension, defined by a BP >140/90 before 20-weeks gestation or prior to pregnancy, and/or hypertension which does not resolve postpartum. Preeclampsia can be superimposed on chronic hypertension, and these patients meet the criteria for both preeclampsia and chronic hypertension. In patients with chronic hypertension, a diagnosis of superimposed preeclampsia is made when there is an increase in blood pressure or proteinuria over baseline, and/or evidence of new end-organ damage. It is important to be aware that these definitions are somewhat arbitrary. Preeclampsia is an unpredictable disease, and women with mild hyper-tension and minimal proteinuria can have a fulminant course resulting in eclampsia. No studies have been able to identify an accurate method for predicting which women will progress to the more severe forms of HELLP or eclampsia. In the past, edema was an important crite-rion for diagnosing preeclampsia, but studies reveal that edema is as common in normal pregnancies, and therefore is not predictive of disease severity. Similarly, in the past an increase of 30 in the systolic BP or 10 in the diastolic BP would define preeclampsia, but studies have not shown increased morbidity in these women, so the absolute value of blood pressure >140/90 is now the accepted criterion.3 However, the American College of Obstetrics and Gy-necology (ACOG), as well as the National High Blood Pressure Education Working Group, still recommend that women with edema or significant changes in their pre-natal blood pressure be followed closely.4 Finally, women without proteinuria, but with elevated blood pressure and evidence of new end-organ damage — in other words, any of the above-mentioned criteria for severe preeclampsia — should be considered preeclamptic and managed iden-tically.5

Placental abruption, also called abruptio placentae, is defined as the premature separation of the placenta from the uterus. It was first described in 1775 as bleeding into the decidual basalis from abnormal small uterine arterial vessels.6,7 Bleeding from both arterial and venous origins has been described. The resulting hematoma may be small and self-limited, resulting in a partial abruption, or it may continue to dissect through decidual layers, resulting in complete separation of the placenta from the underlying uterus, a phenomenon called total abruption. Placenta previa refers to a placenta that is found to cov-er, or be in close approximation to, the internal cervical os. There are 4 different degrees of previa. Total placenta previa occurs when the internal os is completely covered by the placenta. Partial placenta previa means the internal os is partly covered by placenta. In marginal placenta previa, the placental edge is at the margin of the internal os. Finally,

with a low-lying placenta, the placenta is in close proximity to the internal os, but does not touch it. The terms placenta accreta, increta, or percreta are used to describe a placenta that remains firmly attached to the lower uterine segment, and therefore does not deliver nor-mally. These complications are seen in about 7% of cases of placenta previa.8 These women are at increased risk of hemorrhage, hysterectomy, blood transfusions, and death. Mortality is as high as 10%.9

Critical Appraisal Of The Literature

Obtaining Investigational Review Board approval for studies involving pregnant women can be extremely difficult, resulting in too few randomized clinical tri-als on these topics. A January 2004 MEDLINE search on preeclampsia yielded over 7000 articles; however, this list was comprised of an abundance of retrospective and case-control studies, with their well-defined weaknesses. Many studies had small sample sizes, as well, which makes the results even less compelling. An additional problem among preeclampsia papers is that the definitions for hypertension and preeclampsia are not uniform. Further-more, it is likely that preeclampsia is a syndrome, and therefore arbitrary definitions do not adequately reflect the continuum of changes seen in the disease.3 Some authors believe that preeclampsia may represent several different conditions, resulting in a variety of clinical presentations.10 Another issue is raised when reviewing older studies; as the disease has become better understood, clinical definitions have changed, and therefore earlier studies may not reflect today’s definitions.3 For example, earlier studies may have included women with chronic hyper-tension among the preeclampsia group, or women with edema and changes in blood pressure that would not meet today’s criteria for preeclampsia. (See Table 1.) A number of practice guidelines and systematic reviews exist that are relevant to the management of these conditions. The National High Blood Pressure Education Program Working Group has published guidelines on the

Table 1. Risk Factors For Preeclampsia.

Nulliparity

Chronic hypertension

Age under 20 or over 35

Multiple pregnancy

Pregnancy assisted by reproductive technology

Obesity

New paternity

Preexisting vascular, autoimmune, or renal disease

Triploidy

Excessive weight gain in 3rd trimester

Hydatidiform mole

Family history of preeclampsia

History of placental abruption in prior pregnancy

CO

PY

RIG

HTED

MA

TERIA

L—D

O N

OT P

HO

TOC

OP

Y O

R D

ISTRIB

UTE ELEC

TRO

NIC

ALLY

WITH

OU

T WR

ITTEN C

ON

SENT O

F EB P

RA

CTIC

E, LLC

3 Emergency Medicine PracticeDecember 2004 • EMPractice.net

management of hypertension in pregnancy.3 In addition, The American College of Obstetrics and Gynecology has published guidelines on the diagnosis and management of both preeclampsia and eclampsia.4 A systematic review on interventions for suspected placenta previa has been pub-lished in the Cochrane Database.11 And finally, a system-atic review has been published in the Cochrane Database on interventions for treating placental abruption.12

Epidemiology, Etiology, And Pathophysiology

Prevalence About a quarter of all pregnant nulliparous women will develop a hypertensive disorder, and 5-10% will meet di-agnostic criteria for preeclampsia.13 Eclampsia appears to be decreasing in frequency, involving 1/700 deliveries in the 1970s, 1/1150 deliveries in the 1980s, and approximate-ly 1/2300 deliveries in the 1990s.14 This trend is thought to be secondary to improving prenatal care, early detection and delivery of preeclamptic mothers, and prophylactic use of magnesium sulfate. There is also evidence that the onset of eclampsia is shifting towards the postpartum period.15

The incidence of placental abruption is about 6 per 1000 singleton births.16 It is a significant cause of maternal and fetal morbidity and mortality. Perinatal mortality associated with abruption is 119 per 1000, births compared to about 8 per 1000 among all births.16 This condition is responsible for 12-25% of all perinatal deaths.16,17 Maternal complications include hemorrhage requiring transfusion, shock, renal failure, disseminated intravascular coagu-lopathy, couvelaire uterus (also known as uteroplacental apoplexy) that on occasion requires hysterectomy, chorio-amnionitis, and, rarely, death.18,19

Neonatal complications include low birth weight or small for gestational age,16 preterm birth,20 and prema-ture rupture of membranes (PROM).18,19 There is a 9-fold adjusted, relative risk of stillbirth with abruption. The rate of stillbirth significantly increases with severe placental abruption, defined as abruptions involving greater than 50% of the placenta.21

Placenta previa occurs in about 4/1000 singleton de-liveries22 and causes death in about 0.03% of these cases.23 Serious maternal complications include intra- and postpar-tum hemorrhage, hysterectomy, placental abruption, and blood transfusion. Pregnancies complicated with placenta previa necessitate cesarean delivery and also have been associated with higher rates of septicemia and thrombo-phlebitis.23,24 Most of the perinatal morbidity and mortal-ity results from prematurity, since 47% of pregnancies with placenta previa must be delivered prior to full-term. Placenta previa is occurring with increasing frequency and authors speculate that this may be secondary to increasing rates of cesarean section, which is a prominent risk factor.

PathophysiologyPreeclampsiaDespite years of research the cause of preeclampsia re-

mains elusive. There seem to be 2 phases to the syndrome: first, a placental phase, followed by a second, systemic phase, with effects on multiple organs. The link between the 2 phases has not been fully understood. In normal pregnancy, remodeling of the uterine spiral arteries (the terminal branches of the uterine artery) is accomplished by invasion of the arterioles by placental endovascular trophoblasts. The remodeling is completed by the end of the 2nd trimester and results in a low-resis-tance arteriolar system, which accommodates a 10-fold increase in uterine blood flow. In preeclampsia many of the arterioles escape remodeling, thus remaining thick and muscular. This leads to increased vascular resistance, and secondarily decreased blood flow through the preeclamp-tic arterioles. Therefore these vessels are unable to meet the increasing blood flow demands of the fetus leading to placental ischemia.25 The placental ischemia in turn results in the release of certain vasoactive molecules, which act on the maternal vascular endothelium.26,27 Some authors have also implicated oxygen free radicals as a contributing factor in this process.28,29

Most authors feel that endothelial activation is the final common pathway for the changes seen in preeclamp-sia. Endothelial activation has multiple effects, including: release of endothelin and thromboxane, increased sensitiv-ity to angiotensin II, and decreased formation of vasodila-tors, such as nitric oxide (NO) and prostacyclin. These changes are thought to be responsible for the preeclamptic patient’s increased vascular sensitivity to pressors, which results in hypertension, as well as the coagulation abnor-malities common in preeclampsia.30-32

A number of other factors have been proposed as con-tributors to the development of this syndrome. Multiple studies have shown a genetic predisposition to preeclamp-sia. Women with sisters or mothers who had preeclamp-sia have a 4-fold increased risk of severe preeclampsia,33 while increased risk to women with preeclamptic (pa-ternal) grandmothers has also been demonstrated.34 Still other studies suggest that an infectious etiology acts as a contributing factor.35-38 Finally, some studies suggest that an immunologic factor specific to a presumed paternal antigen may play a role in the prevention of the develop-ment of preeclampsia in subsequent pregnancies involving the same parents. Evidence for this mechanism includes the fact that preeclampsia is more common in 1st pregnan-cies, and that it occurs more frequently in multiparous women with new partners (ie, “new paternity”),39 and less frequently in women with a history of prior abortions.40

Risk FactorsMany studies have documented risk factors for pre-eclampsia (Table 1). One of the most significant risk factors is nulliparity. In addition, preeclampsia is more common in women under the age of 20 or over the age of 35. Chron-ic hypertension, multiple or IVF pregnancies, obesity, prior history of severe preeclampsia or placental abrup-tion, diabetes, excessive weight gain in pregnancy, and/or preexisting vascular, autoimmune, or renal diseases have

CO

PY

RIG

HTE

D M

ATE

RIA

L—D

O N

OT

PH

OTO

CO

PY

OR

DIS

TRIB

UTE

ELE

CTR

ON

ICA

LLY

WIT

HO

UT

WR

ITTE

N C

ON

SEN

T O

F EB

PR

AC

TIC

E, L

LC

Emergency Medicine Practice 4 EMPractice.net • December 2004

all been implicated. Hydatiform mole has also been associ-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 AbruptionThe 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 FactorsA 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

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 PreviaAs 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

Table 2. Differential Diagnosis Of Antepartum Hemorrhage.

Differential Diagnosis Diagnostic Criteria Coagulation Profile Fetus Presentation

Acute placental abruption Clinical diagnosis and pathology, ultrasound MAY reveal large clot

Abnormal in about 30% Normal or demise with large abruption

Acute, severe abdominal pain and vaginal bleeding, or concealed bleeding +/- shock

Chronic abruption or marginal sinus abruption

Clinical diagnosis and pathology

Usually normal Usually viable; atincreased risk for prematurity

Chronic mild bleeding with no fetal compromise

Placenta previa Ultrasound Normal Usually viable; atincreased risk for prematurity

Painless vaginal bleeding

Bloody show of normal labor

Clinical diagnosis mini-mal bleeding & fetal well-being

Normal Normal Scant blood mixed with mu-cus and contractions at term

Vasa previa Ultrasound with color Doppler, test for fetal blood in vaginal blood

Normal May be normal, or distress/demise from bleeding

Vaginal bleeding, usually mother hemodynamically stable

Antepartum hemorrhage of unknown origin

Diagnosis of exclusion Normal Increased risk of fetal anomalies and preterm birth

Minimal vaginal bleeding and hemodynamically stable

CO

PY

RIG

HTED

MA

TERIA

L—D

O N

OT P

HO

TOC

OP

Y O

R D

ISTRIB

UTE ELEC

TRO

NIC

ALLY

WITH

OU

T WR

ITTEN C

ON

SENT O

F EB P

RA

CTIC

E, LLC

5 Emergency Medicine PracticeDecember 2004 • EMPractice.net

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.

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

Illustrations by Erin Dart

Figure 3. Partial placenta previa. Figure 4. Complete placenta previa.

Figure 1. Low lying placenta. Figure 2. Marginal placenta previa.

CO

PY

RIG

HTE

D M

ATE

RIA

L—D

O N

OT

PH

OTO

CO

PY

OR

DIS

TRIB

UTE

ELE

CTR

ON

ICA

LLY

WIT

HO

UT

WR

ITTE

N C

ON

SEN

T O

F EB

PR

AC

TIC

E, L

LC

Emergency Medicine Practice 6 EMPractice.net • December 2004

generally painless, women with placenta previa who are 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 PreeclampsiaIt 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

in eclamptic patients.54 A small case-control study has 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

CO

PY

RIG

HTED

MA

TERIA

L—D

O N

OT P

HO

TOC

OP

Y O

R D

ISTRIB

UTE ELEC

TRO

NIC

ALLY

WITH

OU

T WR

ITTEN C

ON

SENT O

F EB P

RA

CTIC

E, LLC

7 Emergency Medicine PracticeDecember 2004 • EMPractice.net

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/TriageUnstable PatientPatients 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.

Stable PatientThe 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

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/ cerebral hemorrhage

CT/MRI scan

Cerebral venous thrombosis CT/MRI scan

Drug- or alcohol-induced seizure Tox screen

Metabolic-related seizure Glucose and electrolytes

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•

CO

PY

RIG

HTE

D M

ATE

RIA

L—D

O N

OT

PH

OTO

CO

PY

OR

DIS

TRIB

UTE

ELE

CTR

ON

ICA

LLY

WIT

HO

UT

WR

ITTE

N C

ON

SEN

T O

F EB

PR

AC

TIC

E, L

LC

Emergency Medicine Practice 8 EMPractice.net • December 2004

not diagnostic, often occur when preeclampsia progresses 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

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-

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.”

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. ▲

CO

PY

RIG

HTED

MA

TERIA

L—D

O N

OT P

HO

TOC

OP

Y O

R D

ISTRIB

UTE ELEC

TRO

NIC

ALLY

WITH

OU

T WR

ITTEN C

ON

SENT O

F EB P

RA

CTIC

E, LLC

9 Emergency Medicine PracticeDecember 2004 • EMPractice.net

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 StudiesA 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

are helpful in assessing kidney function. An elevated uric 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

UltrasoundIn 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

CO

PY

RIG

HTE

D M

ATE

RIA

L—D

O N

OT

PH

OTO

CO

PY

OR

DIS

TRIB

UTE

ELE

CTR

ON

ICA

LLY

WIT

HO

UT

WR

ITTE

N C

ON

SEN

T O

F EB

PR

AC

TIC

E, L

LC

Emergency Medicine Practice 10 EMPractice.net • December 2004

Clinical Pathway: Management Of Bleeding In Late Pregnancy

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.

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.

Hypotension/Tachycardia?

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.

Obtain thorough history and physical

Obtain ultrasound if no prior ultrasound for

previa

Consider bloody show, rupture of membranes

Reassess vital signs regularly to look for

decompensation

•

•

•

•

• Place patient on monitored bed; address airway and breathing problems (Class II)

• High-flow oxygen by facemask (Class III)

• Left lateral decubitus position (Class III)

• Prompt vascular access with large-bore peripheral venous catheters (Class II)

• Check bedside glucose if mental status is not normal, treat hypoglycemia (Class I)

• 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)

• Send complete blood count, blood bank specimen for type and cross and Rh testing

and DIC (Class II)➤

Emergent Obstetric Consultation

Decompensation?

➤

YES

➤

YESNO ➤

➤➤

➤➤

➤

YES

Consult Ob for definitive management:

delivery vs expectant management for

pregnancy remote from term

Consider bedside ultrasound

Pelvic exam to exclude vasa previa and

assess cervical dilation

Continue close monitoring of vital signs

Consider morphine for analgesia

Await Ob for definitive management:

delivery versus expectant management for

pregnancy remote from term

•

•

•

•

•

➤YES

➤

➤

Heavy vaginal bleeding?

Prior ultrasound ruling out previa?

Patient stabilizes with fluid resuscitation?

Placental abruption highly likely

PreviaNo previaPatient stabilizes with fluid resuscitation?

Emergent bedside ultrasound

➤YES

➤YES NO

➤

➤

NO

➤

NO

➤NO

Transfuse 2-4 µ PRBCs

Prepare OR for double set up/rapid delivery

Correct clotting abnormalities as indicated

•

•

•

CO

PY

RIG

HTED

MA

TERIA

L—D

O N

OT P

HO

TOC

OP

Y O

R D

ISTRIB

UTE ELEC

TRO

NIC

ALLY

WITH

OU

T WR

ITTEN C

ON

SENT O

F EB P

RA

CTIC

E, LLC

11 Emergency Medicine PracticeDecember 2004 • EMPractice.net

➤

➤

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.

Clinical Pathway: Management Of TheHypertensive Woman In Late Pregnancy

Blood pressure greater than 140/90?

Hydralazine 5 mg IV or 10 mg IM (Class II)

➤

➤YES

Obtain urine for protein

Check for symptoms of severe preeclampsia:

headache, abdominal pain, visual changes,

nausea/vomiting

Obtain CBC to identify anemia and/or thrombo-

cytopenia, LDH/reticulocyte count and LFTs to

diagnose HELLP

Obtain electrolytes to assess renal function

Obtain uric acid level: marker for severe pre-

eclampsia

Obtain U/S RUQ for abdominal pain

•

•

•

•

•

•

• Place patient on monitored bed in the resuscitation area; address airway and

breathing problems (Class II)

• High-flow oxygen by facemask (Class III)

• Left lateral decubitus position (Class III)

• Prompt vascular access with large-bore peripheral venous catheters (Class II)

• Obtain prompt Ob/Gyn consultation

DBP >110 on two measurements?

➤

YES

NO➤

➤➤

YES

Consult Ob/Gyn for definitive management

of delivery

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

continue after 15 min (Class I)Check bedside glucose if mental status is not normal,

treat hypoglycemia (Class I)Check bedside hemoglobin (if available), identify

anemia (Class II)Frequently reassess vital signs (Class II)For persistent seizures after 2 doses of magnesium,

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

•

•

•

•

•

•

➤YES

Findings suggestive of hypertensive emergency?

(Seizure, pulmonary edema, changes in mental status)

Seizure or postictal?

➤

YES

➤

➤NO

Consult Ob/Gyn for definitive

management, ie, delivery

and/or transfer for pregnancy

remote from term

Diagnosis preeclampsia?

➤

➤

➤

NO

CO

PY

RIG

HTE

D M

ATE

RIA

L—D

O N

OT

PH

OTO

CO

PY

OR

DIS

TRIB

UTE

ELE

CTR

ON

ICA

LLY

WIT

HO

UT

WR

ITTE

N C

ON

SEN

T O

F EB

PR

AC

TIC

E, L

LC

Emergency Medicine Practice 12 EMPractice.net • December 2004

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 TestsThe 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/PreviaUnstable Patient or FetusIn 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 FetusFull-term PregnancyIn the stable patient with suspected abruption or previa,

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 PregnancyMultiple 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

Continued from page 9

CO

PY

RIG

HTED

MA

TERIA

L—D

O N

OT P

HO

TOC

OP

Y O

R D

ISTRIB

UTE ELEC

TRO

NIC

ALLY

WITH

OU

T WR

ITTEN C

ON

SENT O

F EB P

RA

CTIC

E, LLC

13 Emergency Medicine PracticeDecember 2004 • EMPractice.net

(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/ProphylaxisWhile 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

eclampsia with magnesium treatment.86 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

Table 7. Anticonvulsant Dosage For Eclampsia Or Preeclampsia.

Agent Loading Dose Maintenance IM Dosing (Parkland IM Protocol)

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

•

•

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

•

Phenytoin 10-20 mg/kg to a maximum rate of 50 mg/min

•

Diazepam 5 mg/min up to a max of 20 mg•

CO

PY

RIG

HTE

D M

ATE

RIA

L—D

O N

OT

PH

OTO

CO

PY

OR

DIS

TRIB

UTE

ELE

CTR

ON

ICA

LLY

WIT

HO

UT

WR

ITTE

N C

ON

SEN

T O

F EB

PR

AC

TIC

E, L

LC

Emergency Medicine Practice 14 EMPractice.net • December 2004

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.

fetuses have been reported. Other antihypertensive agents 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.)

CorticosteroidsA 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-

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.

IntubationIndications 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 MonitoringSwan-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

PreeclampsiaMuch 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

CO

PY

RIG

HTED

MA

TERIA

L—D

O N

OT P

HO

TOC

OP

Y O

R D

ISTRIB

UTE ELEC

TRO

NIC

ALLY

WITH

OU

T WR

ITTEN C

ON

SENT O

F EB P

RA

CTIC

E, LLC

15 Emergency Medicine PracticeDecember 2004 • EMPractice.net

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.

• 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. ▲

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 PreviaA 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 AbruptionSimilarly, 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

trials need to be performed, in order to identify the opti-mal management strategy for this entity.107

Disposition

DischargeA 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/HospitalizationHospitalization 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

TransferConsider 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.▲

CO

PY

RIG

HTE

D M

ATE

RIA

L—D

O N

OT

PH

OTO

CO

PY

OR

DIS

TRIB

UTE

ELE

CTR

ON

ICA

LLY

WIT

HO

UT

WR

ITTE

N C

ON

SEN

T O

F EB

PR

AC

TIC

E, L

LC

Emergency Medicine Practice 16 EMPractice.net • December 2004

References

Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The find-ings of a large, prospective, randomized, and blinded trial should carry more weight than a case report. To help the reader judge the strength of each refer-ence, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the reference, where available. In addition, the most informative references cited in the paper, as determined by the authors, will be noted by an asterisk (*) next to the number of the refer-ence.

1. Sibai BM. The HELLP syndrome: much ado about nothing? Am J Obstet Gynecol 1990;162(2):311-316. (Review)

2. Sibai BM, Ewell M, Levine RJ, et al. Risk factors associated with preeclampsia in healthy nulliparous women. Am J Obstet Gynecol 1997;177(5):1003-1010. (Randomized prospective study of 4589 women analyzing calcium supplementation in pregnancy)

3. Various. National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Re-port of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol 2000;183(1):s1-s22. (Practice guideline)

4. ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. Int J Gynaecol Obstet 2002 Apr;77(1):67-75.

5.* Lain KY, Roberts JM. Contemporary concepts of the pathogenesis and management of preeclampsia. JAMA 2002;287(24):3183-3186. (Review)

6. Eskes TK. Abruptio placentae. Eur J Obstet Gynecol Reprod Biol 1997;75:63-70. (Review)

7. Speert H. In: Obstetric and Gynecologic Milestones Illustrated. New York, NY: The Parthenon Publishing Group; 1996:313-314. (Textbook)

8. Frederiksen MC, Glassenberg R, Stika CS. Placenta previa: A 22-year analysis. Am J Obstet Gynecol 1999;180(6 Pt 1):1432-1437. (Retrospective analysis of 93,384 deliveries including 514 cases of placenta previa)

9. Gielchinsky Y, Rojansky N, Fasouliotis SJ. Placenta accreta--summary of 10 years: a survey of 310 cases. Placenta 2002;23(2-3):210-214. (Retrospective analysis of 310 cases over 10 years)

10. Pipkin FB. Risk factors for preeclampsia. N Engl J Med 2001;344(12):925-926. (Review article)

11. Neilson JP. Interventions for suspected placenta previa. Cochrane Database Syst Rev. 2000;(2):CD001998. (Review of randomized controlled trials)

12. Neilson JP: Interventions for treating placental abruption. Cochrane Database Syst Rev. 2003;(1):CD003247. (Cochrane review)

13. Levine RJ, Hauth JC, Curet LB, et al. Trial of calcium to prevent preeclampsia. N Engl J Med 1997;337:69-76. (Large prospective randomized study of 4589 women: calcium supplementation in pregnancy).

14. Ventura SJ, Martin JA, Curtin SC, et al. Births: Final data for 1998. Natl Vital Stat Rep 2000 Mar 28;48(3):1-100. (Epidemio-logic data)

15. Chames MC, Livingston JC, Ivster TS, et al. Late postpar-tum eclampsia: A preventable disease? Am J Obstet Gynecol 2002;186(6):1174-1177. (Retrospective analysis of 89 women with eclampsia)

16. Ananth CV, Wilcox AJ. Placental abruption and perinatal mor-tality in the United States. Am J Epidemiol 2001;153(4):332-337. (Large retrospective study of 7,508,655 births between 1995 to1996)

17. Naeye RL, Harkness WL, Utts J. Abruptio placentae and perinatal death: a prospective study. Am J Obstet Gynecol 1977;128(7):740-746. (Retrospective review of 3987 unsuc-cessful deliveries among 53,518 pregnancy records)

18. Saftlas AF, Olson DR, Atrash HK, et al. National trends in the incidence of abruptio placentae, 1979-1987. Obstet Gynecol 1991;78:1081-1086. (Epidemiologic data)

19. Kramer MS, Usher RH, Pollack R, et al. Etiologic determinants of abruptio placentae. Obstet Gynecol 1997;89(2):221-226. (Cohort study 36,875 women 1978-1989)

20. Harris BA, Gore H, Flowers CE. Peripheral placental separa-tion: A possible relationship to premature labor. Obstet Gy-necol 1985;66:774-777. ( Basic science: studied 90 placentas from preterm births compared to 45 controls)

21. Ananth CV, Berkowitz GS, Savitz D,A et al. Placental abrupti-on and adverse perinatal outcomes. JAMA 1999;282(17):1646-1651. (Retrospective cohort study 53,371 pregnancies occur-ring in 40,789 women were analyzed)

22. Sheiner E, Shoham-Vardi I, Hallak M. Placenta previa: Obstet-ric risk factors and pregnancy outcome. J Matern Fetal Med 2001;10(6):414-419. (Retrospective case control study of 78,524 deliveries)

23. Iyasu S, Saftlas AK, Rowley DL, et al. The epidemiology of placenta previa in the United States, 1979 through 1987. Am J Obstet Gynecol 1993;168(5):1424-1429. (Retrospective analysis of 200,000 births from 1979 to 1987)

24. Crane JM, Van den Hof MC, Dodds L, et al. Maternal compli-cations with placenta previa. Am J Perinatol 2000;17(2):101-105. (Retrospective study of 308 cases of placenta previa over 8 years)

25. Granger JP, Alexander BT, Llinas MT, et al. Pathophysiology of hypertension during preeclampsia linking placental isch-emia with endothelial dysfunction. Hypertension 2001;38(3 Pt 2):718-722. (Descriptive review)

26. Roberts JM. Preeclampsia: What we know and what we do not know. Semin Perinatol 2000;24(1):24-28. (Review)

27. Gratton RJ, Gandley RE, Genbacev O. Conditioned medium from hypoxic cytotrophoblasts alters arterial function. Am J Obstet Gynecol 2001;184(5):984-990. (Animal study)

28. Dekker GA, Sibai BM. Etilogy and pathogenesis of preeclamp-sia: current concepts. Am J Obstet Gynecol 1998;179(5):1359-1375. (Review)

29. Sibai BM. Prevention of preeclampsia: a big disappointment. Am J Obstet Gynecol 1998;179(5):1275-1278. (Review)

30. Hayman R, Warren A, Brockelsby J, et al. Plasma from women with pre-eclampsia induces an in vitro alteration in the endothelium-dependent behaviour of myometrial resis-tant arteries. BJOG 2000 Jan;107(1):108-115. (Basic science, plasma collected from 18 women with preeclampsia and 18 normal women and incubated with uterine biopsies from normal women)

31. Ness RB, Roberts JM. Heterogeneous causes constituting the single syndrome of preeclampsia: A hypothesis and its impli-cations. Am J Obstet Gynecol 1996;175(5):1365-1370. (Descrip-tive review)

32. Walker JJ. Pre-eclampsia. Lancet 2000;356(9237):1260-1265. (Review)

33. Cincotta RB, Brennecke SP. Family history of pre-eclampsia as a predictor for pre-eclampsia in primigravidas. Int J Gynaecol Obstet 1998;60(1):23-27. (Prospective trial of 368 women)

34. Esplin MS, Fausett BM, Fraser A. Paternal and maternal components of the predisposition to preeclampsia. N Engl J Med 2001;344(12):867-872. (Retrospective 2998 men and 237 women)

35. Lie RT. Fetal and maternal contributions to the risk of pre-

CO

PY

RIG

HTED

MA

TERIA

L—D

O N

OT P

HO

TOC

OP

Y O

R D

ISTRIB

UTE ELEC

TRO

NIC

ALLY

WITH

OU

T WR

ITTEN C

ON

SENT O

F EB P

RA

CTIC

E, LLC

17 Emergency Medicine PracticeDecember 2004 • EMPractice.net

eclampsia population based study. BMJ 1998;316 :1343-1347. (Population-based study)

36. Robillard PY, Hulsey TC. Association of pregnancy induced hypertension with duration of sexual cohabitation before conception. Lancet 1994;344 :973-975. (Retrospective cohort study, 1011 consecutive women interviewed postdelivery)

37. Jenum PA, Stray-Pedersen B, Melby KK, et al. Incidence of toxoplasma gondii infection in 35,940 pregnant women in Norway and pregnancy outcome for infected women. J Clin Microbiol 1998;36 :2900-2906. (Large population study of incidence of T gondii in 35,940 women)

38. Trogstad LIS, Eskild A, Bruu AL, et al. Is preeclampsia an infectious disease? Acta Obstet Gynecol Scand 2001 Nov;80(11):1036-1038. (Prospective study 978 women)

39. Trupin LS, Simon LP, Eskenazi B. Change in paternity: a risk factor for preeclampsia in multiparas. Epidemiology 1996;7(3):240-244. (Prospective study of 5068 nulliparas and 5800 multiparas)

40. Eras JL, Saftlas AF, Triche E, et al. Abortion and its effect on risk of preeclampsia and transient hypertension. Epidemiol-ogy 2000;11(1):36-43. (Prospective study of 2,739 women)

41. Dommissee J, Tiltman AJ. Placental bed biopsies in placental abruption. Br J Obstet Gynaecol 1992;99:651-654. (Basic sci-ence)

42. Karegard M, Gennser G. Incidence and recurrence rate of ab-ruptio placentae in Sweden. Obstet Gynecol 1986;67:523-528. (Retrospective study of 894,619 births from 1973-1981)

43. Ananth CV, Simulian JC, Dimissie K, et al. Placental abruption among singleton and twin births in the U. S.: Risk Factors. Am J Epidemiol 2001;153:771-778. (Epidemiologic study of 7,465,858 singleton births compared to 193,266 twin births)

44. Ananth CV, Smulian JC, Vintzileos AM. Incidence of placental abruption in relation to cigarette smoking and hypertensive disorders during pregnancy: a meta-analysis of observation-al studies. Obstet Gynecol 1999;93:622-628. (Review)

45. Misra D, Ananth CV. Risk factor profiles of placental abrupti-on in first and second pregnancies: heterogeneous etiologies. J Clin Epidemiol 1999;52:453-461. (Prospective cohort 10,774 first pregnancies 6529 first and second pregnancies)

46. Major CA, De Veciana M, Lewis DF, et al. Obstetrics: Preterm premature rupture of membranes and abruptio placentae: is there an association between these pregnancy complications? Am J Obstet Gynecol 1995;172(2):672-676. (Retrospective cohort study of 756 singleton pregnancies with pre-term premature rupture of membranes compared to 11,240 controls)

47. Rathore SS, McMahon MJ. Racial variation in the frequency of intrapartum hemorrhage. Obstet Gynecol 2001;97:178-183. (Retrospective study of 867,759 singleton births 1990-1997)

48. Ananth CV, Wilcox AJ, Savitz DA, et al. Effect of maternal age and parity on the risk of uteroplacental bleeding disorders in pregnancy. Obstet Gynecol 1996;88:511-516. (Retrospective study of 121,082 singleton births)

49. Rasmussen S, Albrechtsen S, Dalaker K. Obstetric history and the risk of placenta previa. Acta Obstet Gynecol Scand 2000;79(6):502-507. (Large cohort study from birth registry in Norway from 1967 to 1992 of 779,642 women w/ 1,500,000 births)

50. Ananth CV, Smulian JC, Vintzileos AM. The association of pla-centa previa with history of cesarean delivery and abortion: a metaanalysis. Am J Obstet Gynecol 1997;177(5):1071-1078. (Meta-analysis of 36 studies 13,992 women with placenta previa out of 3.7 million women)

51. Hurd WW, Miodovnik M, Hertzberg V, et al. Selective management of abruptio placentae: a prospective study. Obstet Gynecol 1983;61:467-473. (Prospective study of 4,545 deliveries)

52. Chamberlain G, Steer P. ABC of labour care: obstetric emer-gencies. BMJ 1999;318(7194):1342-1345. (Placenta previa on

ultrasound pic in this article) (Review) 53. Chan CC, William WK. Antepartum hemorrhage of unknown

origin-What is its clinical significance? Acta Obstet Gynecol Scand 1999;78(3):186-190. (Retrospective case control study of 718 pregnancies with antepartum hemorrhage of un-known origin compared to 718 controls)

54. Small M. The utility of common clinical and laboratory param-eters to distinguish eclamptic from preeclamptic women in a developing country. Am J Obstet Gynecol 2001;185(6):s176. (Retrospective review of 62 preeclamptics and 20 eclamp-tics)

55. Barrilleaux PS, Rodts-Palenik S, Moore L, et al. Renal compro-mise as a component of HELLP syndrome morbidity. Am J Obstet Gynecol 2001;185(6):s186. (Case control study on 501 patients with HELLP syndrome, of which 55 patients were cases with renal involvement)

56. Witlin AG, Saade GR, Mattar F, et al. Risk factors for abruptio placentae and eclampsia: analysis of 445 consecutively man-aged women with severe preeclampsia and eclampsia. Am J Obstet Gynecol 1999;180(6):1322-1329. (Prospective study of 445 severely preeclamptic women)

57.* Sibai BM. Drug therapy: treatment of hypertension in preg-nant women. N Engl J Med 1996;335(4):257-265. (Review)

58. Holzman RS, Riley LE, Aron E, et al. Perioperative care of a patient with acute fatty liver of pregnancy. Anesth Analg 2001;92(5):1268-1270. (Case reports)

59. Pridjian G, Puschett JB. Preeclampsia. Part 1: clinical and pathophysiologic considerations. Obstet Gynecol Surv 2002 Sep;57(9):598-618. (Review)

60. Olesen AG, Svare JA. Decreased fetal movements: back-ground, assessment, and clinical management. Acta Obstet Gynecol Scand 2004;83: 818-826. (Systematic review)

61. Oyelese OK, Turner M, Lees C, et al. Vasa previa: an avoidable obstetric tragedy. Obstet Gynecol Surv 1999;54(2):138-145. (Review)

62. Sibai BM. Eclampsia. VI Maternal-perinatal outcome in 254 consecutive cases. Am J Obstet Gynecol 1990;163(3):1049-1054. (Retrospective analysis of 254 cases of eclampsia during 12 year period)

63. Meyer NL, Mercer BM, Friedman SA, et al. Urinary dipstick protein: a poor predictor of absent or severe proteinuria. Am J Obstet Gynecol 1994;170(1):137-141. (Retrospective study of 300 women)

64. Ducloy AS, Lee J. Obstetric Anaesthesia - Placental Abruption. World Anesth 2002;14(17):1. (Review article)

65. Neiger R, Krohn HJ, Trofatter MO. Plasma fibrin D-dimer in pregnancies complicated by partial placental abruption. Tenn Med 1997;90(10):403-405. (Prospective study of 25 women with antenatal bleeding compared to 30 controls)

66. Magriples U, Chan DW, Bruzek D, et al. Thrombomodulin: a new marker for placental abruption. Thromb Haemost 1999 Jan;81(1):32-34. (Prospective cohort study of 25 women: 8/25 had abruption)

67. Odunsi K, Bullough CH, Henzel J, et al. Evaluation of chemi-cal tests for fetal bleeding from vasa previa. Obstet Gynecol Surv 1997;52(8):465-466. (Blood from 20 women was mixed with fetal blood and the tests were performed)

68. Taipale P, Hiilesmaa V, Ylostalo P. Transvaginal ultrasonogra-phy at 18-23 weeks in predicting placenta previa at delivery. Ultrasound Obstet Gynecol 1998;12(6):377-379. (Prospective study of 3,696 women)

69. Barton JR, Sibai BM. Hepatic imaging in HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count). Am J Obstet Gynecol 1996;174(6):1820-1825. (Prospective study of 34 patients with HELLP syndrome)

70. Alamia V Jr, Meyer BA. Peripartum hemorrhage. Obstet Gyne-col Clin North Am 1999;26:385-398. (Review)

71. Bonnar J. Massive obstetric haemorrhage. Baillieres Best Pract Res Clin Obstet Gynaecol 2000 Feb;14(1):1-18. (Review)

CO

PY

RIG

HTE

D M

ATE

RIA

L—D

O N

OT

PH

OTO

CO

PY

OR

DIS

TRIB

UTE

ELE

CTR

ON

ICA

LLY

WIT

HO

UT

WR

ITTE

N C

ON

SEN

T O

F EB

PR

AC

TIC

E, L

LC

Emergency Medicine Practice 18 EMPractice.net • December 2004

72. Saller DN, Nagey DA, Pupkin MJ, et al. Tocolysis in the man-agement of third trimester bleeding. J Perinatol 1990;10:125-128. (Retrospective study of 29 women)

73. Knab DR. Abruptio placentae: an assessment of the time and method of delivery. Obstet Gynecol 1978;52:625-629. (Retro-spective study 388 cases abruption and literature review)

74. Towers CV, Pircon RA, Heppard M. Is tocolysis safe in the management of third-trimester bleeding? Am J Obstet Gynecol 1999;180(6):1572-1578. (Retrospective study of 131 cases of abruption and 105 cases of previa, comparing the 95 women with abruption and 76 patients with previa who received tocolysis, to those managed without tocolysis)

75. Scholl J. Abruptio placentae: clinical management in nonacute cases. Am J Obstet Gynecol 1987;156:40-51. (Retrospective study of 130 cases)

76. Combs CA, Nyberg DA, Mack LA, et al. Expectant manage-ment after sonographic diagnosis of placental abruption. Am J Perinatol 1992 ;9:170-174. (Case study, 40 patients)

77. Bond AL, Edersheim TG, Curry L. Expectant management of abruptio placentae before 35 weeks gestation. Am J Perinatol 1989;6(2):121-123. (Prospective study of 43 patients)

78. Sibai BM, Mercer BM, Schiff E et al. Aggressive versus expect-ant management of severe preeclampsia at 28 to 32 weeks’ gestation : A randomized controlled trial. Am J Obstet Gynecol 1994;171:818. (Randomized controlled trial of 95 patients)

79. Odendaal HJ, Pattison RC, Bam R, et al. Aggressive or expect-ant management for patients with severe preeclampsia be-tween 28 and 34 weeks’ gestation: A randomized controlled trial. Obstet Gynecol 1990; 76(6):1070-1075. (Randomized controlled trial of 58 women)

80. Many A, Kuperminc MJ, Pausner D, et al. Treatment of severe preeclampsia remote from term: A clinical dilemma. Obstet Gynecol Surv 1999;54(11):723-727. (Review)

81. Schiff E, Friedman SA, Sibai BM. Conservative management of severe preeclampsia remote from term. Obstet Gynecol 1994;84(4):626-630. (Review)

82. Coppage KH, Polzin WJ. Severe preeclampsia and delivery outcomes: is immediate cesarean delivery beneficial? Am J Obstet Gynecol 2002;186(5):921-923. (Retrospective chart review of 114 patients)

83. Watson KV, Moldow CF, Ogburn PL, et al. Magnesium Sulfate: Rationale for Its Use in Preeclampsia. Proc Natl Acad Sci USA. 1986 Feb;83(4):1075-1078. (Basic science)

84. Group TETC. Which anticonvulsant for women with eclamp-sia? Evidence from the collaborative eclampsia trial. Lancet 1995;345:1455-1463. (Multicenter randomized trial, 1,680 women with eclampsia)

85. Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. N Engl J Med 1995;333(4):201-206. (Randomized trial of 2,138 women with hypertension admitted in labor receiving either magnesium IM or phenytoin IV)

86.* Coetzee EJ, Dommisse J, Anthony J. A randomised controlled trial of intravenous magnesium sulphate versus placebo in the management of women with severe pre-eclampsia. Br J Obstet Gynaecol 1998;105(3):300-303. (Randomized con-trolled double blinded study of 699 women with severe preeclampsia)

87.* Livingston JC, Livingston LW, Ramsey R, et al. Magnesium sulfate in women with mild preeclampsia: a double blind, placebo-controlled trial. Am J Obstet Gynecol 2001;185(6):s75. (Randomized double blinded trial of magnesium versus placebo in 222 women)

88. CREST. 2001. Expert consensus based on RCOG.89. Anonymous. Nifedipine versus expectant management in

mild to moderate hypertension in pregnancy. Gruppo di studio ipertensione in gravidanza. Br J Obstet Gynaecol 1998;105(7):718-722. (Randomized control trial of 283 women)

90. Wide-Swensson DH, Ingemarsson I, Lunell NO, et al. Obstet-rics. Calcium channel blockade (isradipine) in treatment of hypetension in pregnancy: a randomized placebo-controlled study. Am J Obstet Gynecol 1995;173(3):872-878. (Randomized placebo controlled study of 111 women)

91. Sibai BM, Gonzalez AR, Mabie WC, et al. A comparison of labetalol plus hospitalization versus hospitalization alone in the management of preeclampsia remote from term. Obstet Gynecol 1987;70:323-7. (Randomized study of 200 women al-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 Gynecol 1992;167:879-84. (Randomized study of 200 women, 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

CO

PY

RIG

HTED

MA

TERIA

L—D

O N

OT P

HO

TOC

OP

Y O

R D

ISTRIB

UTE ELEC

TRO

NIC

ALLY

WITH

OU

T WR

ITTEN C

ON

SENT O

F EB P

RA

CTIC

E, LLC

19 Emergency Medicine PracticeDecember 2004 • EMPractice.net

review)106. Royal College of Obstetricians and Gynaecologists, Clinical

Green Top Guidelines. Placenta Praevia: Diagnosis and Man-agement (27) -- Jan 2001. Available at: http://www.rcog.org.uk/guidelines.asp?PageID=106&GuidelineID=17. Accessed December 15, 2004. (Guidelines)

107. Nielson JP. Interventions for treating placental abruption. Cochrane Database Syst Rev 2003;(1):CD003247. (Cochrane review)

Physician CME Questions

79. The absence of proteinuria on dipstick definitively excludes the diagnosis of preeclampsia.a. Trueb. False

80. The first-line medication for management of eclamptic seizures is:a. Dilantinb. Phenobarbitalc. Magnesiumd. Tegretole. Valproic Acid

81. The IV antihypertensive most often used in the set-ting of hypertensive urgency with preeclampsia is:a. Esmololb. Labetalolc. Hydralazined. Nipridee. Nifedipine

82. For gestational hypertension, all of the following are true except:a. The BP is >140/90b. Proteinuria is presentc. No other features of preeclampsia are presentd. Blood pressure returns to normal after delivery

83. All of the following are components of HELLP syn-drome except:a. Hemolysisb. Elevated lactatec. Elevated liver enzymesd. Low platelets

84. The prevalence of preeclampsia in pregnant, nul-liparous women is:a. 0.5 – 1%b. 1-2%c. 5-10%d. 15-20%

85. The percentage of patients with placental abruption presenting with either uterine hypertonia or intra-uterine fetal demise is:a. 1%b. 15%c. 30%d. 50%

86. Ultrasound is much more sensitive in detecting placental abruption then placental previa.a. Trueb. False

87. In suspected placental abruption with imminent delivery, vaginal delivery is contraindicated:a. Trueb. False

88. The primary reason to consider expectant manage-ment in confirmed placental previa is to:a. Avoid cesarean sectionb. Minimize blood loss c. Accelerate lung maturity in a preterm fetusd. Prevent Rh sensitization

89. The diastolic blood pressure threshold for initiation of antihypertensive treatment in preeclampsia is:a. 80b. 90c. 100d. 110

90. The primary role for the use of corticosteroids in the treatment of preeclampsia is to:a. Hasten fetal lung developmentb. Prevent hemolysisc. Prevent seizuresd. Prevent encephalopathy

91. Risk factors for preeclampsia include all of the fol-lowing except:a. Multiparityb. Maternal age > 35c. Hydatidiform moled. Chronic hypertension

92. Vaginal bleeding occurs in approximately what percentage of patients with placental abruption:a. 10%b. 20%c. 50%d. 75%

93. Ultrasound is the definitive diagnostic test for pla-cental abruption:a. Trueb. False

CO

PY

RIG

HTE

D M

ATE

RIA

L—D

O N

OT

PH

OTO

CO

PY

OR

DIS

TRIB

UTE

ELE

CTR

ON

ICA

LLY

WIT

HO

UT

WR

ITTE

N C

ON

SEN

T O

F EB

PR

AC

TIC

E, L

LC

Emergency Medicine Practice 20 EMPractice.net • December 2004

Emergency Medicine Practice is not affiliated with any pharmaceutical firm or medical device manufacturer.

Direct all editorial or subscription-related questions to EB Practice, LLC: 1-800-249-5770 • Fax: 1-770-500-1316 • Non-U.S. subscribers, call: 1-678-366-7933

EB Practice, LLC • 305 Windlake Court • Alpharetta, GA 30022E-mail: emp@empractice.net • Web Site: EMPractice.net

Emergency Medicine Practice (ISSN 1524-1971) is published monthly (12 times per year) by EB Practice, LLC, 305 Windlake Court, Alpharetta, GA 30022. Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and is intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The materials contained herein are not intended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of EB Practice, LLC. Copyright 2004 EB Practice, LLC. All rights reserved. No part of this publication may be reproduced in any format without written consent of EB Practice, LLC. Subscription price: $299, U.S. funds. (Call for international shipping prices.)

Publisher: Robert Williford. Executive Editor: Cheryl Strauss. Research Editors: Ben Abella, MD, University of Chicago; Richard Kwun, MD, Mount Sinai School of Medicine.

Physician CME InformationThis CME enduring material is sponsored by Mount Sinai School of Medicine and has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education. Credit may be obtained by reading each issue and completing the printed post-tests administered in December and June or online single-issue post-tests administered at EMPractice.net.

Target Audience: This enduring material is designed for emergency medicine physicians.

Needs Assessment: The need for this educational activity was determined by a survey of medical staff, including the editorial board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for emergency physicians.

Date of Original Release: This issue of Emergency Medicine Practice was published December 17, 2004. This activity is eligible for CME credit through December 1, 2007. The latest review of this material was December 13, 2004.

Discussion of Investigational Information: As part of the newsletter, faculty may be presenting investigational information about pharmaceutical products that is outside Food and Drug Administration approved labeling. Information presented as part of this activity is intended solely as continuing medical education and is not intended to promote off-label use of any pharmaceutical product. Disclosure of Off-Label Usage: This issue of Emergency Medicine Practice discusses no off-label use of any pharmaceutical product.

Faculty Disclosure: In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for this CME activity were asked to complete a full disclosure statement. The information received is as follows: Dr. Selvidge, Dr. Dart, Dr. Freedman, and Dr. Jagoda report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation.

Accreditation: Mount Sinai School of Medicine is accredited by the Accreditation Council for Continuing Medical Education to sponsor continuing medical education for physicians.

Credit Designation: Mount Sinai School of Medicine designates this educational activity for up to 4 hours of Category 1 credit toward the AMA Physician’s Recognition Award. Each physician should claim only those hours of credit actually spent in the educational activity. Emergency Medicine Practice is approved by the American College of Emergency Physicians for 48 hours of ACEP Category 1 credit (per annual subscription). Emergency Medicine Practice has been approved by the American Academy of Family Physicians as having educational content acceptable for Prescribed credit. Term of approval covers issues published within one year from the distribution date of July 1, 2004. This issue has been reviewed and is acceptable for up to 4 Prescribed credits. Credit may be claimed for one year from the date of this issue. Emergency Medicine Practice has been approved for 48 Category 2-B credit hours by the American Osteopathic Association.

Earning Credit: Two Convenient Methods • Print Subscription Semester Program: Paid subscribers with current and

valid licenses in the United States who read all CME articles during each Emer-gency Medicine Practice six-month testing period, complete the post-test and the CME Evaluation Form distributed with the December and June issues, and return it according to the published instructions are eligible for up to 4 hours of Category 1 credit toward the AMA Physician’s Recognition Award (PRA) for each issue. You must complete both the post-test and CME Evaluation Form to receive credit. Results will be kept confidential. CME certificates will be delivered to each participant scoring higher than 70%.

• Online Single-Issue Program: Paid subscribers with current and valid licenses in the United States who read this Emergency Medicine Practice CME article and complete the online post-test and CME Evaluation Form at EM-Practice.net are eligible for up to 4 hours of Category 1 credit toward the AMA Physician’s Recognition Award (PRA). You must complete both the post-test and CME Evaluation Form to receive credit. Results will be kept confidential. CME certificates may be printed directly from the Web site to each participant scoring higher than 70%.

94. The initial dose of magnesium used to prevent sei-zures with preeclampsia is:a. 1-2 gmb. 2-4 gmc. 4-6 gmd. 1-2 mg

This test concludes the July through December 2004semester testing period of Emergency Medicine Practice. The answer form for this semester and a return envelope have been included with this issue. Please refer to the instruc-tions printed on the answer form. All paid subscribers are eligible to take this test.

Monthly online CME testing is available for subscribersat no extra charge at http://www.empractice.net.

Class IAlways acceptable, safeDefinitely usefulProven in both efficacy and ef-fectiveness

Level of Evidence:One or more large prospective stud-ies are present (with rare exceptions)High-quality meta-analysesStudy results consistently positive and compelling

Class IISafe, acceptableProbably useful

Level of Evidence:Generally higher levels of evidenceNon-randomized or retrospective studies: historic, cohort, or case-control studiesLess robust RCTsResults consistently positive

Class IIIMay be acceptablePossibly usefulConsidered optional or alternative treatments

Level of Evidence:Generally lower or intermediate levels of evidence

•••

•

••

••

••

•••

•••

•

Case series, animal studies, consen-sus panelsOccasionally positive results

IndeterminateContinuing area of researchNo recommendations until further research

Level of Evidence:Evidence not availableHigher studies in progressResults inconsistent, contradictoryResults not compelling

Significantly modified from: The Emergency Cardiovascular Care Committees of the American Heart As-sociation and representatives from the resuscitation councils of ILCOR: How to Develop Evidence-Based Guidelines for Emergency Cardiac Care: Quality of Evidence and Classes of Recommenda-tions; also: Anonymous. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. Emergency Cardiac Care Committee and Subcom-mittees, American Heart Association. Part IX. Ensuring effectiveness of com-munity-wide emergency cardiac care. JAMA 1992;268(16):2289-2295.

•

•

••

••••

Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency Medicine Practice

receives a score based on the following definitions.

Coming in Future Issues:

Herbal Toxicities • Wound Care • Hand Injuries