Module 1 Study Guide

Question 1

What is the definition of placental abruption?

Answer 1

Antenatal decidual hemorrhage leads to the premature separation of the placenta. AKA, the placenta detaches from the uterus before the baby is delivered. It can fully or partially separate. This is often caused by sculpture of maternal vessels in the decidua basalis, the bleeding is almost always of maternal origin.

Note: concealed abruption occurs when the separation is in the midsection, and the edges remain attached.

Question 2

What are the risk factors for placental abruption?

Answer 2

Hx of Abruption
Increasing Parity
PPROM
Short interpregnancy interval
Cocaine use in third-trimester
Hx C/S or Leiomyoma (aka fibroids)
Rapid uterine decompression (Mulitple grestation or Polyhydramnios)
Maternal Hx: Thrombophylia, hypothyroidism, asthma, HTN (sig. Increases risk), AMA, smoker, ETOH use
**Blunt trauma
Unexplained elevated maternal serum AFP (protein produced by fetal liver)

Question 3

What are the signs and symptoms of placental abruption?

Answer 3

Early stages: may have no clinically evident signs
Concealed abruption: cramping, contractions, uterine tenderness, back pain
“Classic Signs”: vaginal bleeding with abdominal pain, hypotonic uterus, and tenderness, maternal tachycardia, abnormal FHR. For a posterior placenta, there may be back pain as well.

Question 4

What testing or imaging is available to diagnose placental abruption?

Answer 4

Ultrasound (fresh blood can look like the placenta and may be difficult), symptom-based diagnosis, or diagnosed retrospectively

Question 5

How should placental abruption be managed?

Answer 5

Delivery if >34-36 weeks and or unstable
If bleeding is minor and both the pregnant person and baby are stable and/or preterm may lead to antepartum admission and monitoring.

Question 6

What is the definition of placenta previa?

Answer 6

Abnormally located placenta, near the internal os. If the embryo implants by the cervical os, the placenta will grow there. If it is diagnosed early in the pregnancy, as the uterus grows, it can self-resolve.

Question 7

What are the risk factors for placenta previa?

Answer 7

Hx of placenta previa, multiple gestations (because of more placentas being present), uterine surgery

Question 8

What are the signs and symptoms of placenta previa?

Answer 8

Painless vaginal bleeding

Question 9

What testing or imaging is available to diagnose placenta previa?

Answer 9

Ultrasound to assess the location of the placenta

Question 10

How should placenta previa be managed?

Answer 10

***DO NOT perform cervical exams
If stable: Pelvic rest! Limited physical activity/bed rest. C/S at 34 weeks
If unstable (hemorrhaging/unstable BPs): Urgent/Emergent C/S, blood transfusions as needed

Question 11

What is the definition of vasa previa?

Answer 11

The umbilical cord lies across the cervical os. Often is seen with a velamentous cord insertion.

Question 12

How is vasa previa diagnosed?

Answer 12

Typically diagnosed by routine ultrasound.

Question 13

How should vasa previa be managed?

Answer 13

Antenatal steroids at 30-32 weeks and delivery by C/S at 33-34 weeks

Question 14

What are the signs and symptoms of retained placenta?

Answer 14

When the third stage of labor (i.e. delivery of the placenta) lasts longer than 30 minutes.

Incidence of PPH increases after 17 minutes

If a placenta is retained for >60 minutes, it should be assumed to be invasive (i.e. accreta, increta, percreta)

Question 15

How does retained placenta cause postpartum hemorrhage?

Answer 15

When the placenta is still attached, the blood vessels where it is attached continue to bleed. The uterus is also unable to contract appropriately to stop the blood flow.

Contractions are ineffective when the placenta is retained.

Question 16

What is uterine atony?

Answer 16

Uterine atony refers to the inadequate contraction of the corpus uteri myometrial cells in response to endogenous oxytocin release.

Question 17

What are risk factors for uterine atony?

Answer 17

Uterine overdistention secondary to hydramnios, multiple gestation, use of oxytocin, fetal macrosomia, high parity, rapid or prolonged labor, intra-amniotic infection and use of uterine-relaxing agents.

Question 18

What are the signs of uterine atony?

Answer 18

Excessive bleeding, fundus may be boggy/high/deviated and does not resolve with a massage.

If significant bleeding has occurred, pt may become hypotensive, tachycardic, pale, or dizzy

Question 19

How does uterine atony cause postpartum hemorrhage?

Answer 19

This is the primary cause of PPH. The uterus is not contracting and stopping the blood flow like it should, leading to hemorrhage.

Question 20

What is a uterine inversion?

Answer 20

When the fundus collapses into the endometrial cavity, turning the uterus partially or entirely inside out.
I
ncomplete: Fundus within endometrial cavity
Complete: fundus protrudes through the cervical os
Prolapsed: fundus protrudes to or beyond the vaginal introitus
Total: Both the Uterus and vagina are inverted

Question 21

How does uterine inversion cause postpartum hemorrhage?

Answer 21

It is associated with disseminated intravascular coagulation (DIC). The uterus cannot contract appropriately because it is “inside out”

Note: Most common symptom is maternal shock

Question 22

What is the management for an inverted uterus?

Answer 22

Immediately attempt to reposition the uterus as this is more successful if done before the lower uterine segment and cervix contract. If the placenta is attached, DO NOT remove it. The provider will use their hand to “push” the uterus back into place and then hold it in place with their first while waiting for a physician. Request blood to be prepared or initiate the PPH protocol.

Question 23

How do vaginal and cervical lacerations cause postpartum hemorrhage?

Answer 23

Significant tearing can cause increased bleeding. To stop the bleeding, the tear must be repaired.

Cervical lacerations may not be quickly identified and can be difficult to repair. They may need to be repaired in the operating room for the best visualization.

Question 24

What is the difference between early and late postpartum hemorrhage?

Answer 24

Early PPH occurs within 24 hours of delivery, a late PPH occurs after 24 hours, and up to 12 weeks postpartum. A late PPH is most often the result of subinvolution but could also be due to retained placenta or products of conception.

Question 25

How should an early postpartum hemorrhage be managed?

Answer 25

Varies on cause of hemorrhage. You should immediately start to assess the cause and stop the bleeding. Causes: TTTT-Tone, Trauma, Tissue, Thrombin Medications: Pitocin-*first line 10-40 U in 500-1000 cc IV at 250 cc/hr or 10 U IM Methergine-*2nd line* 0.2 mg IM q2-4h (Note: avoid in HTN due to increased BP, can repeat PO TID-QID for up to 1 week Hemabate-*2nd line* 0.25 IM or intramyometrium q15m x8 (Note: avoid in asthma, causes severe diarrhea) Cytotec 600-800 mcg SL/PO or 800-1000 mcg PR (Note: causes fever and shivering) TXA: to be used in conjunction with other meds. Give within 3 hours of birth (Note: is NOT a uterotonic) PRB-type and cross for 2 units Monitor vital signs: tachycardia and hypotension are signs of significant blood loss Fundal massage/Bimanual massage to remove clots Empty bladder Call for MD backup 2nd IV MD should assume care if PPH is stage 3

Question 26

What is a hematoma?

Answer 26

A pool of mostly clotted blood as a result of damage to blood vessels. They are most common at the vulva, vagina, or retroperitoneum.

Question 27

What are the signs and symptoms of a hematoma?

Answer 27

Significantly worse pain than expected from delivery/type of tear.

Question 28

How are hematomas diagnosed?

Answer 28

Can be diagnosed by a physical exam. Some may not be visible and would require a gentle internal digital exam.

Question 29

How are hematomas managed?

Answer 29

Frequent assessment, Ice packs, pain management, side-lying, IV placement in case of need for volume resuscitation, foley catheter placement, CBC to establish baseline. Note: the midwife SHOULD NOT incise the hematoma without additional aid

Question 30

What is subinvolution?

Answer 30

Subinvolution is delayed return of the enlarged uterus to normal size and function. By 2 weeks PP, the uterus can no longer be palpated abdominally though involution is not complete until 6 weeks PP. When this does not occur in the expected time frame, subinvolution has occurred.

Question 31

What are potential causes subinvolution?

Answer 31

Retained placental fragments or products of conception, infection, leiomyomas (fibroids), exessive maternal activity

Question 32

What are the signs and symptoms of subinvolution?

Answer 32

Prolonged lochial discharge. Irregular or excessive bleeding. Larger than normal uterus. Boggy uterus (occasionally)

Question 33

How is subinvolution treated?

Answer 33

Depends on severity and cause D&C can be performed Medications: the same meds used for an early PPH Treatment of infection

Question 34

What is Rh-D isoimmunization?

Answer 34

Rh factor is a protein on red blood cells. Rh incompatibility is when a mother has Rh-negative blood and her baby has Rh-positive blood. Rh isoimmunization is when the blood from the baby makes the mother's body create antibodies that can harm the baby's blood cells.

Question 35

What affect does Rh-D isoimmunization have on the fetus?

Answer 35

If the mother is Rh- and the baby is Rh+ then the mother's body could “attack” those proteins. This can happen anytime where this is mixing blood due to trauma, bleeding, delivery, etc. In the current pregnancy, it can cause hydrops fetalis and a severe hemolytic disease. It will also affect a future pregnancy if the baby is also Rh+ and can cause IUFD and loss of pregnancy.

Question 36

How can Rh-D isoimmunization be prevented?

Answer 36

300 mcg of Anti-D immunoglobulin (RhoGAM), a human plasma-derived product, is given at 28 weeks gestation and within 72 hours of delivery. In case of trauma, KB stain can be done and 10 mcg/ml of additional RhoGAM given

Question 37

What is the difference in how Rh-D isoimmunization affects the first pregnancy versus subsequent pregnancies?

Answer 37

In the first pregnancy, there tends to be little mixing and, therefore low risk of problems; significant problems are more likely to occur in subsequent pregnancies because those antibodies remain in the maternal immune system and may later cross the placenta.

Question 38

What is ABO incompatibility?

Answer 38

ABO incompatibilities exist between the mother and fetus when the mother is blood type O and the fetus has a different blood type (Type A, B, or AB). The Anti-A and Anti-B antibodies in the mother's serum can cross the placenta and potentially hemolyze fetal RBCs. Most often, ABO incompatibility is less severe than Rh incompatibility.

Question 39

What blood type most commonly has an ABO incompatibility?

Answer 39

Maternal O blood type and fetal A

Question 40

What affect does ABO incompatibility have on the fetus?

Answer 40

This is the most common cause of hemolytic anemia in newborns and is usually mild.

Question 41

How can an ABO incompatibility be managed?

Answer 41

There is no prenatal treatment, only neonatal monitoring and observation for hyperbilirubinemia.

Question 42

What is Kell sensitization?

Answer 42

The third most potent cause of hemolytic disease of the newborn. The disease results when anti-Kell antibodies from the mother cross the placenta to the fetus. The antibodies can cause a more rapid and severe fetal anemia than Rh incompatibility. The antibodies stop the development of red blood cells and lyse blood cells (hemolysis) that are already present.

Question 43

What affect does Kell sensitization have on the fetus?

Answer 43

Can cause hemolytic disease and severe anemia because it suppresses RBC production

Question 44

How should the nurse-midwife manage Kell sensitization when it is recognized?

Answer 44

Any positive antibody warrants: Antibody identification, titer and consult with MD

Question 45

What lab values enable the nurse-midwife to diagnose iron deficiency anemia?

Answer 45

H/H 1st: <11/<33, 2nd: <10.5/<32, 3rd: <11/<33. Diagnostic tests=CBC with indices and serum ferritin (Ferritin <12 is likely IDA)

Question 46

What lab values enable the nurse-midwife to diagnose megaloblastic anemia?

Answer 46

Megaloblastic Anemia (Previously pernicious anemia): Serum B12 and folate levels [One of both def=B12 def and/or Folate Def. If borderline, measure MMA and homocysteine [both increased=B12 Def, only homocysteine increased=Folate Def.)

Question 47

In a patient with anemia, what differential diagnoses can be listed?

Answer 47

Iron Deficiency Anemia Beta/Alpha Thalassaemia Blood Loss Folate Deficiency B12 Deficiency Sickle Cell Megaloblastic Anemia

Question 48

What are the risks of iron deficiency anemia?

Answer 48

Preterm delivery, cesarean section, low fetal birth weight, lower fetal mental and psychomotor performance.

Question 49

What are the risks of megaloblastic anemia?

Answer 49

Pregnancy loss, neural tube defects, cardiac defects, preterm birth, pre-eclampsia, placental abruption, smaller fetal brain size, fetal cognitive defects and behavioral problems, and autism.

Question 50

What are the various approaches to prescribing iron supplementation in pregnancy?

Answer 50

PNV with 30-60 mg/d If Hgb<11 and Ferritin <30: 60-120 mg/d or every other day 2-3x/week. Oral Iron: 40-80 mg/d (Ferrous sulfate/gluconate/fumarate) Injectable Iron transfusions if severe

Question 51

What is the best dietary counseling to give a pregnant patient with anemia?

Answer 51

Heme Iron (Animal sources) is absorbed better than Non-Heme (plant-based and supplements) Sources: Red meat, chicken breasts, lentils, edamame, chickpeas, fortified oatmeal, black beans, chocolate. Megaloblastic Anemia: Green leafy vegetables, lentils, beans, and fortified foods.

Question 52

What populations are most affected by sickle cell trait (Hemoglobin AS) and sickle cell anemia (Hemoglobin SS)?

Answer 52

Hgb AS & SS: People of African descent. 1/12 AA people have sickle cell trait. 1/300 AA has a form of sickle cell disease. 1/600 AA has sickle cell anemia. It is also found in high frequency in Greek, Italian (Sicilian), Turks, Arabs, Southern Iranians, and Asian Indians.

Question 53

What populations are most affected by alpha and beta thalassemia?

Answer 53

Alpha: Southeast Asian, African. Beta Thalassemia: Mediterranean, Middle Eastern, African, and SE Asian ethnicities

Question 54

What is the genetic inheritance pattern (i.e. autosomal recessive, autosomal dominant, etc.) for sickle cell trait/anemia, alpha thalassemia, and beta thalassemia?

Answer 54

Sickle cell trait/anemia: Autosomal recessive Alpha Thalassemia: Autosomal recessive genetic disorder on chromosome 16 [1-4 alpha gene deletion(s)] Beta Thalassemia: Autosomal recessive genetic disorder on chromosome 11 [Point mutation or gene deletion (rare)]

Question 55

What is the difference between alpha thalassemia minor and major?

Answer 55

Minor: MCH=25-27. Alpha Thalassemia minor is often unrecognized and causes no major maternal problems and very little problem for the fetus as well. Mild anemia may occur. Major (Aka Hb Bart Disease): MCH=<25. This is when all four abnormal gene globins are inherited. Oxygen is transported poorly, and these babies are stillborn or are born with hydrops fetalis and die soon after birth.

Question 56

What is the difference between beta thalassemia minor and major?

Answer 56

Minor: Presentation ranges from absence of anemia to mild/moderate anemia characterized by hypochromia and microcytosis. It can cause mild anemia in pregnancy due to ineffective erythropoiesis. It is associated with fetal growth restriction. Major (aka Cooley Anemia): Serious and frequently fatal. Hemolysis is intense and leads to severe anemia. Many patients are transfusion dependent. Pregnancy is safe if the maternal cardiac function is normal. The patient will need transfusions throughout to pregnancy to maintain Hgb of 10 g/dl. Prior to blood transfusion and iron chelation, pregnancy with cooley anemia was rare.

Question 57

What lab test(s) are used to diagnose hemoglobinopathies?

Answer 57

Hemoglobin Electrophoresis. DNA testing must be done to diagnose Alpha Thalassemia.

Question 58

What hemoglobin is present in sickle cell anemia? in alpha thalassemia? in beta-thalassemia?

Answer 58

Sickle Cell Anemia Hb SS Alpha Thalassemia: ABA1 and HBA2 (Rarely Hb H or Hb Bart) Beta Thalassemia: Absence of Hb A. Electrophoresis HbA1 is low, HbA2 is high and HbF is high

Question 59

What are the associated risks of sickle cell anemia?

Answer 59

SAB, Stillbirth, Preterm labor, PPROM, antepartum hospitalization, postpartum infection, IUGR, low birth weight, preterm delivery. Sickle cell crisis, acute chest syndrome, infection, severe anemia, cholecystitis, hypersplenism.

Question 60

What level of interprofessional management is warranted in the care of a patient with sickle cell anemia? thalassemia minor? thalassemia major?

Answer 60

Sickle Cell Anemia: Should be comanaged with perinatology due to risk for complications Thalassemia Minor: Comanage with a physician. Does not typically affect pregnancy beyond anemia. Thalassemia Major: Should be referred for care with perinatology/specialist

Question 61

What is the difference between gestational thrombocytopenia and ITP?

Answer 61

Gestational Thrombocytopenia: Defined as a platelet count below 150,000 in pregnancy ITP: Acquired Autoimmune disorder-IgG antibodies prematurely destroying platelets

Question 62

How does the clinical presentation of ITP differ from gestational thrombocytopenia?

Answer 62

Gestational Thrombocytopenia: More likely to occur in the late 2nd to 3rd trimester and normalizes spontaneously 1-2 months PP. The patient will have no history of low platelets or abnormal bleeding. Typically asymptomatic if over 75,000 ITP: If noted in the first trimester, more likely to be ITP. The majority of cases are pre-existing before pregnancy. May have a history of easy bruising, gums bleeding etc.

Question 63

What labs test/values diagnose gestational thrombocytopenia? What labs test/values diagnose ITP?

Answer 63

Diagnosis of exclusion-there are no specific diagnostic tests. GT is a presumptive diagnosis, official diagnosis can be made after platelets normalize PP. Labs: CBC, Peripheral blood smear, retic count, LFTs, Viral screening (HIV, HCV, HBV)

Question 64

What are the associated risks of gestational thrombocytopenia and ITP?

Answer 64

GT: Generally none. May not have epidural if platelets <80 ITP: Serious problems are rare. Small increased risk of bleeding, PP venous thromboembolism, may not be able to get an epidural.

Question 65

How can gestational thrombocytopenia and ITP be managed by the nurse-midwife?

Answer 65

Both should be comanaged with an OB/hematology

Question 66

What population(s) is/are most affected by G6PD deficiency?

Answer 66

Mediterranean and African descent

Question 67

What is the genetic inheritance pattern (i.e. autosomal recessive, autosomal dominant, etc.) for G6PD?

Answer 67

X-linked

Question 68

What are the signs/symptoms of G6PD?

Answer 68

Ranges from asymptomatic to severe acute/chronic hemolytic anemia. Jaundice. When your skin turns yellow. Amber Urine Fatigue. Paleness Tachycardia Shortness of Breath Enlarged spleen.

Question 69

What risk does G6PD pose to the pregnancy? to the fetus?

Answer 69

ITU, pre-eclampsia, neonatal jaundice, hydrops fetalis, stillbirth

Question 70

How should the nurse-midwife manage a patient with G6PD?

Answer 70

Surgery can cause an episode of hemolysis, therefore any MD that may care for the patient must know about it. Note: Can also be triggered by the following: infection, sulfa, macrobid, NSAIDs, methylene blue, fava beans, and certain legumes.

Question 71

What is indirect bilirubin (unconjugated bilirubin)? How is it excreted from the newborn?

Answer 71

​​Indirect bilirubin is formed by the breakdown of hemoglobin in the red blood cells. Indirect bilirubin is bound to albumin in the blood. The liver converts this bilirubin into direct bilirubin, which can then be released into the intestine by the gallbladder for elimination. It is excreted in stool or urine.

Question 72

What are the causes of elevated indirect bilirubin in the newborn?

Answer 72

Physiologic jaundice: immature liver, short lifespan on RBCs in newborns. Usually occurs on day 2-4 PP and resolves in 2 weeks. Pathologic jaundice: Occurs in the first 24 hours of life. Breastfeeding jaundice: occurs in the first week of life due to inadequate feeding/dehydration. There is decreased intestinal motility and decreased elimination of bilirubin. Breast milk jaundice: occurs late in the first week and resolves by week 12 and is less common than breastfeeding jaundice. Higher levels of free fatty acids result in increased enterohepatic circulation.

Question 73

What is pathologic hyperbilirubinemia? How does pathologic hyperbilirubinemia differ from physiologic jaundice?

Answer 73

Pathologic: the most serious type of jaundice. It occurs within 24 hours after birth, and is characterized by a rapid rise in a baby's bilirubin level. The most likely cause is blood incompatibility or liver disease. Pathologic jaundice presents in the first 24 hours and physiologic presents later and is a normal result of the short lifespan of RBCs in newborns and immature liver.

Question 74

What laboratory testing is available to evaluate newborn bilirubin levels?

Answer 74

Total bilirubin levels

Question 75

At what level(s) is/are total serum bilirubin (TSB) levels considered abnormal?

Answer 75

As total serum bilirubin levels increase, jaundice progresses cephalocaudally from the face (5 mg/dL) to the trunk (upper chest 10 mg/dL, abdomen 12/mg/dL) and extremities, eventually including the palms and soles (>15 mg/dL) (Porter & Dennis, 2002) (progresses below the nipple line).

Question 76

What is Bhutani's nomogram?

Answer 76

The Bhutani Nomogram is used to determine the level of risk based on the Infant's hours of age and serum bilirubin result.

Question 77

How does acute bilirubin encephalopathy differ from kernicterus?

Answer 77

Bilirubin encephalopathy: refers to cerebral symptoms associated with hyperbilirubinemia such as irritability, high-pitched cry, hypertonia or hypotonia, seizures, and possibly death if left untreated. Kernicterus: used to describe the chronic and permanent sequelae of ABE in infants who sustain permanent cerebral damage as the result of hyperbilirubinemia.

Question 78

What are early signs of acute bilirubin encephalopathy?

Answer 78

Extreme jaundice, absent startle reflex, poor feeding/sucking, lethargy/low muscle tone

Question 79

What are risk factors for newborn anemia?

Answer 79

Alloimmunization, infection (parvovirus), genetic disorders (G6PD def.), fetomaternal hemorrhage.

Question 80

What is polycythemia?

Answer 80

Increased circulating red blood cell mass. Polycythemia in the newborn is a central venous Hct over 65% or a Hgb above 22.

Question 81

What are the associated risks of polycythemia?

Answer 81

Maternal DM, inherited, intrapartum hypoxia, Twin to twin tr

Question 82

What are the signs and symptoms of polycythemia?

Answer 82

Lethargy, irritability, jitteriness, tremors, seizures, cerebrovascular accidents, oliguria and/or hematuria, respiratory distress, cyanosis, and apnea.

Question 83

What are the potential complications of polycythemia?

Answer 83

Thrombosis, ischemia of end organs, hypoperfusion to lungs and renal system by decreasing blood flow. Hypoperfusion to the brain due to a change in oxygen content.