Uterine bleeding associated with an obstetric complication can lead to severe hemorrhage, hypovolemic shock, infection and coagulation disorders. Not only is the pregnant patient at risk for increased morbidity and mortality, but the fetus may also be adversely affected. In the prehospital setting, a patient complaint of vaginal bleeding during pregnancy heightens the suspicion that the uterus is the source of hemorrhage. This is alarming, since the pregnant uterus is very vascular and has a rich blood supply. Interestingly, it is possible for the pregnant patient to be experiencing severe uterine bleeding but present with little to no vaginal bleeding.
Vaginal bleeding during pregnancy can occur at any time and may be due to a variety of conditions. Bleeding that occurs prior to the 20th week of gestation commonly results from ectopic pregnancy or spontaneous abortion. Vaginal bleeding in late pregnancy is considered to occur during or after the 20th week of gestation. Approximately 4% of pregnant patients will experience bleeding after the 20th week of gestation. Late-pregnancy bleeding often arises from abnormal or premature separation of the placenta from the innermost uterine wall. Abnormal separation of the placenta exposes uterine blood-filled sinuses, which are small, irregular vascular channels in the endometrium that form during pregnancy, and placental vessels, which leads to hemorrhage.
Following fertilization, the ovum travels down the fallopian tube over one to five days and enters the uterus. Once it reaches the uterus, it begins to develop as a blastocyst. After one to three days in the uterus, the blastocyst implants itself in the innermost uterine wall-the endometrium. Implantation typically occurs in the upper portion of the uterus, in or near the fundus, where the uterine blood supply is very rich. The blastocyst typically does not implant in the lower segment of the uterus or near or on the cervix, due to a much poorer blood supply. If attachment does occur in the lower uterine segment, vessel and tissue growth usually extends upward toward the fundus, where the endometrium is much more vascular. Once implantation has occurred, thread-like structures begin to invade and grow into the endometrium. Cells from both the blastocyst and endometrium grow rapidly to form the placenta and other structures associated with pregnancy.
The placenta is a temporary organ of pregnancy; however, it is one of the most vital organs for fetal survival. It is the life support system for the growing fetus. In essence, it provides for fetal respiration, nutrition and elimination of wastes. The placenta is a disk-shaped structure that is about 15 to 20 cm in diameter and 1.5 to 3.0 cm thick. The side of the placenta that is adhered to the uterus has a rough surface, representing the structures of attachment and circulation; the side facing the fetus is smooth. The umbilical cord connects the fetus to the placenta and contains one vein and two arteries.
The primary functions of the placenta are diffusion of oxygen and nutrients from the mother's circulation through the placenta and into the fetal circulation, and removal of carbon dioxide and other waste products through diffusion from the fetal circulation, through the placenta and into the mother's blood. Early in pregnancy, the permeability is low and the surface area for effective diffusion is small. However, in later pregnancy, the diffusion is great due to the increase in surface area and thin placental membrane allowing for greater permeability.
If abnormal and premature separation of the placenta from the uterine wall occurs, a disturbance in the diffusion of oxygen, nutrients and waste products may result, leaving the fetus hypoxic and without an effective means of nutrition or elimination of waste products. In addition, the mother may suffer serious hemorrhage from the exposed rich vascular uterine tissue, which then may lead to hypovolemic shock. The vasoconstriction of vessels associated with the maternal response to shock may significantly reduce perfusion to the placenta, further decreasing fetal oxygenation, nutrition and waste elimination. Two common etiologies associated with abnormal placental separation and uterine bleeding are abruptio placentae and placenta previa.
Abruptio placentae is premature separation of the placenta from the uterine wall after the 20th week of gestation. It is important to note that the placenta is normally positioned high in the uterus in this condition. It occurs in about 1% of all pregnancies and accounts for approximately 30% of the bleeding episodes late in pregnancy and 15% of fetal perinatal deaths. About 50% of fetal deaths are due to maternal hypoxia. Maternal and fetal mortality are related to severe maternal hemorrhage, hypovolemic shock and a coagulation disorder. The severity of the condition depends on the degree of placental separation, extent of hemorrhage, gestational age of the fetus, health status of the mother and fetus, and access to advanced obstetric care.
Abruptio placentae is thought to occur as a result of degenerative changes in the arterioles that nourish the inner uterine lining (deciduas basalis) and supply blood to the placenta. As a result of the loss in blood supply, the decidua tissue begins to die, making the vessels prone to rupture. Because the pregnant uterus is distended, the smooth muscle can't contract effectively to tamponade the bleeding vessels. A hematoma forms behind the placenta, increasing the pressure and causing further separation from the uterine wall with increased hemorrhage. Compression of the placental vessels and tissue by the hematoma can compromise circulation to the fetus. If the margins of the placenta remain intact, the bleeding may stay concealed while pressure within the hematoma continues to build. The buildup of blood causes the uterus to become irritable and tender. Eventually, the blood may permeate through the placenta and be released into the amniotic sac and into the peritoneal cavity. This may weaken the bulky middle uterine muscle layer (myometrium) and make it prone to rupture with increasing pressure. The ruptured uterus would cause severe maternal hemorrhage and hypovolemic shock. The placenta may also be separated at its margin, allowing the blood to flow freely into the uterus. As a result of the severe bleeding, the maternal blood-clotting cascade is triggered and may lead to disseminated intravascular coagulation (DIC), an acute coagulation (clotting) disorder. Both severe maternal and fetal distress will occur. If a complete or near-complete abruption is present, fetal death is almost inevitable, unless an emergency cesarean section can be immediately performed.
Blunt trauma to the pregnant abdomen may also be an etiology of abruptio placentae. The placenta is a relatively inelastic organ, whereas the uterus is relatively elastic. This may cause the placenta to be traumatically sheared from the uterine wall when significant blunt force is applied to the abdomen, causing the uterus to stretch at the time of impact.
The exact cause of abruptio placentae is still unknown; however, there are certain conditions or behaviors that place the patient at an increased risk. The most consistent and common risk factor is maternal hypertension, which occurs in approximately 44% of all cases. This may be a result of pregnancy-induced hypertension (PIH) or chronic hypertension. Hypertension in the pregnant patient is defined as a blood pressure of 140/90 mmHg or greater, or a systolic blood pressure greater than 30 mmHg and a diastolic blood pressure greater than 15 mmHg beyond the pre-pregnancy baseline blood pressure. Hypertension is thought to cause changes in the placental vessel integrity and separation at the decidua layer. Other predisposing factors include:
Increasing maternal age (generally over 35 years of age)
Cigarette smoking (causing vasoconstriction of the arteries in the decidua)
Premature rupture of the amniotic sac at less than 34 weeks of gestation
Vascular disease (includes diabetes mellitus)
Trauma to the pregnant abdomen (1.5% to 9.4% of all cases)
Previous abruptio placentae
Needle puncture from an amniocentesis
Alcohol (ethanol) consumption (14 or more drinks per week)
Cocaine and methamphetamine abuse (causes hypertension and vasoconstriction of decidual arteries)
Multiparity (usually greater than five pregnancies) leads to more damaged and thinner endometrial layer
Short umbilical cord
Signs and Symptoms
The signs and symptoms of abruptio placentae depend on the type and amount of placental separation from the uterus. The types of separation are:
Partial separation with the placental margins intact
Bleeding occurs behind the placenta and is not able to escape due to the intact margins. Vaginal bleeding will not be present; however, the patient may complain of abdominal pain and uterine tenderness, and may present with signs and symptoms of hemorrhage and shock.
Partial separation without an intact placental margin
The bleeding will be allowed to escape from the placental margin that is torn free from the uterine wall. The patient will present with vaginal bleeding and most likely abdominal pain and uterine tenderness. The amount of vaginal bleeding is dependent on the severity of uterine bleeding.
The placenta has completely separated from the uterine wall. The patient will likely complain of abdominal pain, uterine tenderness, uterine contractions and vaginal bleeding, and exhibit signs and symptoms of hypovolemia. If a complete central separation occurs but the margins of the placenta remain intact, vaginal bleeding will not initially be present; however, the patient may present with signs and symptoms of hypovolemia, shock and abdominal pain. The abdomen will also likely enlarge and the uterus will be rigid.
Abruptio placentae may also be classified as mild, moderate and severe. A mild abruption occurs when less than one-sixth of the placenta is separated from the uterus. If it is a central abruption and the margins of the placenta are intact, vaginal bleeding would not likely be present. If it is a mild partial separation, vaginal bleeding would be evident. If the abruption is mild, the pregnant patient may complain of what appear to be labor pains or false labor, which are associated with uterine irritation. The uterus may be tender and the patient may complain of a backache. Approximately half of abruptions are mild.
A moderate abruption is defined as a one-sixth to two-thirds separation of the placenta from the uterus. The patient will complain of moderate to severe uterine tenderness with possible contractions. Vaginal bleeding may or may not be present, depending on whether the placental margins remain intact. The fetus will typically exhibit signs of distress, such as fetal bradycardia. Moderate abruption comprises approximately one-quarter of the cases.
A severe abruption is associated with greater than two-thirds placental separation from the uterus. If the margins are not intact, severe vaginal bleeding will be present. The uterus will be tender and rigid, and the patient will complain of severe abdominal pain. The fetus will be in severe distress and is prone to fetal death unless immediate delivery can be accomplished. If the entire placenta separates, severe maternal hemorrhage, hypovolemic shock, fetal and/or maternal death, and DIC are likely to occur.
The patient experiencing an abruptio placentae will typically present with the following:
Abdominal pain or lower lumbar pain and uterine tenderness (70%)
Vaginal bleeding (80%)
Abnormal uterine contractions (35%)
Fetal distress (60%).
Another system to classify abruptio placentae according to clinical characteristics is as follows:
Grade 0 or Class 0
The patient is asymptomatic. A retroperitoneal clot is found after delivery of the placenta.
Grade I or Class 1
The patient presents with mild to no vaginal bleeding, slight uterine tenderness, normal maternal heart rate and blood pressure, and no fetal distress.
Grade II or Class 2
The patient presents with moderate to no vaginal bleeding, moderate to severe uterine tenderness, possible uterine contractions, maternal tachycardia and orthostatic vital signs, and fetal distress.
Grade III or Class 3
The patient presents with severe to no vaginal bleeding; severe uterine pain; hypotension; pale, cool, and clammy skin; tachycardia; and a narrow pulse pressure. Fetal death is likely.
Placenta previa is another common cause of vaginal bleeding in the latter half of pregnancy. It is associated with abnormal implantation of the placenta over or near the cervical os (opening). When the uterus undergoes change in preparation for labor and delivery, the placenta may be torn away from the uterine wall, leading to hemorrhage. Placenta previa occurs in approximately 0.3% to 0.5% of all pregnancies. Prior cesarean section delivery increases the risk by 1.5 to 5 times; thus, this is important information to obtain when gathering the patient history. Fetal mortality is approximately 2%-3%.
Placenta previa occurs when the placenta is abnormally implanted near the margin of, or partially or totally covering, the cervical os. As the cervix begins to elongate and thin (effacement) or dilate during labor, the placenta is sheared from the uterine wall, exposing torn vessels and the uterine sinus. The uterus is not able to adequately contract to stop the bleeding from the open vessels or sinuses, leading to potential severe hemorrhage.
Placenta previa is generally classified by the site of placental implantation. The classifications are:
Low-lying placenta previa
The placenta is implanted in the lower uterine segment with the edges positioned approximately 2-5 cm from the cervical os.
Marginal placenta previa
The edge of the placenta is implanted at the margin of the internal cervical os.
Partial placenta previa
The internal cervical os is partially covered by the placenta.
Total placenta previa
The internal cervical os is completely covered by the abnormally implanted placenta.
In addition to hemorrhage and possible hypovolemic shock, other complications include preterm delivery, abnormal fetal presentations (hand, foot), disseminated intravascular coagulation and abruptio placentae. Fetal mortality most often resulting from maternal hemorrhage and preterm delivery ranges from 12%-29%.
The actual cause of placenta previa remains unknown; however, several factors are associated with an increased incidence of the condition. These factors are:
Maternal age >35 years (uterus is not as vascular as a younger uterus)
Multiparity (permanent damage may occur to endometrium from previous placental implantations)
Uterine scarring (Cesarean section, abortion or other uterine surgeries)
A short umbilical cord (weight of the fetus may pull the placenta downward)
Multiple gestation (lack of space in uterus causes low uterine implantation)
Dilation and curettage (D and C)
Endometritis (possible damage to vascular network and defective endometrial lining)
Large placenta (may cause placenta to migrate downward toward cervix)
Smoking (causes reduced blood supply to uterine lining)
Cocaine use (causes reduced blood supply to uterine lining)
Previous placenta previa.
Signs and Symptoms
The hallmark sign of placenta previa is painless vaginal bleeding in late pregnancy. The onset of bleeding is associated with the amount of placenta covering the cervical os. Typically, the more placenta covering the cervical os, the earlier the onset of bleeding. The bleeding may occur with or without uterine contractions. Detachment of the placenta is not painful, thus, if the mother is in labor, she will not experience uterine pain between contractions. This is unlike abruptio placentae, where the patient experiences abdominal pain and uterine tenderness.
Common signs and symptoms of placenta previa include:
Vaginal bleeding (usually occurs in third trimester, may be bright red) that is painless
Hypotension if bleeding is severe
Uterus remains soft and nontender.
Prehospital Management of Abruptio Placentae and Placenta Previa
Prehospital emergency care is focused on supporting vital functions: establish and maintain an adequate airway, ventilation, oxygenation and circulation. Provide a high concentration of oxygen. Establish at least one large-bore intravenous line and infuse lactated Ringer's (LR) or normal saline to maintain maternal and fetal perfusion. Continuously monitor vital signs, since the amount of vaginal bleeding may not truly represent the stage of hemorrhage the patient is experiencing. It is important to note that the pregnant patient may lose up to 30% of her circulating blood volume before she exhibits obvious signs and symptoms of hypovolemic shock, especially hypotension, due to the 40%-50% increase in the circulating blood volume experienced in pregnancy. Even though the pregnant patient is not presenting with obvious signs of shock while bleeding, the blood supply to the placenta and fetal circulation may be drastically reduced prior to reaching the 30% maternal blood loss. If possible, monitor the fetal heart tones.
Fetal bradycardia is an indication of fetal distress. Fetal heart rates should be evaluated in all pregnant patients with the complaint of abdominal pain, uterine cramping or vaginal bleeding. In the field, fetal heart tones can be evaluated by use of a Doppler. When using Doppler on the abdomen of a pregnant patient, it is imperative to ensure that the fetal heart rate obtained by Doppler does not correlate with the mother's heart rate. If so, it is likely that the fetal heart tones are being mistaken for the pulse heard at the maternal abdominal aorta. If the pulse obtained by Doppler is different from the mother's, it is the fetal heart tones that you are hearing. If fetal bradycardia is present, or the patient has vaginal bleeding, uterine cramping or abdominal pain, transport her to a medical facility that has obstetric capabilities.
Anath CV, Oyelese Y, Yeo L, et al. Placental abruption in the United States, 1976 through 2001: Temporal trends and potential determinants. Am J Obstet Gynecol 192(1):191-198, 2005.
Collins NJ. Abruptio placentae. www.nursingceu.com/courses/81/index_nceu.html. January 1, 2005.
Collins N. Placenta previa. www.nursingceu.com/courses/48index-nceu.html. January 1, 2005.
Creasy R, Resnick R. Maternal and Fetal Medicine, 3rd ed. Philadelphia: Saunders, 2000.
Gaufberg SV. Abruptio placentae. www.emedicine.com/emerg/topic12.htm. August 29, 2006.
Getahun D, Oyelese Y, Salihu HM, Anath CV. Obstet Gynecol 107(4):771-778, 2006.
Gilbert E, Harmon J. High Risk Pregnancy and Delivery, 3rd ed. St. Louis: Mosby Inc., 2003.
Gorrie T. Foundations of Maternal-Newborn Nursing, 2nd ed. Norwalk: Appleton & Lange, 2000.
Guton AC, Hall JE. Textbook of Medical Physiology, 10th ed. Philadelphia: W.B. Saunders, 2001.
Joy S. Placenta previa. www.emedicine.com/med/topic3271.htm. June 13, 2006.
Ko P. Placenta previa. www.emedicin.com/emerg/topic427.htm. January 6, 2005.
Lowdermilk D, Bobak I, Perry S. Maternity and Women's Healthcare, 7th ed. St. Louis: Mosby Inc., 2000.
Marx JA, Hockberger RS, Walls RM. Rosen's Emergency Medicine: Concepts and Clinical Practice, 5th ed. St. Louis: Mosby, Inc., 2002.
Mahlmeiser L, May K. Comprehensive Maternity Nursing, 4th ed. Philadelphia: Lippincott, 2003.
Miller DA, Chollet JA, Goodwin TM. Clinical risk factors for placenta previa-placenta accreta. Am J Obstet Gynecol 177(1):210-214, Jul 1997.
Nichols F, Zwelling E. Maternal-Newborn Nursing, 3rd ed. Philadelphia: Saunders, 2003.
Oyelese Y, Smulian JC. Placenta previa, placenta accreta, and vasa previa. Obstet Gynecol 107(4):927-941, 2006.
Reeder S. Maternity Nursing: Family, Newborn, and Women's Health Care, 17th ed. Philadelphia: Williams and Wilkins, 2000.
Salihu HM, Bekan B, Aliyu MH, et al. Perinatal mortality associated with abruptio placentae in singletons and multiples. Am J Obstet Gynecol 193(1):198-203, Jul 2005.
Tikkanen M, Nuutila M, Hiilesmaa V, et al. Clinical presentation and risk factors of placental abruption. Acta Obstet Gynecol Scand 85(6):700-705, 2006.
Wong D, Perry S, Hess C. Maternal and Child Nursing Care, 2nd ed. St. Louis: Mosby, Inc., 2002.
Joseph J. Mistovich, MEd, NREMT-P, is a professor and the chair of the Department of Health Professions at Youngstown (OH) State University, author of several EMS textbooks and a nationally recognized lecturer.
William S. Krost, BSAS, NREMT-P, is an operations manager and flight paramedic with the St. Vincent/Medical University of Ohio/St. Rita's Critical Care Transport Network (Life Flight) in Toledo, Ohio, and a nationally recognized lecturer.
Daniel D. Limmer, AS, EMT-P, is a paramedic with Kennebunk Fire-Rescue in Kennebunk, Maine, and a faculty member at Southern Maine Community College. He is the author of several EMS textbooks and a nationally recognized lecturer.