Abnormal pregnancy Flashcards
1
Q
Ectopic pregnancy
- most common site
- incidence
- risk factors
A
Most common site –> ampulla of fallopian tube
Incidence
- true incidence is uncertain –> estimated as 2%, likely underestimated
- increase in cases due to increased use of assisted reproductive technologies
- remains the leading cause of maternal mortality, despite great improvements –> bleeding can occur when the implanting pregnancy erodes into blood vessels or ruptures through structures
Risk factors –> most cases are thought to be due to tubal disease
- previous tubal surgery
- infections (salpingitis/PID)
- previous ectopic (15% recurrence)
- endometriosis
- pelvic or abdominal surgery
- failed tubal ligation
Other risk factors
- smoking
- infertility and use of infertility tx
- DES exposure in utero
2
Q
Ectopic pregnancy
- clinical symptoms
A
- abdominal pain or pelvic pain
- amenorrhea
- vaginal bleeding
- –> Any sexually active woman of reproductive age who presents with any of these symptoms should have ectopic pregnancy as part of her initial differential dx
Other symptoms
- pregnancy symptoms - vomiting
- intraabdominal bleeding –> syncope, dizziness, shoulder pain
3
Q
ectopic pregnancy
- differential diagnosis
A
- ectopic pregnancy
- early intra-uterine pregnancy
- miscarriage
- PID
4
Q
Ectopic pregnancy
- physical exam/lab findings
A
Physical findings
- abdominal tenderness
- adnexal tenderness
- adnexal mass
- hypotension + tachycardia –> from internal bleeding
Lab findings –> pregnancy test
- urine test detects hcg 14 days after conception
- serum test detects after 5 days
- follow hcg levels at 2 day intervals –> should double every 48 hours early in pregnancy
- a viable intra-uterine pregnancy demonstrates a minimal increase of 66% every 48 hours in serum hcg levels
- hcg levels alone can not distinguish ectopic pregnancy from normal or abnormal intrauterine pregnancy
- inappropriate rising hcg signals an abnormal pregnancy but does not identify the location
- if hcg levels have not risen appropriately, we know its either a miscarriage or ectopic pregnancy
5
Q
Ectopic pregnancy
- diagnosis
A
Locate the pregnancy
Transvaginal US
- should identify a viable intra-uterine pregnancy by 5.5 weeks gestation (hcg of more than 1500)
- transabdominal US should identify an intrauterine pregnancy when hcg > 6000
- –> if intrauterine pregnancy is not seen at these levels = likely ectopic
- signs of ectopic gestation = embryo, heart rate, sac with “ring of fire”
Uterine curettage (D and C)
- when pregnancy is clearly non-viable, but location is inconclusive, uterine curettage can help distinguish ectopic vs. uterine in case of abnormally rising hcg
- can also be done if pregnancy is undesired
Laparoscopy = gold standard
- invasive procedure –> insert probe through umbilicus to search for pregnancy
- hcg >1500 + no intrauterine sac in trans-vaginal US = diagnostic
- hcg <1500, active vaginal bleeding, no villi in D and C, less than minimal increase in hcg level = diganostic
Classic clinical triad = pain, bleeding + skipped menses
6
Q
Ectopic pregnancy
- management
A
Surgical
- conservative –> linear salpingostomy unruptured ectopic
- salpingectomy
Medical = methotrexate
- folic acid antagonist
- inhibits DNA synthesis and cell reproduction, primarily in actively proliferating cells such as malignant cells, trophoblast, and fetal cells
- toxic to hepatocytes
- renal clearance
- prior to administration should check: serum creatinin, liver transaminases, CBC, type and screen
Follow up
- patient must be followed post therapy with serial hcg measurements to monitor complete regression of the pregnancy
- sucess rate depends on the initial hcg level, the size of the pregnancy and the presence of cardiac activity
7
Q
Preterm labor
- overview
- risk factors
A
Preterm labor is the most common cause of perinatal morbidity and mortality
- only 12% of infants are borm prematurely, however they account for more than 50% of all perinatal morbidity and mortality in the US
- definition = regular uterine contractions causing cervical change before 37 weeks
Risk factors
- history of prior preterm birth –> RR=4
- multiple gestation –> RR=6
- bleeding in pregnancy –> RR=3
- uknown = 50% –> we don’t know what causes most preterm births, so we can’t prevent them
8
Q
Preterm labor
- clinical symptoms
A
- menstrual like cramps
- low, dull backache
- abdominal or vaginal pressure
- abdominal cramping
- increase or change in vaginal discharge
- uterine contractions (can be painless)
9
Q
Preterm labor
- differential dx
A
- preterm labor
- UTI
- vaginitis
- round ligament pain
- muscular pain
- broxton hicks contractions
10
Q
Preterm labor
- physical exam/lab findings
A
Lab
- WBC count
- urinalysis and culture
- cervical culture
- vaginal wet prep –> vaginal infections
11
Q
Preterm labor
- diagnosis
A
Regular uterine contraction
- > 6 contractions/hour
- moderate/severe intensity
Cervical change –> advancing effacement or dilation in serial exam
- cervical length –> short cervical length = higher risk of preterm birth
Fetal fibronectin –> a glycoprotein found in the ECM of the membranes of the amniotic sac
- presence in cervico-vaginal secretions between 22-34 weeks represents disruption of maternal-fetal interface
- low positive predictive value - if its there, we don’t know for sure that its preterm labor
- high negative predictive value - if its not there, we know that its not preterm labor
No one single modality has a good detection rate on its own
- uterine contractions = 18% sensitivity
- cervical length = 60% sensitivity
- FFN = 50% sensitivity
- combined cervical length + FFN = 71% sensitivity
- IL6 –> 82% sensitivity but have to perform an invasive, risky procedure to obtain measurement
12
Q
Preterm labor
- management
A
Goal is to delay delivery until fetal lung maturity is attained, if possible
- IV hydration
- tocolysis –> give drugs to delay labor
- administration of steroids to promote lung maturity = 2 doses of betamethasone 24 hours apart –> helps fetal survival but does not prevent preterm birth
- neuroprotection –> mg sulfate
- antibiotics –> group B strep propylaxis
Effective
- steroids (bethametasone/dexamethason)
- progesterone –> prevents preterm birth if patient has a history of prior preterm birth
- neuroprotection with mg sulfate
Ineffective –> prolonged tocolysis (after 48 hours)
13
Q
Tocolysis
A
Goal is to stop contractions until 24 hours after 2nd dose of steroids to obtain greatest lung maturity
Mg sulfate –> competes with ca for entry into cells
- often first line tx
- at high levels, can cause resp distress, pulm edema, cardiac depression
Nifedipine –> ca channel blocker
- prevents ca entry into muscle cells
Indomethacin –> pg synthetase inhibitor
- decrease pg by blocking conversion of free arachidonic acid to pg
- premature closure of ductus arteriosis with use after 32 weeks –> need to be careful
- decreased amnihotic fluid with prolonged use
- must use cautiously, and don’t use after 32 weeks
14
Q
Contraindications to tocolysis
A
- evidence of intrauterine infection
- significant vaginal bleeding
- fetal distress
- no tocolysis after 34 weeks
- –> decreased risk of morbidiy/mortality from prematurity
- –> no role for betamethasone administration
15
Q
PPROM = preterm rupture of membranes
A
Often iatrogenically caused or due to preterm labor
Diagnosis
- pooling –> water coming out of the cervix = 100% sensitive
- nitrazine –> pH testing to tell you whether its likely amniotic fluid
- ferning –> indicates presence of salt, telling you if its amniotic fluid
16
Q
Risks after PPROM
A
- infection –> its unclear whether infection is a cause or consequence of PPROM
- cord prolapse –> more common in non-vertex presentations
- placental abruption –> placenta separates from attachment earlier
- pulmonary hypoplasia –> correlates with gestational age at time of rupture
- –> sufficient levels of amniotic fluid are necessary for normal fetal lung development
- –> 19 wks = 50%
- –> 22 wks = 25%
- –> 26 wks = <10%
17
Q
Management of PPROM
A
- expected management
- if there is an infection, we deliver the baby immediately (not good for baby or mom for baby to stay inside)
- antibiotics for latency –> if no signs of infection, we give prophylactic antibiotics to prevent strep B
- bethametazone course –> helps devt of lungs
- tocolysis until completion of bethametazone course
- delivery if patient develops signs or symptoms of chorioamnionitis
- delivery after 34 weeks gestation
18
Q
Hypertensive disorders of pregnancy
A
Second leading cause of maternal mortality, accounting for almost 15% of deaths
- occurs in 6-8% of pregnancies
- causes both maternal and fetal morbidity and mortality –> placental abruption, DIC, cerebral hemorrhage, hepatic and renal failure
- the most significant unsolved problem in OB
systolic > 140 diastolic > 90 --> at least two occasions --> at least 4 hours apart --> within 1 week period
19
Q
Classification of hypertension in pregnancy
A
Chronic Hypertension = elevated BP before 20 weeks of gestation or beyond 6 weeks postpartum
- 25% of patients with chronic htn will develop preeclampsia/eclampsia
Gestational Hypertension = htn without other signs or symptoms of preeclampsia or preexisting htn
- no proteinuria
- onset occurs after 20 wks gestation and BP must return normal within 6 weeks after delivery
Preeclampsia
- Without or with severe features
Chronic Hypertension with superimposed preeclampsia
HELLP syndrome
Eclampsia
20
Q
Preeclampsia
A
- BP greater than or equal to 140/90 on 2 occasions at least 4 hours apart after 20 weeks of gestation in a woman with a previously normal BP
- BP greater than or equal to 160/110 –> htn can be confirmed iwthin a short interval to facility quick tx
AND
proteinuria –> greater than or equal to 300 mg per 24 hour urine collection, or protein/cr ratio greater than or equal to 0.3
OR - in the absence of proteinuria, new onset hypertension with the new onset of any of the following
- platelet count less than 100,000
- serum cr conc greater than 1.1
- elevated liver enzymes to 2x normal
- pulm edema
- cerebral or visual symptoms
21
Q
Severe preeclampsia
A
Management is different than preeclampsia
- BP is 160/110 or higher on 2 occasions at least 4 hours apart white patient is on bed rest
- thrombocytopenia (less than 100,000)
- impaired liver function = abnormally elevated liver enzymes to 2x normal
- progressive renal insufficiency
- pulm edema
- new onset cerebral or visual disturbance
22
Q
HELLP syndrome
A
A variant of severe preeclampsia
- hemolysis = microangiopathic hemolytic anemia
- –> abnormal peripheral blood smear
- –> elevated indirect bilirubin
- –> low serum haptoglobin
- –> elevated LDH - elevated liver enzymes –> ALT/AST > 70 IU/L
- low platelets –> <100,000
23
Q
Risk factors for pre-eclampsia
A
- nulliparity
- extremes of age (40)
- african american
- chronic htn
- chronic renal disease
- diabetes - disturbs blood vessles
- multifetal gestations
24
Q
Eclampsia
A
Preeclampsia with seizures
- 0.5-4% of deliveries
- 25% of eclamptic seizures occur in first 72 hours after delivery
- Mg sulfate is used to prevent and treat eclamptic seizures - can reduce the rate of seizures by 50%
25
Pathophysiology of preeclampsia
Abnormal placentation in preeclampisa
- in normal placental devt, invasive cytotrophoblasts of fetal origin invade the maternal spiral arteries, transforming them from small caliber resistance vessels to high caliber capacitance vessels capable of providing placental perfusion adequate to sustain the growing fetus
- in preeclampsia, this process fails to occur --> the arteries remain small caliber resistance vessels
- when the placenta is deprived of blood, it secretes 2 endogenous circulating antiangiogenic proteins = sFlt1 and sEng --> inhibit VEGF and TGF beta signaling so that more angiogenesis can occur in the placenta specifically
- inhibition of VEGF and TGF beta in the vasculature results in endothelial cell dysfunction = decreased prostacyclin, NO production, and increased release of pro coagulant proteins
Endothelial dysfunction causes:
- proteinuria = increase creatinine, oliguria and increased uric acid
- CNS = brisk reflexes, headaches, seizures, stroke
- RUQ pain = increased liver function tests + thrombocytopenia
- blood vessels = vasoconstriction, edema, increased HCT, hemolysis
26
Evaluation of preeclampsia
- review of records
- obtain history including symptoms
- physical exam including maternal weight, serial BP readings, edema, deep tendon reflexes, elicit RUQ tenderness
- assess fetus
- lab findings
27
Management
Individualized care --> risks and benefits of delivery vs. continued monitoring for both the mother and fetus
If term --> mg sulfate to prevent maternal seizures and deliver
If preterm
- with severe features --> mg sulfate to prevent complications in baby and deliver
- without severe features --> expectant management until term or becomes severe
28
Causes of obstetric hemorrhage
Vulva
- varicose veins
- tears or lacerations
Vagina - tears or lacerations
Cervix - poly, cervicitis, carcinoma
Intrauterine
- placenta previa
- placenta
- morbidly adherent placenta
- vasa previa
29
Obstetric hemorrhage
| - management
Initial management
- stabilize the patient
- --> assessment of hemodynamic stability
- --> IV fluids
- --> blood products
- locate the placenta with US
30
Placenta previa
Abnormal location of the placenta over or in close proximity to the internal cervical os
- 1/250 pregnancies
- no cervical exam!! will cause bleeding
- painless bleeding --> differentiates from abruption
- can occur spontaneously or after intercourse
If mother and fetus are stable, expectant management until close r to the expected due date
- deliver by C section
31
Placental abruption
Premature separation of the normally implanted placenta from the uterine wall
- vaginal bleeding - can be visible or concealed
- usually with abdominal discomfort (can be severe) and/or uterine contractions
- difficult to detect by US
Etiology
- maternal htn
- cocaine use
- smoking
- abdominal trauma
Fetal blood supply is compromised
- can result in fetal heart rate abnormalities and need for emergent delivery or fetal demise
- associated with DIC
32
Complications of multiple gestations
Preterm delivery
- singleton - 40 wks
- twins - 36 wks
- triplets - 32 weeks
- quadruplets - 28 weeks
Spontaneous abortion
Gestational diabetes
Preeclampsia
Maternal hemorrhage at deliver
33
Incidence
Spontaneous twins = 1/90 pregnancies in the US
- higher in blacks, lower in white
- 31/1000 live births
Spontaneous triplets = 1/800 pregnancies
- 1/8/1000 live births
34
Monozygotic twins
Division of fertilized ova after conception - unknown etiology
- 1/250 pregnancies
- 4-5/1000 births
- dichorionic diamniotic = separate at 4 days - each has its own amniotic sac and placenta
- monochorionic diamniotic = separate at 4-8 days- each has its own amniotic sac but share a placenta
- monochorionic monoamniotic = separate at 8-13 days - share an amniotic sac and a placenta
- conjoined twins = separate greater than 13 days
35
Dizogotic twins
Two ova fertilized by two different sperm
- 1/20 in certain african countries
- increasing age
- familial
- assisted reproductive technologies
Any twins in utero can have cord entanglement
36
twin-twin transfusion syndrome
- monochorionic-diamniotic twins = each has its own amniotic sac but share a placenta
- vascular anastomoses resulting in net blood flow from one twin to the other
- donor = impaired growth, anemia, hypovolemia, low amniotic fluid
- recipient = hypervolemia, hypertension, polycythemia, CHF, increased amniotic fluid
Management - separate the placenta and make dichorionic type placenta - can save at least one of the babies
