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CCP 344 Perinatal Emergencies 🤰 Flashcards

1
Q

list the different Hypertensive disorders of pregnancy

A
  1. chronic HTN with or without superimposed pre-eclampsia/eclampsia
  2. gestational HTN
  3. preeclampsia with or without severe features
  4. Hemolysis, Elevated Liver Enzymes and Low Platelet Count (HELLP) syndrome
  5. eclampsia
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2
Q

define Chronic hypertension (outside the context of pregnancy)

A

Chronic HTN is diagnosed as an in-office measurement with SBP >140mmHg or DPB >90mmHg confirmed with either ambulatory BP monitoring, home BP monitoring, or BP evaluation with serial office visits, with elevated pressures at least 4 hours apart prior to 20 weeks gestation.

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3
Q

define Gestational hypertension

A
  1. defined as SBP >140mmHg or DPB >90mmHg on two separate occasions at least 4 hours apart after 20wks of pregnancy when previous BP was normal.
  2. Alternatively, a patient with any single episode of SBP >160mmHg or DBP >110mmHg can be confirmed to have gestational HTN
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4
Q

define pre-eclampsia

💵💵💵 MONEY SLIDE 💵💵💵

A

defined as SBP >140mmHg or DPB >90mmHg on two separate occasions at least 4 hours apart after 20wks of pregnancy when previous BP was normal

OR

a patient with any single episode of SBP >160mmHg or DBP >110mmHg can be confirmed to have gestational HTN

WITH

≥300mg urine protein excretion in a 24-hour period OR a protein/creatinine ratio of greater than or equal to 0.3 OR new-onset hypertension with thrombocytopenia, OR renal insufficiency, OR pulmonary edema, OR impaired liver function, OR new-onset headache unresponsive to medications with no alternative cause

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5
Q

define eclampsia

💵💵💵 MONEY SLIDE 💵💵💵

A

pre-eclampsia → generalized tonic-clonic seizures (typically intrapartum through up to 72 hours postpartum)

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6
Q

define and describe HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count)

💵💵💵 MONEY SLIDE 💵💵💵

A
  1. syndrome in pregnant and postpartum women characterized by hemolysis, elevated liver enzymes, and a low platelet count
  2. can be a form of severe pre-eclampsia, however 15-20% of patients with HELLP do not have antecedent HTN or proteinuria
  3. Criteria: hemolysis as evident by LDH >600IU/L, liver injury from AST and/or AST >2 times upper limit of normal, and thrombocytopenia of less than 100,000 x 10(9)/L
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7
Q

define and describe Hyperemesis gravidarum

A
  1. nausea + vomiting that cause starvation metabolism, weight loss, dehydration, and prolonged ketonemia and ketonuria.
  2. Initial management involves rehydration with IV fluids, antiemetics, and demonstration of ability to take oral hydration.
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8
Q

discuss Thromboembolism in Pregnancy

A
  1. Thromboembolic disease accounts for almost 20% of obstetric mortality, making it the LEADING CAUSE OF DEATH in pregnancy.
  2. Doppler ultrasonography is the first-line test for the diagnosis of DVT. CT angiography and lung scintigraphy are used for the diagnosis of PE.
  3. LMWH is preferred for anticoagulation.
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9
Q

list risk factors for ectopic pregnancy

A
  • Older women
  • Women of minority groups
  • Previous ectopic pregnancy
  • Prior spontaneous abortion
  • Medically induced abortion
  • History of infertility
  • IUD
  • Smoking
  • Prior tubal infection (50% of cases)
  • PID
  • Anatomic abnormalities of the fallopian tubes,
  • assisted reproduction (especially multiple embryo transfers),
  • abnormal endometrium (host factors).
  • Prior tubal surgery (tubal sterilization, removal of previous ectopic)
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10
Q

differentials for bleeding in late (2nd and 3rd trimesters) pregnancy

A 
Placental abruption
Placenta previa
Early labour
Occult marginal placental separations
Cervical or vaginal lesions
Lower genital tract lesions
Hemorrhoids
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11
Q

list risk factors for pre-eclampsia

A
  • Women younger than 20 years
  • Primigravidas
  • Twin or molar pregnancies
  • Hypercholesterolemia
  • Pregestational diabetes
  • Obesity
  • Those with a family history of pregnancy-induced hypertension
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12
Q

list potential complications arising from pre-eclampsia

A
  1. HELLP syndrome
  2. spontaneous hepatic and splenic hemorrhage
  3. abruptio placentae
  4. Eclampsia (may present up to 4 weeks after delivery)
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13
Q

list potential maternal complications arising from eclampsia

A
  1. permanent CNS damage from recurrent seizures
  2. intracranial bleeding
  3. renal insufficiency
  4. death
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14
Q

list potential neonatal complications arising from eclampsia

A
  1. placental infarcts
  2. intrauterine growth retardation
  3. premature delivery
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15
Q

Describe the management of eclampsia

A

For ongoing seizures/actively seizing patient the first line therapy is always benzos!

  1. stat bolus dose MgSO4 4g IV over 20 - 30 minutes, followed by MgSO4 1g/hr IV (Consider other seizure causes – drugs, hypoglycemia)
  2. If seizures refractory to magnesium: Obtain CT head to exclude cerebral venous thrombosis or ICH
  3. Consider control of HTN if DBP > 105 and MgSO4 therapy given: Hydralazine 5 mg IV, repeat 5-10 mg IV q20m prn to keep DBP <105 mmHg
  4. Maintain euvolemia
  5. Assess for end organ dysfunction – liver, kidney, heme (CBC, LFTS, Coags, Renal panel)
  6. Facilitate delivery!
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16
Q

What is HELLP syndrome?

💵💵💵 MONEY SLIDE 💵💵💵

A

severe form of preeclampsia that develops in 5% to 10% of women who have preeclamptic symptoms,

  1. hemolysis (microangiopathic hemolytic anemia)
  2. elevated liver enzyme levels (alanine transaminase [ALT] and aspartate transaminase [AST] > 70 U/L)
  3. low platelet count (<100,000/mL).

PT/aPTT and fibrinogen level are normal, and blood studies reveal microangiopathic hemolytic anemia.

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17
Q

list risk factors for miscarriage

A 
↑ maternal age (especially > 40 yrs)
↑ parental age
↑ parity
Hx of prior miscarriage
Hx of vaginal bleeding
ETOH use
Poorly controlled disease
Diabetes
Thyroid disease
Obesity
Low prepregnancy BMI
Maternal stress
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18
Q

fetal effects of pre-eclampsia

A

Intra-uterine growth restriction
Oligohydramnios
abnormal Doppler
abnormal electronic fetal monitoring

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19
Q

Indications for Delivery in pre-eclampsia

A

Worsening maternal status

  1. ↑ BP
  2. HELLP syndrome (↑ LFTs, ↓ platelets)
  3. Eclampsia (seizures)
  4. ↑ serum creatinine
  5. Placental Abruption / DIC

Compromised fetal status

  1. IUGR
  2. Oligohydramnios
  3. Abnormal Doppler studies
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20
Q

define Severe Preeclampsia

💵💵💵 MONEY SLIDE 💵💵💵

A
  1. Onset < 34 weeks
  2. BP ≥ 160 / 110 mm Hg
  3. Proteinuria ≥0.3g (300mg) in a 24hr period
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21
Q

define preterm labour

💵💵💵 MONEY SLIDE 💵💵💵

A
  1. Preterm labor is labor occurring between after 20 and before 37 weeks gestation.
  2. Preterm labors are subcategorized as early or late preterm.
  3. Early preterm labor occurs prior to 33 weeks gestation,
  4. late preterm labor occurs between 34 and 36 weeks gestation.
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22
Q

Early preterm labor definition

A

Early preterm labor occurs prior to 33 weeks gestation,

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23
Q

late preterm labor definition

A

late preterm labor occurs between 34 and 36 weeks gestation

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24
Q

list Early maternal signs and symptoms of preterm labour

A
  1. increase or change in vaginal discharge
  2. pain resulting from uterine contractions (sometimes perceived as back pain)
  3. pelvic pressure
  4. vaginal bleeding
  5. fluid leak.
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25
Q

Demographic and psychosocial factors linked to preterm labour

A 
Extremes of age
Lower socioeconomic status
Tobacco use
Cocaine use
Prolonged standing (occupation)
Psychosocial stress
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26
Q

Reproductive & Gynecologic factors linked to preterm labour

A 
Prior preterm delivery
Diethylstillbestrol exposure
Multiple gestations
Anatomic endometrial cavity anomalies
Cervical incompetence
Low pregnancy weight gain
First-trimester vaginal bleeding
Placental abruption or previa
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27
Q

Surgical factors linked to preterm labour

A

Prior reproductive organ surgery

Prior paraendometrial surgery other than genitourinary (appendectomy)

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28
Q

Infectious factors linked to preterm labour

A

UTIs
Nonuterine infections
Genital tract infections

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29
Q

absolute Contraindications to Tocolysis

A 
Acute vaginal bleeding
Fetal distress (not tachycardia alone)
Lethal fetal anomaly
Chorioamnionitis
Preeclampsia or eclampsia
Sepsis
DIC
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30
Q

relative Contraindications to Tocolysis

A 
Chronic hypertension
Cardiopulmonary disease
Stable placenta previa
Cervical dilation >5cm
Placental abruption
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31
Q

what classic treatments for preterm labour are INEFFECTIVE

A

In women with an acute episode of preterm labor, bedrest, hydration, sedatives, antibiotics, and progesterone supplementation are ineffective for preventing preterm birth

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32
Q

define and describe Prelabor rupture of the membranes (PROM)

A
  1. Prelabor rupture of the membranes (PROM) refers to rupture of the fetal membranes prior to the onset of regular uterine contractions.
  2. It may occur at term (≥37 weeks of gestation) or preterm (<37 weeks of gestation); the latter is designated preterm PROM (PPROM)
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33
Q

key diagnostic features of PROM

A

History
1. Spontaneous gush of watery fluid, followed by a mild persistent seepage.

Physical

  1. Direct digital examination is AVOIDED
  2. Visualization of a umbilical cord
  3. Visualization of a fetal part

Special tests

  1. pH testing – amniotic fluid has a pH of 7-7.5 (but there are many other falsely alkaline things that can fool you)
  2. Nitrazine (amniotic fluid turns nitrazine paper blue)
  3. Ferning (amniotic fluid crystallizes) GOLD STANDARD
  4. Smear combustion (amniotic fluid turns white & crystallizes)
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34
Q

complications of PROM

A
  • preterm labour and delivery
  • fetal / neonatal infection
  • maternal infection
  • umbilical cord compression / prolapse
  • failed induction resulting in cesarean section
  • pulmonary hypoplasia (early, severe oligohydramnios)
  • fetal deformation (< 20 wks)
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35
Q

management of PROM

A

management depends on several factors, including the gestational age and fetal maturity, presence of active labor, presence or absence of infection, presence of placental abruption, and degree of fetal well-being or distress

  1. Avoid digital cervical exam (speculum assessment only)
  2. Steroids for fetal lung maturity (if <34 weeks)
  3. Treat with antibiotics with any suspicion of infection
    - Preterm PROM = ampicillin or clindamycin
    - Term PROM = ampicillin or penicillin if GBS +
  4. Surveillance for infection/fetal distress
    - ultrasound
    - Start fetal monitoring
  5. Pediatric/Neonatology consult
  6. Consider transfer to higher level of care
  7. induction of labor in women with term PROM ≥37wk
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36
Q

define and describe Placenta previa

A
  1. presence of placental tissue that extends over the internal cervical os
  2. A “low-lying placenta” is where the edge is within 2 to 3.5 cm from the internal os.
  3. “Marginal” placenta previa is where the placental edge is within 2cm of the internal os.
  4. Nearly 90% of placentas identified as “low lying” will ultimately resolve by the third trimester due to placental migration
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37
Q

Summarize and describe the clinical manifestations of placenta previa

A
  1. Vaginal bleeding 2nd to placenta previa can lead to postpartum hemorrhage requiring a blood transfusion, hysterectomy, maternal intensive care admission, septicemia, and maternal death
  2. Postpartum hemorrhage is blood loss ≥1000mL accompanied by signs or symptoms of hypovolemia occurring within 24 hours after delivery, regardless of the route of delivery.
  3. This condition may necessitate blood transfusion, uterotonics, uterine artery embolization, iliac artery ligation, balloon tamponade, and hysterectomy.
  4. Placenta previa that is not diagnosed early enough or managed improperly can lead to morbidity and mortality for both the mother and fetus.
  5. Placenta previa is also associated with preterm birth, low birth weight, lower APGAR scores, longer duration of hospitalization, and higher blood transfusion rates
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38
Q

Detail the pathophysiology of Intramniotic infection (IAI) (Chorioamnionitis)

A
  1. ascending infection, originating in the lower GU tract and migrating to the amniotic cavity
  2. can occur before labor, during labor, or after delivery. can be acute, subacute, or chronic
  3. Vertical transmission has been documented in bacterial and viral infections transmitted to the fetus
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39
Q

Summarize and describe the clinical manifestations of Intramniotic infection (IAI) (Chorioamnionitis)

A
  1. febrile illness assoc. w/ ↑ WBC count, uterine tenderness, abdominal pain, foul-smelling vaginal discharge, and fetal/maternal tachycardia.
  2. fever of at least 39 C or between 38 C and 39 C within 30 minutes and one of the clinical symptoms
  3. The majority of women presenting with chorioamnionitis are in labor or have ruptured membranes.
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40
Q

Maternal Signs & Symptoms of Intramniotic infection (IAI) (Chorioamnionitis)

A 
Premature rupture of membranes (PROM)
Uterine tenderness
Fever
Tachycardia (maternal or fetal)
Malodorous vaginal discharge
Leukocytosis
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41
Q

Fetal Signs & Symptoms of Intramniotic infection (IAI) (Chorioamnionitis)

A

Decreased activity
Abnormal biophysical profile
Fetal tachycardia
Decreased variability of fetal heart rate

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42
Q

Management of Intramniotic infection (IAI) (Chorioamnionitis)

A

Treatment = Delivery + Broad spectrum antibiotics iv

Ampicillin PLUS gentamicin
Cefoxitin
Pip-tazo
Ertapenem

If post partum:

Ampicillin PLUS gentamicin PLUS (Clindamycin or metronidazole)

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43
Q

What’s the difference between PROM and PPROM?

A
  1. The word premature in PROM refers to rupture before labor, not to fetal prematurity.
  2. In 8% of PROM cases, the fetus is at or near term, and PROM may result in normal labor.
  3. When PROM occurs before 37 weeks, it is called preterm PROM and is associated with significant fetal morbidity and mortality.
  4. PROM is the inciting event in one-third of all preterm deliveries.
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44
Q

define and describe Polyhydramnios

A
  1. Polyhydramnios is an increase in amniotic fluid in pregnancy associated with increased maternal and neonatal morbidity and mortality.
  2. The severity of this disease process varies, but up to 20% of neonates affected by this condition are born with a congenital anomaly
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45
Q

define and describe Oligohydramnios

A
  1. Oligohydramnios is a disorder of amniotic fluid resulting in decreased amniotic fluid volume for gestational age.
  2. Low amniotic fluid volumes can be the result of numerous maternal, fetal, or placental complications and can lead to poor fetal outcomes
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46
Q

define EARLY post partum hemorrhage

A

blood loss that occurs within first 24hrs

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47
Q

define LATE post partum hemorrhage

A

hemorrhage 24 hours to 6 weeks after delivery

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48
Q

define and describe Shoulder dystocia

A

failure of the shoulders to spontaneously traverse the pelvis after delivery of the fetal head.

occurs in 0.2 to 3 percent of births

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49
Q

define and describe McRoberts maneuver

A
  1. initial approach for releasing the impacted shoulder in shoulder dystocia
  2. Maternal leg flexion to a knee-chest position may disengage the anterior shoulder, allowing rapid vaginal delivery to follow.
  3. This maneuver “walks” the pubic symphysis over the anterior shoulder and flattens the sacrum, helping the fetus pass through the birth canal, one shoulder at a time.
  4. This method, although requiring very little effort, is often successful in alleviating shoulder dystocia.
  5. The McRoberts maneuver requires two assistants, each of whom grasps a maternal leg and sharply flexes the thigh back against the abdomen (knee to chest position).
  6. This procedure relieves shoulder dystocia via marked cephalad rotation of the symphysis pubis and subsequent flattening the sacrum, thus removing the sacral promontory as an obstruction site
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50
Q

describe Breech presentation

A

presentation of the fetal feet or buttocks and is associated with a higher rate of morbidity for the mother and the fetus compared with normal cephalic (head-first) presentation

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51
Q

Frank breech

A

Both hips are flexed and both knees are extended such that the feet are next to the fetal head. This is the most common type of breech (50%-70%)

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52
Q

Complete breech

A

Both hips and both knees are flexed (5%-10%)

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53
Q

Incomplete breech

A

One or both hips not completely flexed (10%-40%)

54
Q

list the 3 types of breech presentation

💵💵💵 MONEY SLIDE 💵💵💵

A
  1. Frank breech: Both hips are flexed and both knees are extended such that the feet are next to the fetal head. This is the most common type of breech (50%-70%).
  2. Complete breech: Both hips and both knees are flexed (5%-10%).
  3. Incomplete breech: One or both hips not completely flexed (10%-40%).
55
Q

outline the significance of the different types of breech presentation

A
  1. Frank and complete breech presentations are more favorable for vaginal delivery, because the fetal thighs, buttocks, and trunk pass through the birth canal simultaneously. Together, this large presenting part will usually allow for smooth passage of the aftercoming shoulders and head.
  2. Incomplete breech is less favorable for vaginal delivery, because one of the hips is not flexed; thus, a foot or knee could slip through an incompletely dilated cervix, and larger parts such as the head could become entrapped. Cord prolapse is also more likely in incomplete breech
56
Q

Risk factors for breech presentation

A 
Preterm gestation
Multiple gestation
Intrauterine growth restriction (IUGR)
Previous breech presentation 
Uterine abnormalities (bicornuate uterus, septate uterus, fibroids)
Placental abnormalities
Multiparity
Polyhydramnios or oligohydramnios
Abnormal fetal cephalic anatomy
57
Q

Zavanelli maneuver (shoulder dystocia)

A

pushing the baby’s head back up the birth canal

used for stat c-section in cases of un-fixable shoulder dystocia

58
Q

if the McRobert’s manoeuvre fails to deliver the shoulder in dystocia, what is the next immediate action (ALARM mnemonic)

A

A - Ask for help
L - Legs back (McRobert’s manoeuvre)
A - Anterior shoulder (Apply Suprapubic pressure to ↑ the effectiveness of the McRoberts’ manoeuvre)
R - Rotate the posterior shoulder (Wood’s manoeuvre) or rotate mom (Gaskins Maneuver)
M - Manual removal of posterior arm

59
Q

initial approach to the Critical Patient with Postpartum Hemorrhage

💵💵💵 MONEY SLIDE 💵💵💵

A
  1. Begin empiric uterine massage.
  2. Start uterotonics (Oxytocin 20-40 international units diluted in 500 mL of 0.9% sodium chloride IV, titrate to sustain uterine contractions and counteract uterine atony)
  3. tranexamic acid (TXA) 1 g IV.
  4. Call the blood bank to initiate the MTP
  5. Consider the placement of an intrauterine balloon tamponade device.
  6. Consult the OB immediately.
  7. Consult Interventional Radiology immediately
60
Q

American College of Obstetricians and Gynecologists (ACOG) postpartum hemorrhage definitions

💵💵💵 MONEY SLIDE 💵💵💵

A
  1. cumulative blood loss ≥1,000 mL or

2. bleeding associated with signs/symptoms of hypovolemia within 24 h of birth, regardless of the delivery route

61
Q

PRIMARY postpartum hemorrhage definition

A

PPH which occurs within the first 24 h of birth.

62
Q

SECONDARY postpartum hemorrhage definition

A

excessive bleeding that occurs >24 h after delivery and up to 12 wk postpartum.

63
Q

the “4 T’s” mnemonic for causes of primary PPH

💵💵💵 MONEY SLIDE 💵💵💵

A

Tone (70%-80% of cases are due to uterine atony)
Trauma (rips/tears to canal)
Tissue (retained placental tissue)
Thrombin (coagulopathic)

64
Q

Treatment of PPH targeting uterine tone

A

Begin aggressive uterine massage.

Initiate uterotonic medications:

  1. Oxytocin: First-line
  2. Carboprostol
  3. Methylergonovine
  4. Misoprostol

Placing an intrauterine balloon tamponade is another helpful adjunct to treating atony.

65
Q

Pathophysiology of postpartum hemorrhage

💵💵💵 MONEY SLIDE 💵💵💵

A
  1. By term, blood flows to the uterus at 500-700 mL/min and accounts for approximately 15% of CO → high potential for massive and rapid hemorrhage following delivery
  2. The uterus is a unique organ with its own mechanisms for hemostasis (Mechanical hemostasis from contraction of the myometrium that compresses blood vessels; local and systemic coagulation factors that cause clotting)
  3. A helpful way to remember the causes of primary PPH is the four T’s (Tone, trauma, tissue, thrombin)
  4. Tone (uterine atony): #1 cause of primary PPH (70%-80% of cases), should be considered first. Causes include: prolonged use of oxytocin, high parity, prolonged labor, use of general anesthesia, and uterus overdistention in cases of multiple-gestation pregnancies, polyhydramnios, or fetal macrosomia
  5. Trauma: large source of hemorrhage and is ~20% of PPH cases. Causes include: vaginal lacerations, uterine rupture, uterine inversion, or vulvar hematomas
  6. Tissue: Retained placental tissue can occur ~3% of deliveries. Any retained placenta minimizes the uterus’ ability to contract after delivery, which → hemorrhage, since the blood sinuses will stay open.
  7. Thrombin: Any coagulopathic state ↑ the risk of PPH. Disorders such as idiopathic thrombocytopenic purpura, thrombotic thrombocytopenic purpura, vWD, and various hemophilias may be present prior to delivery. Pregnant patients specifically can develop other secondary acute coagulopathies such as hemolysis, elevated liver enzyme levels, HELLP syndrome, DIC, which can be caused by severe preeclampsia, amniotic fluid embolism, sepsis, placental abruption, and other conditions.
66
Q

define and describe the Placenta accreta spectrum (PAS)

A
  1. Placenta accreta spectrum (PAS) is a general term comprising placenta accreta, increta, and percreta.

Placenta accreta – The placenta attaches itself too deeply and too firmly into the uterus.
Placenta increta – The placenta attaches itself even more deeply into the muscle wall of uterus.
Placenta percreta – The placenta attaches itself and grows through the uterus, sometimes extending to nearby organs, such as the bladder.

these patients bleed like a motherfucker. potential life threatening PPH

67
Q

Secondary PPH causes and pathophysiology

A
  1. Secondary PPH is excessive vaginal blood loss occurring at least 24 h to 12 wk after the completion of the third stage of labor.
  2. The most common cause of secondary PPH is retained tissue or products of conception. Uterine infection is another cause
  3. Anticoagulation medications and other coagulopathic states may ↑ the risk of secondary PPH.
68
Q

describe the role of TXA in PPH

A
  1. TXA inhibits enzyme breakdown of fibrinogen + fibrin
  2. In 2017, a large international RCT (WOMAN trial) showed TXA reduces death d/t hemorrhage in the postpartum woman without any increase in adverse effects (namely thrombosis).
  3. TXA 1 g IV may be used in PPH if initial medical therapy fails. benefits of TXA for PPH are strongest the earlier the medication is given
69
Q

describe the approach to treating “tone” component of PPH

A
  1. administer prophylactic uterotonic medication(s), such as oxytocin 10 international units IV or IM immediately after delivery of the placenta.
  2. At the same time, check the uterus for tone and begin uterine massage
70
Q

describe how to perform external uterine massage

A
  1. Place one hand in a cupped position on the lower uterine segment
  2. Place the other hand on the uterine fundus and aggressively massage the uterus between the two hands until the uterus becomes firm and contracted or the bleeding stops
71
Q

define and describe placental abruption

A
  1. occurs when a normally implanted placenta separates from uterus before delivery of the fetus
  2. can be d/t chronic pathologic vascular process or acute insults (trauma)
  3. should be suspected in women at >20 wk GA w/ vaginal bleeding +/- abdominal pain or a history of trauma, or unexplained preterm labor
72
Q

What is the role of glucocorticoids in antenatal preterm pregnancy?

A
  1. Glucocorticoids accelerate the production of type 1 and 2 alveolar cells.
  2. Type 2 alveolar cells produce surfactant.
  3. They also enhance the exposure of Na-K-ATPase which assist in fetal lung fluid clearance.
73
Q

Why is 24 weeks GA typically the cutoff for extrauterine fetal survival?

A
  1. Alveoli are barely developed at this GA, the majority of the lung is composed of terminal bronchi.
  2. Alveoli develop in the third trimeter, and dramatically ↑ up to age 2, then gradually to age 8
74
Q

What are the antenatal corticosteroid dosages?

A
  1. Betamethasone = 12mg x 2 doses, 24 hours apart. (first choice)
  2. Dexamethasone = 6mg x 4 doses, 12 hours apart (2nd line if beta not available)
75
Q

When are antenatal corticosteroids indicated?

A
  1. < 34 weeks GA with expected vaginal delivery.

2. < 37 weeks GA with scheduled cesarian delivery.

76
Q

What four questions should be asked of the mother during imminent birth?

A
  1. ROM — Time and characteristics
  2. GA
  3. Approximate birth weight if known
  4. Other extenuating factors
77
Q

How long is induction/cesarian typically delayed once antenatal corticosteroids are administered?

A
  1. One week

2. Benefits are seen as of 4 hours post-initiation of therapy, but greatest after one week

78
Q

What is PROM?

A

Premature rupture of membranes

79
Q

What is PPROM?

A

preterm Premature rupture of membranes

80
Q

What is the most common organism to cause neonatal sepsis?

A

Group B streptococcus.

E. Coli is the second most common cause.

81
Q

What does blood in the amniotic fluid typically indicate?

A

Placental abruption

82
Q

What are the two most common causes of premature fetal delivery?

A
  1. Infection

2. Cervical incompetence

83
Q

What are the three most common causes of preterm delivery without labour?

A

Hypertension
Fetal distress
Polyhydramnios

84
Q

Why do we give MgSO4 to preeclamptic mothers?

A
  1. Prevent seizure of the mother (thought to be from NMDA receptor action, increasing the threshold for seizure).
  2. Fetal neuroprotection (unknown mechanism)
85
Q

How do you determine minimum MAP in the first 48 hours of life?

A

MAP = GA in weeks. (ie. GA 30 weeks should have a MAP > 30)

86
Q

What are the most common causes of maternal transfers?

A
  1. Preterm labour

2. PPROM

87
Q

How is pregnancy dated? (estimated gestational age)

A
  1. Perinatal ultrasound.

2. Dated from the first day of the woman’s last menstrual period

88
Q

What does EDD stand for?

A

Expected date of delivery

89
Q

What does EGA stand for?

A

Estimated gestational age

90
Q

What are the most common causes of death in preterm babies

A

RDS, ICH, and NEC

91
Q

List four predisposing factors to PTD

A
  1. Cervical shortening
  2. Incompetent cervix
  3. PPROM
  4. Preterm labour
92
Q

List some risk factors for PTD

A
  1. Maternal → Previous PTD, pre-existing disease, uterine anomaly
  2. Fetal → IUGR, fetal anomaly, multiple gestation
  3. Placental → Poor implantation, antepartum hemorrhage
93
Q

Define abortion

A

Delivery of a dead fetus prior to 20 weeks GA

94
Q

Define live birth

A

Delivery of a live newborn at any GA

95
Q

Define stillbirth

A

Delivery of a dead newborn at or beyond 20 weeks

96
Q

Define gestational age

A

measure of the age of a pregnancy which is taken from the beginning of the woman’s last menstrual period

Take 40 + 6 and subtract the date of the START of the woman’s last period = estimated GA

Example → 25 weeks GA refers to 25+6 weeks

97
Q

What is the survivability of a fetus born at 32 weeks, compared to 40 weeks GA?

A

Approximately the same

98
Q

What is considered a “short” cervix?

A

Cervical length <2.5 cm before 24 weeks

99
Q

What is an incompetent cervix?

A
  1. It is essentially the opening of the cervix without labour.
  2. Defined as painless cervical dilation, typically before 24 weeks GA.
  3. The management of an incompetent cervix is to place a stitch, in order to maintain the pregnancy.
100
Q

Define preterm labour (PTL)

A
  1. PTL is defined as regular contractions twice in 10 minutes (“2 in 10”), as well as changes in length or dilation of the cervix
101
Q

What are the components of the initial assessment of PTL?

A
  1. GA
  2. Palpation of contractions
  3. Sterile speculum exam (cultures, rule out PROM, fetal fibronectin testing)
  4. Digital exam
102
Q

What is fetal fibronectin (fFN) testing?

A
  1. fFN is a protein detectable during labour. It is produced when there is separation of the placenta from the uterine wall
  2. The negative predictive value is very good at ruling out PTL
  3. positive fFN does not mean true labour, but will win you a transfer
103
Q

What are the goals of tocolytic therapy?

A
  1. Allow time for steroid therapy
  2. Allow time for antibiotic therapy
  3. Allow time for Transport
104
Q

What is a normal fetal heart rate?

A

110 to 160

105
Q

Define PROM

A

ROM prior to labour

106
Q

Define PPROM

A

ROM prior to labour with GA < 37 weeks

107
Q

What are the consequences of PROM?

A
  1. PTD within 1 week in 50% of births.
  2. Fetal pulmonary hypoplasia
  3. Fetal skeletal maldevelopment (contractures)
  4. Ascending infection (maternal/neonatal sepsis, GBS)
  5. baby gets neurologically fucked (cerebral palsy)
108
Q

What is ferning? (lab test)

A
  1. Microscopic investigation into fluid obtained from speculum exam.
  2. Presence of ferning indicates PROM
109
Q

Outline the management of PPROM

A
  1. <23 weeks → Termination of pregnancy
  2. 24 to 34 weeks → ABX, corticosteroids, delivery at 34 to 36 weeks GA
  3. 36 to 36 + 6 weeks → Weighed risk of ascending infection vs benefit of continued pregnancy, ABX
110
Q

What are the initial steps of in the delivery of a fetus with shoulder dystocia? (ALARM mnemonic)

A

A - Ask for help
L - Legs back (McRobert’s manoeuvre)
A - Anterior shoulder (Apply Suprapubic pressure to ↑ the effectiveness of the McRoberts’ manoeuvre)
R - Rotate the posterior shoulder (Wood’s manoeuvre)
M - Manual removal of posterior arm

111
Q

What is the most common cause of iatrogenic preterm delivery?

A

Hypertension

112
Q

What medication reduces preeclampsia risk by ~50%?

A

Aspirin

113
Q

Define hypertension in pregnancy

A

SBP or DBP >140/90

114
Q

Define severe hypertension in pregnancy

A

SBP or DBP >160/110

115
Q

Define gestational hypertension

A

Non-preexisting hypertension that develops beyond 20 weeks GA

116
Q

What are the criteria needed for the diagnosis of preeclampsia?

A
  1. Gestational hypertension with one of the following:

- New proteinuria OR associated symptoms.

117
Q

At what GA does preeclampsia/eclampsia develop?

A

> 20 weeks GA

118
Q

What is the pathophysiology of preeclampsia?

A
  1. Poor placental implantation → inadequate development of placental blood flow.
  2. This results in release of antiangiogenic factors from the placenta into the maternal circulation, which binds with vascular endothelial growth factor → widespread endothelial dysfunction
119
Q

Define HELLP syndrome

A

Complication of preeclampsia involving hemolysis, elevated liver enzymes, and low platelet count

120
Q

What symptoms should prompt investigation into HELLP syndrome?

A
  1. Nausea/vomiting

2. RUQ pain (liver tenderness)

121
Q

Can HELLP syndrome occur without hypertension?

A

Yes

122
Q

Outline the management of hypertensive disorders of pregnancy

A
  1. Initial therapy → nifedipine + Labetalol

2. Second line therapy → Methyldopa and other beta blockers.

123
Q

Why should ACE inhibitors and ARBs be avoided in the management of hypertensive disorders of pregnancy?

A

ACE-Is and ARBs are fetotoxic

124
Q

What is the leading cause of death in women with preeclampsia?

A

Pulmonary edema (be careful with your IV fluids)

125
Q

Define oligohydramnios

A
  1. amniotic fluid volume that is less than expected for gestational age
  2. diagnosed by ultrasound
126
Q

Why does hypertension often peak in the days following delivery?

A
  1. return of blood volume from the uterus → HTN.

2. Eclampsia can occur up to 6 weeks post-partum

127
Q

What is placenta accreta?

A
  1. Placental growth into the uterus.

2. Placenta accreta is associated with massive hemorrhage and high rates of mortality

128
Q

What are the benefits of delayed cord clamping?

A
  1. ↑ blood volume (20-40 ml/kg additional blood)
  2. ↑ stem cell transfer
  3. ↑ iron volume
  4. ↑ oxygen carrying capacity
  5. Decreased risk of NEC.
  6. Decreased risk of IVH (likely due to stabilized blood pressure from additional blood volume)
129
Q

What are the disadvantages of delayed cord clamping?

A

Higher risk of jaundice, though minimal

130
Q

When is delayed cord clamping contraindicated?

A
  1. Absent blood flow to neonate.

2. Multiple gestations that are sharing a placenta (though can be utilized on the last baby)

131
Q

What are the physiological differences between pregnant and non-pregnant patients?

🥼🥼🥼MEGA PIMPABLE TOPIC🥼🥼🥼

A
  1. CNS: N/A
  2. CVS: ↑ preload from a rise in blood volume. ↓afterload from ↓ SVR. ↑ HR by ~20 beats per minute. Left axis deviation.
  3. RSP: Progesterone stimulation produces an ↑ respiratory drive, reducing PaCO2 to 30-32, creating a chronic respiratory alkalosis. PaO2 elevation to 104-108 as a result of ↑ CO and minimization of VQ mismatch in the lung. Upward displacement of the diaphragm → 20% decrease in FRC. Oxygen consumption ↑ by 20%.
  4. GI: ↑ risk of gastric aspiration 2° to ↓ lower esophageal sphincter tone
  5. GU: ↑ GFR w/ ↑ renal blood flow, decreasing creatinine to 35-45.
  6. MSK: N/A.
  7. LABS: Plasma volume ↑ by 50% by 32 weeks. RBC ↑ only by 20-30%, resulting in hemodilution and normal Hgb of 100-110 (preggo patients have ↑ Hgb but it normalizes d/t ↑ circulating plasma volume). Mild leukocytosis. Small reduction in platelets

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