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Postpartum Hemorrhage in Emergency Medicine Clinical Presentation

  • Author: Maame Yaa A B Yiadom, MD, MPH; Chief Editor: Bruce M Lo, MD, CPE, RDMS, FACEP, FAAEM, FACHE  more...
Updated: Nov 08, 2015


The clinical history should be taken as a primary survey (ABCs) of the patient. This should include collecting an initial set of vital signs to guide the patient’s management, as the patient is positioned to begin the physical examination. Keep in mind, that if the bleeding is very brisk, the patient’s mental status may wane. As a result, this first set of questions should include queries about signs and symptoms that are most crucial in managing potential circulatory collapse, identifying the cause of postpartum hemorrhage (PPH), and selecting appropriate therapies.[10]

Severity of bleeding

Consider the following:

  • Is the placenta delivered?
  • What has been the duration of the third stage of labor?
  • How long has the bleeding been heavy?
  • Was initial postdelivery bleeding light, medium, or heavy?
  • Are symptoms of hypovolemia present such as dizziness/lightheadedness, changes in vision, palpitations, fatigue, orthostasis, syncope or presyncope?
  • If evaluating a patient with delayed postpartum hemorrhage, what has been the bleeding pattern since delivery?

Intervention guides

Obtain the following information:

  • Is there a history of transfusion? What was the reason for transfusion? Is there a history of a transfusion reaction?
  • Past medical history (particularly cardiovascular, pulmonary, or hematologic conditions)
  • Allergies

Predisposing factors and potential etiology

Obtain the following information:

  • History of postpartum hemorrhage
  • Gravity, parity, length of most recent pregnancy, history of multiple gestations
  • Number of fetuses for the most recent pregnancy
  • Pregnancy complications (polyhydramnios, infection, vaginal bleeding, placental abnormalities)
  • If the placental was delivered, was it spontaneous, or was manual delivery required?
  • Current and past history of vaginal delivery versus cesarean delivery
  • If cesarean delivery, was it planned in advance, decided upon after a failed vaginal delivery attempt, or performed emergently?
  • Other uterine surgeries such as myomectomy (transvaginal vs transabdominal), uterine septum removal
  • Personal or family history of bleeding disorder
  • Medications such as prescribed, over the counter, diet supplements, or vitamins (with particular attention to anticoagulants, platelet inhibitors, uterine relaxants, and antihypertensives)
  • Vaginal penetration since delivery (tampons, finger, other foreign object, vaginal intercourse)
  • Signs or symptoms of infection such as uterine pain or tenderness, fever, tachycardia, or foul vaginal discharge
  • Information helpful for continued management
  • When and where was the delivery?
  • Who assisted the delivery?
  • Where and with whom was prenatal care?
  • Healthy infant(s) delivered (any complications or concerns before, during, or after delivery)?
  • Past surgical history


As mentioned earlier, patients with postpartum hemorrhage (PPH) should be managed like all emergency department resuscitation situations, with the history and physical examination occurring simultaneously while following acute life support algorithms.

The physical examination should focus on determining the cause of the bleeding. The patient may not have the typical hemodynamic changes of shock early in the course of the hemorrhage due to physiologic maternal hypervolemia.

Important organ systems to assess include the pulmonary system (evidence of pulmonary edema), the cardiovascular (heart murmur, tachycardia, strength of peripheral pulses), and neurological systems (mental status changes from hypovolemia).The skin should also be checked for petechiae or oozing from skin puncture sites, which could indicate a coagulopathy, or a mottled appearance, which can be indicative of severe hypovolemia.

Looking for occult postpartum hemorrhage—in the form of a pelvic, vaginal, uterine, or abdominal wall hematoma, or intra-abdominal or perihepatic bleeding—is always an important consideration when unstable hemodynamic findings are present without evidence of excessive vaginal blood loss.

Having a gynecologic examination bed is helpful but not necessary. The patient's pelvis can always be elevated on an inverted bedpan (thick-side toward the patient's feet) cushioned with towels and a sheet for comfort.

Ensure that good lighting and suction are available before beginning the following evaluations:

  • Abdominal examination: Pain and tenderness (concerning for retained placenta tissue, rupture, or endometritis), distension, boggy or grossly palpable uterus (at or above the umbilicus) is suggestive of atony. Palpation of an overdistended bladder may indicate a barrier to adequate uterine contraction.
  • Perineal examination: A brisk bleed should be visible at the introitus; identify any perineal lacerations.
  • Speculum examination: Gently suction blood, clots, and tissue fragments as needed to maintain the view of the vagina and cervix. Careful inspection of the cervix and vagina under good light may reveal the presence and extent of lacerations.
  • Bimanual examination: Bimanual palpation of the uterus may reveal bogginess, atony, uterine enlargement, or a large amount of accumulated blood. Palpation may also reveal hematomas in the vagina or pelvis. Assess if the cervical os is open or closed.
  • Placental examination: Examine the placenta for missing portions, which suggest the possibility of retained placental tissue.


The 4Ts of postpartum hemorrhage (PPH) +1: tone, trauma, tissue, thrombosis, and traction. More than one of these can cause postpartum hemorrhage in any given patient.

Uterine atony


Atony is by far the most common cause of postpartum hemorrhage. Uterine contraction is essential for appropriate hemostasis, and disruption of this process can lead to significant bleeding. Uterine atony is the typical cause of postpartum hemorrhage that occurs in the first 4 hours after delivery.

Risk factors for atony include the following:

  • Overdistended uterus (eg, multiple gestation, fetal macrosomia, polyhydramnios)
  • Fatigued uterus (eg, augmented or prolonged labor, amnionitis, use of uterine tocolytics such as magnesium or calcium channel blockers)
  • Obstructed uterus (eg, retained placenta or fetal parts, placenta accreta, or an overly distended bladder)

Laceration or hematoma


Trauma to the uterus, cervix, and/or vagina is the second most frequent cause of postpartum hemorrhage. Injury to these tissues during or after delivery can cause significant bleeding because of their increased vascularity during pregnancy. Vaginal trauma is most common with surgical or assisted vaginal deliveries. It also occurs more frequently with deliveries that involve a large fetus, manual exploration, instrumentation, a fetal hand presenting with the head, or spontaneously from friction between mucosal tissue and the fetus during delivery. Cervical lacerations are rarer now that forceps-assisted deliveries are less common. They are more likely to occur when delivery assistance is provided before the cervix is fully dilated.

Risk factors for trauma include the following:

  • Delivery of a large infant
  • Any instrumentation or intrauterine manipulation (eg, forceps, vacuum, manual removal of retained placental fragments)
  • Episiotomy

Retained placenta


Retained placental tissue is most likely to occur with a placenta that has an accessory lobe, deliveries that are extremely preterm, or variants of placenta accreta. Retained or adherent placental tissue prevents adequate contraction of the uterus allowing for increased blood loss.

Risk factors for retained products of conception include the following:

  • Prior uterine surgery or procedures
  • Premature delivery
  • Difficult or prolonged placental delivery
  • Multilobed placenta
  • Signs of placental accreta by antepartum ultrasonography or MRI

Clotting disorder


During the third stage of labor (after delivery of the fetus), hemostasis is most dependent on contraction and retraction of the myometrium. During this period, coagulation disorders are not often a contributing factor. However, hours to days after delivery, the deposition of fibrin (within the vessels in the area where the placenta adhered to the uterine wall and/or at cesarean delivery incision sites) plays a more prominent role. In this delayed period, coagulation abnormalities can cause postpartum hemorrhage alone or contribute to bleeding from other causes, most notably trauma. These abnormalities may be preexistent or acquired during pregnancy, delivery, or the postpartum period.

Potential causes include the following:

  • Platelet dysfunction: Thrombocytopenia may be related to preexisting disease, such as idiopathic thrombocytopenic purpura (ITP) or, less commonly, functional platelet abnormalities. Platelet dysfunction can also be acquired secondary to HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count).
  • Inherited coagulopathy: Preexisting abnormalities of the clotting system, as factor X deficiency or familial hypofibrinogenemia
  • Use of anticoagulants: This is an iatrogenic coagulopathy from the use of heparin, enoxaparin, aspirin, or postpartum warfarin.
  • Disseminated intravascular coagulation (DIC): This can occur, such as from sepsis, placental abruption, amniotic fluid embolism, HELLP syndrome, or intrauterine fetal demise.
  • Dilutional coagulopathy: Large blood loss, or large volume resuscitation with crystalloid and/or packed red blood cells (PRBCs), can cause a dilutional coagulopathy and worsen hemorrhage from other causes.
  • Physiologic factors: These factors may develop during the hemorrhage such as hypocalcemia, hypothermia, and acidemia.

Uterine inversion

"Traction": The traditional teaching is that uterine inversion occurs with an atonic uterus that has not separated well from the placenta as it is being delivered, or from excessive traction on the umbilical cord while placental delivery is being assisted. Studies have yet to demonstrate the typical mechanism for uterine inversion. However, clinical vigilance for inversion, secondary to these potential causes, is generally practiced. Inversion prevents the myometrium from contracting and retracting, and it is associated with life-threatening blood losses as well as profound hypotension from vagal activation.

Contributor Information and Disclosures

Maame Yaa A B Yiadom, MD, MPH Staff Physician, Department of Emergency Medicine, Cooper University Hospital, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School

Maame Yaa A B Yiadom, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Public Health Association, National Medical Association, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


Daniela Carusi, MD, MSc Instructor, Obstetrics and Gynecology and Reproductive Biology, Harvard Medical School; Consulting Physician, Department of Obstetrics and Gynecology, Medical Director, Department of General Ambulatory Gynecology, Brigham and Women's Hospital

Daniela Carusi, MD, MSc is a member of the following medical societies: American College of Obstetricians and Gynecologists, Association of Reproductive Health Professionals, Massachusetts Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Mark Zwanger, MD, MBA Assistant Professor, Department of Emergency Medicine, Jefferson Medical College of Thomas Jefferson University

Mark Zwanger, MD, MBA is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Bruce M Lo, MD, CPE, RDMS, FACEP, FAAEM, FACHE Medical Director, Department of Emergency Medicine, Sentara Norfolk General Hospital; Associate Professor, Assistant Program Director, Core Academic Faculty, Department of Emergency Medicine, Eastern Virginia Medical School

Bruce M Lo, MD, CPE, RDMS, FACEP, FAAEM, FACHE is a member of the following medical societies: American Academy of Emergency Medicine, American Association for Physician Leadership, American College of Emergency Physicians, American College of Healthcare Executives, American Institute of Ultrasound in Medicine, Emergency Nurses Association, Medical Society of Virginia, Norfolk Academy of Medicine, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Assaad J Sayah, MD, FACEP Chief, Department of Emergency Medicine; Senior Vice President, Primary and Emergency Care, Cambridge Health Alliance

Assaad J Sayah, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, Massachusetts Medical Society, National Association of EMS Physicians

Disclosure: Nothing to disclose.


Special thanks to Dr. Donnie Bell for his assistance with the "Imaging" section for this topic.

The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous author, Michael P Wainscott, MD, to the development and writing of this article.

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