Abruption/Dead Fetus Case File

Abruption/Dead Fetus Case File

Eugene C. Toy, MD, Edward Yeomans, MD, Linda Fonseca, MD, Joseph M. Ernest, MD

Case 7

A 26-year-old G1P0 at 34 3/7 weeks by last menstrual period (LMP) consistent with a first-trimester ultrasound (US) with singleton gestation presents to L&D because of mild contractions for the last 2 hours that are increasing in frequency and intensity. She also endorses decreased fetal movement since the onset of these contractions and had an episode of vaginal bleeding on arrival. She denies leakage of fluid or abdominal trauma. She has received scant prenatal care. She is Rh negative but has not received Rh immune globulin this pregnancy. She denies medical problems or surgeries.

Initial vital signs: T = 97.9°F, BP = 110/69 mm Hg, Pulse = 90 bpm, respiratory rate (RR) = 18 breaths/min. She appears uncomfortable due to contractions, lungs are clear, chest has regular rate and rhythm with grade 3/4 systolic ejection murmur, abdomen is tender in all quadrants and uterus feels hypertonic, extremities with 2+ edema bilaterally but without tenderness. The nurse is unable to detect fetal heart rate by external Doptones but contractions are detected by tocodynamometer every 2 to 3 minutes. A bedside US is performed and no fetal cardiac activity is detected. The placenta appears fundal and there is no evidence of retroplacental clot. Amniotic fluid is normal and fetal biometry is consistent with stated gestational age. On speculum examination, there is a golf-size clot in the vault and active bleeding noted. Her cervix is dilated to 2 cm, cervical length is 1 cm, and station is −2 on digital examination.

➤ What is the differential diagnosis?

➤ What is the most likely diagnosis?

➤ What should be involved in the management of this patient?

ANSWERS TO CASE 7:

Abruption/Dead Fetus

Summary: This is a primigravida at term with vaginal bleeding, fetal demise, preterm contractions, and hypertonic uterus.

➤ Differential diagnosis of the patient’s pain: Placental abruption, placenta previa, and vasa previa are important consideration in any patient that presents with bleeding during pregnancy. Other conditions that should be considered but are less likely based on the clinical presentation are appendicitis, urinary tract infections, labor, fibroid degeneration, and ovarian pathology.

➤ Most likely diagnosis: The most likely diagnosis in this case is placental abruption severe enough to kill the fetus.

➤ Next step in the management of this patient: Maternal stabilization is the priority in this case involving fetal demise. Close monitoring of hemorrhage, vital signs, urine output, and laboratory results for assessment of anemia and coagulopathy will help to determine hemodynamic status.

ANALYSIS

Objectives

1. Describe the clinical presentation of placental abruption.
2. List the risk factors of placental abruption.
3. Describe the diagnostic strategy and therapy for abruption.
4. List the complications of placental abruption.

Considerations

This 26-year-old woman is noted to have significant vaginal bleeding and a dead fetus. The most likely diagnosis is placental abruption. The diagnosis is a clinical one, and also to rule out other causes of vaginal bleeding, such as an ultrasound to assess placental location. Meanwhile, the patient should have two large-bore IVs placed and receive fluid resuscitation. This individual very well could have a coagulopathy, and should have a clinical assessment for overt coagulopathy, as well as a red top for clot retraction testing. Delivery is important, and a vaginal delivery should be the plan.

The diagnosis of placental abruption is a clinical one, however, presentation may vary. Most cases present with vaginal bleeding (66%) or abdominal pain/back pain (78%). Other signs/symptoms include fetal heart rate abnormalities (60%), preterm labor (22%), high-frequency contractions (17%), uterine hypertonus (17%), and dead fetus (15%)1 (Level II-2). The sensitivity of ultrasound in detecting placental abruption is poor (approximately 25%). As illustrated in this case, the absence of a retroplacental clot should not exclude this diagnosis when it is clinically suspected2 (Level II- 2). On the other hand, when a retroplacental clot is visualized by ultrasound the positive predictive value for an abruption at delivery is high.

Once the diagnosis is made, maternal resuscitation takes precedence in this patient of severe abruption with fetal demise. Regardless of gestational age, a vaginal delivery is recommended as long as the maternal hemodynamic status is stable. When the abruption is severe enough to kill the fetus, maternal blood loss can be estimated as approximately 50% of her blood volume3 (Level II-2). Therefore, it is important to have blood crossed for at least 4 units of packed red blood cells (PRBCs) when considering this principle; however, each case should be individualized based on the severity of abruption. Abruption involving a dead fetus also has a high risk of causing disseminated intravascular coagulopathy (DIC). Critical laboratory tests that should be drawn at regular intervals are as follows: CBC with platelets, coagulations studies (PT/INR/aPTT, fibrinogen, fibrin degradation products), and a comprehensive metabolic panel. Correction of anemia and/or DIC should be undertaken according to the patient’s hemodynamic status and/or laboratory results (see Table 7–1). Urine output should be closely monitored to ensure a minimum of 30 cc/h. Volume replacement with crystalloid or colloid applying the “3:1 rule” (3 mL of fluids for every 1 mL of blood loss) should be undertaken. Visual estimation of blood loss during an emergency is appropriate, however, weighing pads and chucks is a more accurate approach to the estimation of blood loss. This is done by subtracting the dry weight of disposable items (ie, pads) from the soiled material remembering that 1 g = 1 mL. If there is ongoing bleeding, a multidisciplinary team approach should be undertaken involving nursing staff, obstetricians, anesthesiologists, neonatologists (with viable fetus), specialists in gynecologic oncology, interventional radiologist, critical care as well as the laboratory, blood bank, and pharmacy personnel.

Preeclampsia labs should be drawn as well even in the absence of hypertension as elevated blood pressures may become apparent only after the maternal intravascular compartment has been refilled. Evaluation for fetalmaternal hemorrhage is important in this nonsensitized Rh-negative patient in order to determine the dose of Rh immune globulin to be administered. Toxicology screen should be considered if drug use such as cocaine is suspected. The placenta should be sent for pathologic examination.

Once maternal stabilization has been accomplished, induction or augmentation of labor should be initiated. The use of oxytocin, prostaglandins (E1 or E2), or mechanical dilators should be individualized. It is important to keep in mind that it is not the interval of time to delivery but rather maternal resuscitation

Table 7–1 BLOOD COMPONENT THERAPY
THERAPY	INDICATION	VOLUME PER UNIT	DOSE	RESULT
Packed red blood cells	Anemia; ↑O2 carrying capacity	250 mL		↑Hgb 1 g/dL ↑Hct 3% per unit
Platelets	Bleeding/DIC or surgery with platelets < 50,000/mm3	50-75 mL	6 units (1 unit per 10 kg weight)	↑Platelets by 5,000/mm3 per unit
Fresh frozen plasma	Clotting factor deficiencya	200-250 mL	4-6 units (10-20 mL/kg)	↑Fibrinogen 10 mg/dL per unit
Cryoprecipitate	Fibrinogen < 100 mg/dL, concern for volume overload	~15 mL	1 unit per 10 kg weight	↑Fibrinogen 5-15 mg/dL per unit

aProlonged PT/aPTT/INR, fibrinogen < 100 mg/dL.

with fluid and blood that predicts maternal outcome. Therefore, cesarean delivery should be considered only with special circumstances involving maternal hemodynamic instability or contraindications to vaginal delivery.

APPROACH TO

Abruption/Dead Fetus

Placental abruption is by definition premature separation of a normally implanted placenta. The frequency in which it occurs has been reported to be 1 in 200 deliveries. The incidence of placental abruption severe enough to kill a fetus has been reported as 1 in 1600 deliveries in recent years.4

Over half of all pregnancies complicated by placental abruption deliver preterm. Abruption is more common between 24 and 27 weeks gestational age5 (level III). The perinatal mortality rate for placental abruption is 119 per 1000 births compared with 8.2 per 1000 for all others. Although this high rate can be strongly associated with preterm delivery, the perinatal mortality was 25-fold higher with placental abruption at term.6 The risk of neurologic injury depends on gestational age and severity of abruption.

Risk Factors

There are many known risk factors for placental abruption. The most significant risk factor is hypertension including preeclampsia, gestational or chronic. The risk of abruption with early onset severe preeclampsia is in the order of 4% to 30%. It is also important to note that approximately 50% of abruption cases severe enough to kill a fetus involve a hypertensive disorder that may not become apparent until the intravascular compartment has been adequately refilled7 (Level II-3).

The risk of abruption with premature rupture of membranes is 4% to 12%. Abdominal trauma also increases the risk of placental abruption as well as fetal hemorrhage. Clinically evident abruption occurs in up to 40% of severe abdominal trauma and in only 3% of minor direct abdominal trauma. Uterine leiomyomas may also be a risk factor for abruption especially when they are large and retroplacental in location. Other risk factors include increased parity, maternal age, multiple gestation, polyhydramnios, chorioamnionitis, thrombophilias, smoking, and cocaine use.

The recurrence rate of severe placental abruption is approximately 12%8 (Level II-2) although up to 35% has been reported9 (Level II-2). Recurrence has also been reported to occur 1 to 3 weeks prior to the gestational age of the previous abruption.

Pathophysiology

The precise pathophysiology that leads to abruption is unknown in many instances. Most would agree that the most important factor is hemorrhage at the decidual-placental interface. Acute vasospasm of small vessels may precede hemorrhage and placental separation. Progressive hemorrhage causes compression of the overlying intervillous space with subsequent destruction of placental tissue. Gross examination of the placenta often reveals an organized clot on a depressed area of maternal surface. The “age” of the clot is often difficult to determine. The placenta may also appear completely unremarkable if abruption occurs just before delivery not allowing enough time for clot formation. Data from the New Jersey–Placental Abruption Study showed that concordance between clinical and histologic criteria is poor. Of the clinically diagnosed cases of abruption, the sensitivity and specificity for a histologic confirmation of abruption were 30% and 100%, respectively. Retroplacental clots were the most common (77%) findings in clinically apparent cases. Acute lesions associated with abruption included chorioamnionitis and funisitis while placental infarction was the only chronic histologic lesion associated with abruption10 (Level II-2).

A chronic placental disorder may be the underlying etiology of a placental abruption. Abnormal trophoblast invasion may lead to rupture of spiral arteries and premature separation of the placenta. There is also evidence suggesting that inflammatory cells which secrete cytokines and tumor necrosis factors (TNF) can lead to trophoblasts production of matrix metalloproteinase leading to premature placental detachment11 (Level II-2). Intrauterine growth restriction, preeclampsia, and oligohydramnios are associated with placental abruption providing further evidence of placental insufficiency as a causative factor.

Clinical Presentation

In addition to the previously mentioned signs and symptoms of abruption (see case discussion) there are other important clinical consequences. Abruption is the most common etiology in obstetrics of DIC. Consumptive coagulopathy is seen in approximately 30% of abruption cases severe enough to kill the fetus (fibrinogen <150 mg/dL in 38% and <100 mg/dL in 28%)3 (Level II-2). Thromboplastin release from placental separation activates the extrinsic pathway of the coagulation cascade. This event, in combination with retroplacental fibrin deposition (although to a lesser extent), contributes to depletion of clotting factors. Fibrin degradation productions are elevated in 85% to 100% of patients with DIC and are formed from the degradation of fibrinogen and fibrin by plasmin. Placental separation associated with abruption contributes to an increase in higher than normal FDP levels after delivery. Data supports a direct pathophysiologic relationship between high FDP (fibrin degradation products) levels (>300 mg/dL) and postpartum hemorrhage associated with abruption. Elevated FDP levels interfere with myometrial contractility12 (Level II-2). Couvelaire uterus is caused by extravasation of blood into the uterine musculature and serosa. This rarely interferes with myometrial contractility and is an unlikely reason for postpartum hemorrhage.

Acute renal failure secondary to under perfusion is common in untreated hemorrhage. Most cases are due to reversible acute tubular necrosis and less often due to irreversible cortical necrosis.

Concealed hemorrhage occurs when the placenta separates to some degree and the collection of blood behind the placenta is retained by the margins of the placenta or membranes that remain attached to the uterine wall or by the fetal head applied to the cervix. Concealed abruption is by far less common than external hemorrhage but just as clinically significant (Figure 7–1).

Management

The management of placental abruption depends on the presentation, gestational age, and the degree of maternal and fetal compromise.

A delay in recognizing hypovolemia due to hemorrhage can occur as a result of some of the normal physiologic changes that occur during pregnancy.

Figure 7–1. Abruption/Dead fetus (Reproduced, with permission, from DeCherney AH, Nathan L, Goodwin TM, et al. Current Diagnosis & Treatment: Obstetrics & Gynecology, 10th ed.New York:McGraw-Hill 2007:332.)

Pregnancy is normally a state of hypervolemia due to an approximate 50% increase in blood volume. With blood loss, vasoconstriction of vessels occurs to maintain perfusion of vital organs. This results in compensatory tachycardia and an increase in systemic vascular resistance. Blood pressures usually remain stable (normal to high) until blood loss exceeds 30% of the pregnancy blood volume. It is therefore important to remember that the first vital sign to change is heart rate (tachycardia) and the last to change is blood pressure (hypotension). Interventions to replace fluid and blood should not be delayed until hypotension develops. Preeclamptics are less tolerant of blood loss due to a constricted intravascular compartment. Normal blood pressures in a previously hypertensive patient should always be concerning for hemorrhage. Similarly, a normal hematocrit should not be considered reassuring in preeclamptics. Hemoconcentration is expected due to an underfilled intravascular compartment. It is therefore important to replace volume in these women in the early phase as they are more susceptible to renal failure compared to non-preeclamptics.

Although it is important to individualize each case according to severity of complications, the basic principles of resuscitation apply in all cases. Two large-bore infusion lines and Foley catheter should be inserted immediately. Type and cross, complete blood count, comprehensive metabolic panel, and coagulation studies should be sent stat. The decision on how much blood to cross should be individualized based on the severity of abruption. The clot assay is a useful and inexpensive bedside test for hypofibrinogenemia if laboratory results are not available within a reasonable time. A sample of blood is collected in a red-topped tube. If a clot does not form in 6 minutes or forms and lyses in 30 minutes, then the fibrinogen level is most likely less than 150 mg/dL.13 Correction of anemia and/or coagulopathy should be undertaken. Vaginal delivery is preferable and usually proceeds quickly in the setting of abruption. This is because many patients are already experiencing signs of labor at presentation. Patients with any degree of placental abruption are at risk of postpartum hemorrhage and preparation in case of atony is critical. Uterotonic agents should be readily available. It is also important to be familiar with hospital resources in case there is a need for uterine artery embolization or peripartum hysterectomy.

Severe Abruption with Stillbirth See Case Discussion.

Fetus is alive at or near term When the fetus is alive at or near term, delivery should be expedited. If spontaneous labor is absent, induction or augmentation of labor may be necessary if the fetus is vertex and there is no contraindication for vaginal delivery. If delivery does not occur within a reasonable time and the patient has ongoing hemorrhage and is difficult to stabilize, then cesarean delivery is recommended. Cesarean delivery should also be performed at any time when the fetal heart rate tracing is concerning or for any contraindications to vaginal route of delivery. Surgery in a patient with DIC is life-threatening and must be corrected prior to surgery.

Fetus is alive at 24 to 34 weeks’ gestation If the maternal and fetal status is reassuring, conservative management is reasonable with close monitoring. Antenatal steroids can be administered during this period of observation given the high risk of preterm birth. Consultation with maternal-fetal medicine and neonatology specialists is important for counseling regarding maternal and neonatal outcomes. The patient needs to be counseled that abruption is unpredictable, that fetal death can occur at any time, and that normal fetal testing can occur before a catastrophic event. The risks to both mother and fetus associated with conservative management need to be balanced against the neonatal risks associated with preterm birth. Coexisting conditions such as preterm premature rupture of membranes (PPROM),

preeclampsia, or intrauterine growth restriction should be factored into the decision on whether to recommend expectant management versus delivery. The use of tocolytics in the setting of abruption and contractions is controversial and not enough evidence exists to support or refute routine practice. Continued hospitalization until bleeding subsides is reasonable and outpatient management can be considered in well-selected cases, depending on the clinical circumstances.

Fetus is alive less than 24 weeks Antepartum bleeding in the second trimester is usually attributed to some degree of placental abruption. Exclusion of other causes such as previa, rupture of membranes or cervical causes should be undertaken before attributing bleeding to abruption. There is limited data to guide management of abruption prior to viability. Expectant management is reasonable as long as maternal hemodynamic status is stable. Intrauterine growth restriction, oligohydramnios, recurrent bleeding, previable and/or preterm birth, and cesarean delivery are potential risks of pregnancies complicated by early abruption. The goal of conservative management is to prolong the pregnancy in order to improve fetal/neonatal outcome. This must be balanced against the risks to the mother such as hemorrhage, anemia requiring blood transfusion or lifesaving procedure such as hysterectomy, and rarely maternal death. Consultation with maternal-fetal medicine specialists is recommended given that there are several factors to consider when determining the most reasonable management plan. One factor to consider is gestational age since counseling regarding prognosis may differ when the gestational age is 16 weeks versus 23 weeks, for example. The severity of abruption and coexisting maternal conditions (hypertension, cardiac disease, renal disease) are also important considerations as they affect pregnancy outcome. Most importantly, the patient’s own wishes should be considered and the risks/benefits of both options, expectant management and termination of pregnancy, should be explained.

Abdominal Trauma If direct abdominal trauma has occurred and there is no evidence of maternal or fetal compromise, a period of observation to monitor for placental abruption is warranted. Delayed abruption is unlikely in the absence of frequent contractions (< 6 contractions per hour) with normal fetal heart rate tracing over a 4 to 6 hour period. The recommended monitoring period is a minimum of 4 hours from the trauma event. Further monitoring is also reasonable with other concerning signs or symptoms such as uterine tenderness, abdominal ecchymoses, vaginal bleeding, or frequent contractions14 (Level III).

Hemorrhage from most cases of abruption is maternal in origin. With blunt traumatic abruption, fetal bleeding is more common as a result of a tear or fracture in the placenta. An evaluation of fetal-maternal hemorrhage with flow cytometry or Kleihauer-Betke test is useful in nonsensitized Rh-negative women with abruption, (traumatic or nontraumatic) as the information obtained guides in administering the appropriate dose of Rh immune globulin necessary to prevent alloimmunization. There is little evidence that tests of fetal-maternal hemorrhage (flow cytometry or Kleihauer-Betke test) in Rh-positive women predict adverse fetal or neonatal outcome due to fetal hemorrhage15 (Level II-2). Significant fetal hemorrhage from abruption that would impact neonatal outcome usually results in fetal heart rate tracing abnormalities such as tachycardia, loss of variability, late decelerations, or

sinusoidal pattern14 (Level III). It is important to keep in mind that a negative test does not exclude the diagnosis of abruption and similarly a positive test does not confirm the diagnosis. A positive test for fetal-maternal hemorrhage simply guides the management of Rh-immune-globulin dose that needs to be administered in nonsensitized women.

Comprehension Questions

7.1 A 21-year-old G1P0 at 32 weeks’ gestation presents to L&D after a fall involving direct abdominal trauma. She denies leakage of fluid, vaginal bleeding, contractions, or abdominal pain. On examination her vitals are normal and stable and her abdominal examination is nontender without evidence of trauma. Her cervix is closed and 2 cm in length. The fetal heart rate tracing is reassuring but irregular, infrequent contractions (every 25 min) are noted on external monitoring. She is Rh positive and has no medical problems. If her cervix is unchanged in 2 hours, how long will you observe her from the time of the traumatic event?

A. 1 hour

B. 2 hours

C. 4 to 6 hours

D. Until her contractions resolve

7.2 A 40-year-old woman G3P1010 at 39 weeks’ gestation is being induced for preeclampsia. She has been on intravenous oxytocin, and is now at 5 cm dilation. Amniotomy is performed and bright red blood mixed with fluid is seen. Her BP is 143/89 mm Hg, pulse is 98, urine output is 55 cc/h, and abdomen is nontender although she has an epidural. The fetal heart rate tracing is reassuring with a baseline of 140, moderate variability, and no decelerations. Contractions are occurring every 2-4 minutes. Her obstetrical history is significant for one-term uncomplicated vaginal delivery. What is your next step in management?

A. Place two large-bore IVs, repeat preeclampsia labs and coagulation studies.

B. Recommend cesarean delivery at this time.

C. Recommend amnioinfusion.

D. Prepare for transfusion.

ANSWERS

7.1 C. The recommended time to observe a patient for abruption after direct abdominal trauma is 4 to 6 hours, however, reasonable judgment should be exercised. If this patient’s contractions increase in frequency or if other worrisome signs/symptoms develop then she should be observed longer to evaluate for preterm labor and abruption.

7.2 A. This patient may continue to labor as long as the fetal heart rate tracing remains reassuring and she is progressing well in labor. At this time there is no need to prepare for transfusion given that her vitals signs are appropriate, however, close monitoring of vitals, urine output, and estimated blood loss is necessary. Preeclampsia labs should be repeated and coagulation studies should be ordered for suspected abruption.

Clinical Pearls

See US Preventive Services Task Force Study Quality levels of evidence in Case 1

➤ Over half of all pregnancies complicated by placental abruption deliver preterm.

➤ The sensitivity of ultrasound in detecting placental abruption is poor and therefore the absence of a retroplacental clot should not exclude this diagnosis when it is clinically suspected (Level II-2).

➤ When the abruption is severe enough to kill the fetus, maternal blood loss can be estimated as approximately 50% of her blood volume (Level II-2).

➤ Half of all cases of abruption cases severe enough to kill a fetus involve a hypertensive disorder that may only become apparent after the intravascular compartment has been adequately refilled (Level II-3).

➤ Consumptive coagulopathy is seen in approximately 30% of abruption cases severe enough to kill the fetus (Level II-2).

➤ Elevated FDP levels interfere with myometrial contractility and this increases the risk for postpartum hemorrhage (Level II-2).

➤ The first vital sign to change during hemorrhage is heart rate (tachycardia) and the last to change is blood pressure (hypotension). Volume replacement should not be delayed until there is hypotension since 30% of blood volume has been lost by this point.

➤ It is not the interval of time to delivery but rather maternal resuscitation with fluid and blood replacement that predicts maternal outcome in an abruption.

➤ In any case of antepartum or postpartum hemorrhage, a multidisciplinary team approach ensures both maternal and fetal/neonatal safety.

CONTROVERSIES

• Routine assessment of fetal-maternal hemorrhage in all cases of abruption involving Rh-positive women as there is little evidence that testing predicts fetal or neonatal outcome.

REFERENCES

1. Hurd WW, Miodovnik M, Hertzberg V, et al. Selective management of abruption placentae: a prospective study. Obstet Gynecol. 1993;61:467. A prospective study of 50 cases of placental abruption between 20 and 34 weeks’ gestation. There was a significant increase in respiratory distress and low Apgar scores in study infants compared to controls but without a correlation with regard to mode of delivery or diagnosis to delivery interval (Level II-2). 

2. Glantz C, Purnell L. Clinical utility of sonography in the diagnosis and treatment of placental abruption. J Ultrasouund Med. 2002;21:837. (Level II-2) 

3. Pritchard JA, Brekken AL. Clinical and laboratory studies on severe abruptio placentae. Am J Obstet Gynecol. 1967;97:681. (Level II-2) 

4. Cunningham FG, Leveno KJ, Bloom SL, et al. Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010. 

5. Oyelese Y, Ananth CV. Placental Abruption. Obstet Gynecol. 2006;108:1005- 1016. (Level III) 

6. Ananth CV, Wilcox AJ. Placental abruption and perinatal mortality in the United States. Am J Epidemiol. 2001;153:332. 

7. Pritchard JA, Cunningham FG, Pritchard SA, et al. On reducing the frequency severe abruption placentae. Am J Obstet Gynecol. 1991;165:345. (Level II-3) 

8. Pritchard JA, Mason R, Corely M, et al. Genesis of severe placental abruption. Am J Obstet Gynecol. 1970;108:22. (Level II-2) 

9. Matsaseng T, Bagratee JS, Moodley J. Pregnancy outcomes in patients with previous history of abruptio placentae. Int J Gynecol Obstet. 2006;92:253-254. (Level II-2) 

10. Elsasser DA, Ananth CV, Prasad V, Vintzileos AM. Diagnosis of placental abruption: relationship between clinical and histopathological findings. Eur J Obstet Gynecol Reprod Biology. 2009;6762. A multicenter case-control study (New Jersey–Placental Abruption Study) which showed that the concordance between clinical and pathologic criteria for abruption is poor (Level II-2). 

11. Ananth CV, Getahun D, Peltier MR, et al. Placental abruption in term and preterm gestations. Evidence for heterogeneity in clinical pathways. Obstet Gynecol. 2006;107:785-792. (Level II-2) 

12. Basu HK. Fibrinolysis and abruption placenta. J Obstet Gynaecol Br Commonw. 1969; 76:481-496. (Level II-2) 

13. Gabbe SG, Niebyl JR, Simpson JL. Normal and Abnormal Pregnancy. 4th ed. Philedelphia, PA: Churchill Livingstone; 2001. 

14. Brown HL. Trauma in pregnancy. Obstet Gynecol. 2009;114:147-160. (Level III) 

15. Boyle J, Kim J, Walerius H, Samuel P. The clinical use of the Kleihauer-Betke test in Rh positive patient. Am J Obstet Gynecol. 1996;174:343. (Level II-2)

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