Question | Answer |
developmental age | number of weeks and days since fertilization |
gestational age | number of weeks and days measured from the last menstrual period; can also be determined by fundal height, quickening, fetal heart tones, and ultrasound |
nagele's rule | 9 months + 7 days since last menstrual period = estimated date of delivery |
levels of hCG double approximately every ________ during early pregnancy | 48 hours |
physiologic change to the cervix | softening and cyanosis at approximately four weeks (Goodell's sign). Thick mucus plug in the cervical oss expelled at or near labor("bloody show"). mucus appears granular microscopically due to progesterone. |
physiologic changes to the uterus during pregnancy | softening of the uterus after six weeks (Ladin's sign). palpated above the pubic synphysis at 12 weeks. |
when can you feel the uterus above the pubic symphsis during pregnancy? | 12 weeks. |
What is Ladin's sign | softening of the uterus after 6 weeks |
during pregnancy what changes do the vagina undergo? | thick acidic secretions; violet colorations from increased blood flow |
what is chadwick's sign | violet colorations of the vagina due to increased blood flow |
what happens to the cardiovascular system during pregnancy | increased cardiac output, heart rate adn stroke volume; decreased systemic vascular resistance and decreased BP in the 1st trimester which normalizes by 40 wks. |
what murmurs are normal in pregnancy | systolic murmur and audible S3 |
what murmurs are NOT normal in pregnancy | NEW diastolic murmur |
why does cardiomegaly occur on CXR during pregnancy? | the heart is displaced by the uterus upward and to the left. |
what happens to thyroid hormone in pregnancy? | increased estrogen levels increases TBG leading to increase in total and bound T3/T4; but active unbound hormone is unchanged |
what is human placental lactogen | a hormone that increases lipolysis and FFAs, and acts as a ninsulin antagonist to maintain fetal glucose levels --> postprandial hyperglycemia, fasting hyperinsulinemia/hypertriglyceridemia and exaggerated starvation ketosis. Changes can worsen GDM. |
what happesn to cortisol during pregnancy? | increased total and free cortisol because the fetal adrenal gland and placenta produce cortisol. |
changes in the GI system during pregnancy | nausea and vomiting usually resolves in 14-16 weeks, increased acid reflux because of decreased GEJ(x) tone; constipation from decreased bowel motility and increased water resorption; increased biliary cholesterol saturation predisposes to gallstones. |
what is physiologic anemia of pregnancy? | unequal increase in plasma volume and RBC mass leads to decreased hemoglobin and hematocrit. however, a hemoglobin of <11.0 mg/dL is never normal and is likely due ot iron deficiency. |
T/F. WBC stay the same during pregnancy | WBC can increase to a mean of 10.5 million/mL but during labor can become >20 million/mL. |
what is the leading nonobstetric cause of postpartum death? | DVT -->PE: pregnancy creates ah hypercoagulable state. |
musculoskeletal changes during pregnancy | increased motility of sacroiliac, sacrococcygeal and pubi joints. |
pulmonary changes | increased tidal volume, decreased TLC, RV, ERV; RR unchanged but increased minute ventilation --> increased alveolar and arterial PO2 and decrease arterial and alveolar pCO2. |
what is dyspnea of pregnancy | it is common and likely caused by increased tidal volume and decreased PCO2 |
renal changes in preganncy | GFR increases by 50%, BUN and creatinine decrease by 25%, renal plasma flow increases by 30%; kidneys dilate and there's physiologic hydronephrosis b/c uterus compresses the ureter; increased risk of asymptomatic UTIs, increased RAA --> water retention |
changes in the skin during pregnancy | increased estrogen --> striae, spider angiomas, palmar erythema; hyperpigmentation over the abdominal midline (linea nigra), face (chloasma/melasma), nipples and perineum is due to increased alpha melanocyte stimulating hormone and steroids. |
what is diastasis recti | rectus muscles may separate in the midline, leaving part of the anterior uterus covered only by skin, fascia and peritoneum. |
how much weight should a pregnant woman gain | 25-35lbs for averate weight woman |
how many extra calories does a pregnant woman need | 100-300kcal |
how many extra calories does a breast feeding woman need | 500kcal/day |
what vitamin/mineral supplements should be given | 0.4mg qday folic acid; 30mg/d of elemental iron = 325mg FeSO4 |
what vitamin should be avoided during pregnancy in excess amounts | vitamin A |
how much exercise is encouraged during pregnancy | 30 minutes |
how often should a pregnant woman see her doctor | wks 0-28: q4wks; wks 29-36 - q2wks; wks36-birth: qweekly. |
what labs should an ob get on a first prenatal visit | CBC, blood type, Rh factor, and antibody screen. UA and culture, rubella antibody titier, HBVsAg, syphilis screen, cervical gonorrhea and chlamydia PCR/culture, PPD, HIV. Pap smear, glucose challenge, sickle prep. |
what labs should be gotten at 15-20 wks of pregnancy | materal serum AFP or quad screen or triple screen; offer amniocentesis to patients >35 yoa. |
what labs should be done at 18-20wks of pregnancy | US to determin GA and to survey fetal anatomy, amniotic fluid volume, and placental location |
what labs should be done at 26-28wks of pregnancy | glucose challege test |
what labs should be done at 32-36 wks of pregnancy | cervical chlamydia, gonorrhea cultures; HIV, RPR; repeat Hematocrit; GBS screening (GBS = group B strep), pap |
what do you do if someone is GBS positive during pregnancy | give penicilin during labor to prevent transmission to the infant. |
differential for elevated materal serum alpha fetoprotein | >2.5 MoMs: open neural tube defects, abdominal wall defects, multiple gestation, incorrect gestational dating, fetal death and placental abnormaliites |
differentail for low materal serum alpha fetoprotein | <0.5 MoM warrent amniocentesis and karyotyping to rule out chromosomal abnormalities |
what is the quad screen | sensitivity for detecting chromosomal abnormalities is increased by adding inhibinA, estriol, beta-hCG and MSAFP together. |
what are the results in the quad screen for trisomy 18 | all four characteristics are down |
what are the results in teh quad screen for trisomy 21 | afp and estrio are decreased; beta hCG and inhibin A are increased |
when is amniocentesis performed? | at wks 15-17 in women who will be >35 yoa at the time of delivery, in those with abnormal quad screens, in Rh sensitized preganncy to obtain fetal blood type or detect fetal hemolysis and to evaluate fetal lung maturity via lecithin-shpingomyelin ratio |
what are advantages to chorionic villus sampling | has a diagnostic accuracy comparable to that of amniocentesis; availability at 10-12 wks gestation. |
waht are disadvantages to chorionic villus sampling | risk of fetal loss and inability to diagnose neural tube defects is 0.5-1% greater than with amniocentesis. |
why is chorionic villus sampling not done earlier during gestation | limb defects have been associated with chorionic villus sampling performed at <9wks of age |
what is percutaneous umbilica blood sampling | transabdominal phlebotomy of the umbilical cord. performed in 2nd and 3rd trimesters, when umbilical cord vessels are lager enough to pucture safely. not done any more except to diagnose fetal hemolytic disease and fetal infection. |
leopold's maneuvers do what | determin fetal lie (longitudinal or transverse) and fetal presentation (breech or cephalic) |
5 aspects of a bishop score | dilation,effeacement, station, cervical position and cervical consistency. A bishop score of >8 is consisten with a cervix favorable for both spontaneous and induced labor. |
should the speculum exam be steril or non steril | if ROM is suspected sterile |
fetal alcohol syndrome | growth restriction before and after bith, mental retardation, idfacial hypoplasia, renal and cardiac defects |
extra androgens and testosterone during pregnancy | virilization of females; advanced genital development in males |
ACEIs during pregnancy | fetal renal tubular dysplasia and neonatal renal failure, oligohydramnios, intrauterine growth restriction, lack of cranial ossification |
coumadin during pregnancy | nasal hypoplasia, stippled bone epiphysis, developmental delay, IUGR, ophthalmologic abnormalities |
carbamazepine during pregnancy | neural tube defects, finger nail hypoplasia, microcephaly, developmental delay, IUGR |
folic acid antagonists (e.g. methotrexate, aminopterin)during pregnancy --> | increased spontaneous abortion rate |
cocaine during pregnancy --> | bowel atresias; congenital malformations of the heart, limbs, face and genitourinary tract; microcephaly; IUGR; cerebral infarctions |
diethylstilbestrol (DES)during pregnancy --> | clear cell adenoma of the vagina or cervix, vaginal adenosis, abnormalities of the cervix and uterus or testes, possible infertility. |
lead during pregnancy --> | increased spontaneous abortion rates; still births. |
lithium during pregnancy --> | congential heart disease - Ebstein's anomaly (opening of TV displaced towards RV) |
organic mercury during pregnancy --> | cerebral atrophy, microcephaly, mental retardation, spasticity, seizures, blindness. |
phenytoin during pregnancy --> | IUGR, metal retardation, microcephaly, dysmoprhic craniofacial features, cardiac defects, fingernail hypoplasia |
radiation during pregnancy --> | microcephaly, mental retardation, medical diagnostic radiation delivering <0.05 Gy to the fetus has no teratogenic risk. |
streptomycin and kanamycin during pregnancy --> | hearing loss; CN VIII damage |
tetracyclines during pregnancy --> | permanent yellow-brown discoloration of the deciduous teeth, hypoplasia of tooth enamel. |
thalidomide during pregnancy --> | bilateral limb deficiencies, anotia, microtia, cardiac and GI anomalies |
trimethadione and peramethadione during pregnancy --> | cleft lip or cleft palate, cardiac defects, microcephlay, mental retardation. |
valproic acid during pregnancy --> | neural tube defects, minor craniofacial defects |
vitamin A and derivatives during pregnancy --> | increase spontaneous abortion rate, microtia, thymic agenesis, cardiovascular defects, craniofacial dysmorphis, microphthalmia, cleft lip or cleft palate, mental retardation. |
defects found on congenital CMV | microcephaly, hydrocephaly, chorioretinits, cerebral calcifications, IUGR, microphthalmos, metnal retardation, hearing loss |
most common congenital infection | CMV |
congenital rubella | microcephaly, mental retardation, cataracts, hearing loss, congenital heart disease |
congential syphilis defects | fetal hydrops (severe); abnormalities of hte skin, teeth, and bones (mild). |
congenital toxoplasmosis defects | microcephaly, hydrocephaly, crebral calcifications, chorioretinitis. |
how is toxoplasma gondii is transmitted to humans | by raw meat or through exposure to infected cat feces. |
congenital varicella | skin scarring, chorioretinitis, cataracts, microcephaly, hypoplasia of the hands and feet, muscle atrophy. |
most common obstetric procedure | fetal heart rate monitoring: in patients w/o complications, done every 30 min in 1ststage of labor & every 15 min in 2nd stage of labor. in Patients w/ complications every 15 min in 1st stage of labor, & every 5 min in the 2nd stage of labor. |
first stage of labor | divided into latent (onset o flabor to 3-4cm of cervical dilation) and active (4 cm of cervical dilation at least) |
what prolongs the latent first stage of labor | excessive sedation, hypertonic uterine contractions |
what prolongs the active first stage of labor | cephalopelvic disproportion |
how long is the first stage of labor | latent and combined can be anywhere from 6-18 hours. |
how long is the 2nd stage of labor | complete cervical dilation to delivery of infant |
how long does it take to go through the 2nd stage of labor | 0.5-3hours |
what is the 3rd stage of labor | delivery fo the infant to delivery of placenta 0-0.5 hrs; placental separates and uterus contracts to establish hemostasis. |
common causes of acceleration of fetal heart rate patterns | fetal movements can cause a visually apparent increase (onset to peak in <30s) in FHR from the most recent baseline |
what is early deceleration | vissually apparent, gradual decrease in fetal heart rate with retun to baseline that mirrors uterine contraction |
common cause of early fetal heart rate deceleration | head compression from the uterine contraction |
late deceleration | a vissually apprent, gradual, decrease in fetal heart rate with retun to bseline whose onset, nadir and recovery occur after the beginning, peak and end of uterine contraction respectively. |
what causes late deceleration | fetal hypoxemia and uteroplacental insufficiency |
umbilical cord compression | (most often 2' to oligohydramnios) causes what changes to the fetal heart rate patterns? variable decerleration |
what is variable deceleration | an abrupt vissual apparent decrease in fetal heart rate below baseline lasting more than 15 s, but less than 2 min |
what is bradycardia at baseline? | a fetal heart rate of less than 110bpm |
what causes fetal bradycardia | congenital heart malvormations, severe hypoxia (2' to uterine hyperstimulation, cord prolapse, rapid fetal descent). |
fetal tachycardia | baseline fetal heart rate >160 bpm |
what causes fetal tachycardia | hypoxia, maternal fever, anemia |
what is considered an antepartum fetal surveillance technique | fetal movement assessment; nonstress test; contraction stress test, biophysical profile, modified biophysical profile, umbilical artery doppler velocimetry, oligohydramnios |
fetal movement assessment | assessed by the mother as the number of fetal movements over one hour; avg is 10-20; materal reports of decreases in fetal movements should be followed with additional antepartum fetal surveillance |
nonstress test= | monitor fetal HR & uterine contractions (use a tocodynamometer). NORMAL response: 2 accels. of >15 bpm above baseline for >/= 15s over 20 min. Lack of fetal accelerations: GA <32wks, fetal sleep, fetal CNS anomalies & maternal sedative/narcotic use. |
contraction stress test = | in lateral recumbent positions, fetal HR is monitored during contractions. a +ve CST = late decelrations following >/=50% of contractions in a 10 min window and this is worrisome, and delivery is usually warrented. |
biophysical profile = | real time ultrasound is used t assign a score (0=abnormal; 2 = normal); to 5 parameters. a total score of 0-4 is extremely worrisome for fetal asphyxia. |
5 parameters of a biophysical profile | fetal tone, breathing, movement, amniotic fluid volume and NST |
modified biophysical profile | combines the NST with the amniotic fluid index; normal if NST is reactive/normal and AFI >5cm |
amniotic fluid index = | AFI, sum of measurements of hte deepest cord free amniotic fluid in each of the abdominal quadrants |
umbilical artery doppler velocimetry = | with IURGR, there is a reduction and even reversal of umbilical artery diastolic flow. the test is of benefit only when IUGR is suspected |
oligohydramnios = | AFI <5cm = always warrants further workup. |
absolute contraindiations to regional anaesthesia | refractory maternal hypotension; maternal coagulopathy, maternal use of once daily dose of LMWH, untreated maternal bacteremia; skin infection over hte site of needle placement, increased intracranial pressure caused by a mass lesion |
what is used to reduce gastric acidity and prevent acid aspiration syndrome during delivery? | sodium citrate |
advantages of using parenteral analgesia (opioid agonists and agonist-antagnoists) | provides an adequate level fo pain relief without the risks of anaesthesia |
disadvantages of parenteral analgesia/anestehsia (opioids) | limited analgesic effect in labor as it mostly sedates; increases risk fo neonatal naloxone administration of apgar scores of <7 |
advantages of epidural | provides the most effective form of pain relief; can also be used for C-section or postpartum tubal ligation. |
disadvantages of epidruals | can result in pruritus, fever, hypotension and transient fetal heart rate deceleration |
advantages of spinal analgesia | rapid, provides excellent pain relief for procedures of limited duration |
disadvantages of spinal analgesia | acts for a limited duration; puts patients at risk for hypotension, postdural puncture headache, and transient neurologic symptoms |
advantages of combined spinal epidural | offers the rapid onset of spinal analgesia combined with the ability to prolong the duration of analgesia with continuous epidural infusion. |
disadvantages of combined spinal epidurals | carries the risks of both procedures, increase hte risk of bradycardia and emergent C-section over epidural analgeisa alone |
advantages of general anesthesia | used in emergent c-sections and indicated in some cases of fetal HR abnormality; can be useful in cases where regional anaesthesia is absolutely contraindicated |
disadvantages of general anaesthesia | requires airway control; carries a significant risk fo maternal aspiration and neonatal depression; associated with higher maternal m orbidity rates than epidurals. |
advantage of local anaesthesia/analgesia | provides anesthesia before episiotomy and during repair of lacerations; can be used to perform a pudendal block |
disadvantages of local anesthesia and analgesia | in rare circumstances, can cause seizures, hypotension and cardiac arrhythmias. |
hyperemesis gravidarum = | persistent vomiting not related to other causes, acute starvation and weight loss |
frequency of hyperemesis gravidarum | 0.5-2%, more common in nulliparas, multiple gestations, and molar pregannacies. |
ddx for hyperemesis gravidarum | differentiate from "morning sickness", acid reflux, gastroenteritis, hyperthyroidism and neurologic conditions. |
workup for hyperemesis gravidarum | evaluate for ketonemia, ketonuria, hyponatremia, hypokalemia, hypochloremic metabolic alkalosis. measure liver enzymes, serum bilirubin, and serum amylase/lipase. check beta-hCG level. |
treatment for hyperemesis gravidarum | vitamin B6 +/- doxylamine for nausea and vomiting of pregnancy. Can also consider most antiemetics. ginger, IV hydration, hospitalization and parenteral nutrition may also be used. |
gestational diabetes mellitus | carbohydrate intolerance of variable severity diagnosed first during pregnancy |
frequency of GDM | 3-5% of all pregnancies, usually in late pregnancy |
risk factors for GDM | obesity, family/personal Hx of diabetes, recurrent abobrtions, stillbirths, maternal age >25 yoa, prior macrosomic infant, or an infant with congenital anomalies and prior polyhydramnios |
workup for GDM | glucose challenge test, UA with glycosuria |
treatment for GDM | start w/ ADA diet, regular exercise, & strict glucose monitoring (4x/day). Add insulin if dietary control is insufficient. get US & NSTs to assess fetal growth & well being. It may be necessary to induce labor at 39-40wks. |
complications of GDM | later on DM, in fetus, large for gestation age, increased risk fo congential malformations, increased maternal/fetal morbidity during labor and delivery |
workup for diabetic moms | fasting morning BS<90 mg/dL, 2hr post-meal<120 mg/dL. 18-20 wks:US 4 fetal age, growth, heart & polyhydraminios; quad screen. 32-34 wks: fetal surveillance (e.g.NST, CST, BPP); Admit if matenral DM has been poorly controlled/fetal parameters are concern. |
C-section in GDM if estimated fetal weight is _____________ | >4500 g |
maternal complications in diabetic pregnancies | DKA/HHNK; preeclampsia/eclampsia; cephalopelvic disproportion and need for C-section; preterm labor; infection; polyhydramnios; postpartum hemorrhage; maternal mortality |
fetal complications in diabetic pregnancies | macrosomia, cardiac and renal defects, neural tube defects (e.g. sacral agenesis; hypocalcemia, polycythemia, intrauterine growth restriction, hypoglycemia from hyperinsulinemia, respiratory distress syndrome, birth injury, perinatal mortality |
gestational hypertension (formerly known as pregnancy-induced hypertension) | idiopathic HTN w/o significant proteinuria (<300 mg/L) that develops at >20 wks gestation. as many as 25% progress to preeclampsia. |
treatment for hypertension during pregnancy. | NOOOOO ACEIs or diuretics. use methyldopa, labetalol, nifedipine. |
preeclampsia | defined as a new onset hypertension (SBP >140 mmHg or DBP >90 mmHg) and proteinuria (>300 mg of protein in a 24 hour period) occurring at >20wks gestation. |
eclampsia | is defined as new onset grand mal seizures in women with preeclampsia |
HELLP | variant of preeclampsia with poor prognosis (see mnemonic) = hemolysis, elevated LFTs, and Low platelets (thrombocytopenia); etiology is unknown but vasospasm --> hemorrhage and organ necrosis |
risk factors for HELLP syndrome | risk factors include nulliparity, black ethnicity, extremes of age (<20 or >35 wks), multiple gestation, molar pregnancy, renal disease, family history of preeclampsia, and chronic hypertension |
workup after dx with preeclampsia | UA, urine protien 24 hr, CBC, BMP, Uric acid, fetal age US, amniocenteseis to assess fetal lung maturity, LFTs, PT/PTTT, etc. |
cure for preeclampsia/eclampsia | delivery of the fetus |
antepartum hemorrhage | any bleeding after 20 wks gestation. complicates 3-5% of pregnancies. the most common causes are placental abruption and placenta previa. but can be due to ruptured uterus, genital tract lesions and trauma. |
management for mild preeclampsia | if patient close to term deliver; if not - bed rest and expectant management. |
mild preeclampsia = | BP >140-90 on 2 occasions >6 hours apart. Proteinuria (>300 mg/d or 1-2 + urine dipsticks) |
management of severe preeclampsia | control BP with labetalol/hydralazine; deliver; prevent seizures with continuous MgSO4 drip; continue seizure prophylaxis for 24 hours post partum. |
treatment of Mg2+ toxicity | IV Ca2+ gluconate (also used to prevent arrhythmias in pt w/ hyperkalemia or hypocalcemia) |
signs of Mg2+ toxicity | loss of DTRs, respiratory paralysis, coma |
s/sx of severe preeclampsia | BP>160/110 on 2 occasions >6 hrs apart. Renal: proteinuria (>5g/d or 3-4 +urine dipsticks) or oliguria (<500 ml/24 hrs); headache, somnolence; blurred vision, scotomata; hyperactive reflexes/clonus; HELLP syndrome |
s/sx of eclampsia | HA, visual changes, RUQ/epigastric pain, seizures are severe if not controlled with anticonvulsant therapy |
management of eclampsia | ABCs with supplemental Oxygen. Seizure control/prophylaxis with MgSO4, if seizures recur, give IV diazepam. Control BP (Labetalol and or hydralazine). Limit fluids, fetal monitoring, initiate delivery if patient is stable and confulsions are controlled. |
postpartum management for eclampsia | differs how from pre-eclampsia? it does not differ. |
when do most seizures occur during eclampsia? | post partum within 48 hours of delivery. |
complications of preeclampsia | prematurity, fetal distress, stillbirth, placental abruption, seizure, DIC, cerebral hemorrhage, serous retinal detachment, fetal/maternal death |
complications of eclampsia | cerebral hemorrhage, aspiration pneumonia, hypoxic encephalopathy, thromboembolic events, fetal/maternal death. |
total placenta previa = | placenta covers the cervical os |
marginal placenta previa = | placenta extends to the margin of the os |
low-lying = | placenta is in close proximity to the os |
placental abruption | premature separation of normally implanted placenta = pathophysiology |
incidence of placenta abruption | 1/100 |
incidence of placenta previa | 1/200 |
risk factors for placental abruption | hypertension, abdominal/pelvic trauma, tobacco or cocaine use, previous abruption, rapid decompression of overdistended uterus |
risk factors for placental previa | prior C-section, grand multiparous, advanced maternal age, multiple gestation, prior placenta previa |
symptoms of placental abruption | painful, dark vaginal bleeding that does not spontaneously cease. abdominal pain, uterine hypertonicity. fetal distress |
symptoms of placenta previa | painless bright red bleeding tha toften ceases in 1-2 hours with or without uterine contractions. usually no fetal distress. |
transabdominal/transvaginal sensitivity for placental abruptio vs. previa | 50 vs 90% |
management of placental abruption | stabilize patients with mild abruption and a premature fetus; manage expectantly; moderate to severe abruption: immediate delivery (vaginal delivery with amniotomy if mother and fetus are stable; C-section for maternal or fetal distress). |
management for placental previa? | no vaginal exam! stablize patients with a premature fetus, manage expectantly, give tocolytics. serial ultrasounds to assess fetal growth and resolution of partial previa. give betamethasone to help with fetal lung maturity, and deliver by C-section. |
indications for delivery for placenta previa | labor, life-threatening bleeding, fetal distress, documented fetal lung maturity, and 36 weeks GA |
complications of placental abruption | hemorrhagic schock. coagulopathy, recurrence risk, fetal hypoxia. |
risk of DIC in placental abruption | 10% |
placental previa complications | increased risk fo placenta accreta, vasa previa (fetal vessels crossing hte internal os). preterm delivery, PROM, IUGR, congential anomalies, recurrence risk |
dystocia | slow abnormal progression of labor leading to indication for C-section. |
risk factors for dystocia | chorioamnionitis, occiput posterior position, nulliparity, and elevated birthweght. |
diagnosing ectopic pregnancy | serial hCG testing in conjunction with transvaginal ultrasound |
treatment of ectopic pregnancy | medical treatment (methotrexate) for small, unruptured tubal pregnancies; surgical options for salpingectomy (laproscopy vs. laparotomy). |
complications of ectopic pregnancy | tubal rupture... |
intrauterine growth restriction | EFW <10th percentile for GA |
risk factors for IUGR | uteroplacental insufficiency, maternal substance abuse, placenta previa, and multiple gestations |
diagnosing IUGR | serial fundal height measurements confirmed by ultrasound |
treatment for IUGR | explore underlying etiology, correct if possible; administer steroids to acclerate fetal lung maturity; fetal monitoring - a non reassuring status near term may prompt delivery |
complication of intrauterine growth restriction | increased perinatal morbidity and mortality |
fetal macrosomia = | BW > 90th percentile |
treatment for macrosomia | planned cesarean esp >5000 g or 4500 for GDM |
complications of fetal macrosomia | increased riks of shoulder dystocia (--> brachial plexus injury and erb duchenne palsy) as birth weight increases |
oligohydramnios = | AFI <5cm on ultrasound |
etiologies for oligohydramnios | fetal urinary tract abnormalities (e.g. renal agenesis, GU obstruction), chronic uteroplacental insufficiency and rupture of membranes |
diagnosing oligohydramnios | summation of deepeset amniotic fluid pocket in all four abdominal quadrants. Rule out inaccurate gestational dates. |
treating oligohydraminios | treat the underlying cause if possible |
complications of oligohydramnios | associated with a 40X increase in perinatal mortality. other complications include musculoskeletal abnormalities (e.g., clubfoot, facial distortion), pulmonary hypoplasia, umbilical cord compression, and IUGR. |
complications of polyhydramnios | preterm labor, fetal malpresentation, cord prolapse. |
polyhydraminios = | AFI > 20 on US. may present in normal pregnanacies; but fetal chormosomal and developmental abnormalities are common. |
treatment for polyhydarmnios | etiology specific |
diagnosis of polyhydramnios | evaluation includes ultrasound for fetal anomalies, glucose testing for DM and Rh screen |
etiologies of polyhydramnios | maternal DM, multiple gestation, isoimmunization, pulmonary abnormalities (e.g. Cystic lung malformations), fetal anomalies (e.g. duodenal atresia, tracheoesophageal fistula anencephaly), and twin to twin transfusion syndrome. |
complications of polyhydramnios | preterm labor, fetal malpresentation, cord prolapse. |
Rh isoimmunization | fetal RBCs leak into the maternal circulation; maternal anti-Rh IgG antibodies form that can cross the placenta --> hemolysis of fetal Rh RBCs (erythroblastosis fetalis). |
what titer levles indicate Rh- troubles? | 1:16; do US to assess fetal hemolysis |
treatment of Rh isoimmunization | in severe cases, initiate preterm delivery when fetal lungs are mature; prior to delivery intrauterine blood transfusions may be given to correct low fetal hematocrit. |
prevention of Rh isoimmunization | if the mother is Rh- @ 28 wks & the father is Rh+/unknown give RhoGAM; if the baby is Rh+ give RhoGAM postpartum, give RhoGAM to RH- mothers who undergo abortion or who have had ectopic pregnancy, amniocentesis, vaginal bl |
gestational trophoblastic disease (GTD) | a range of proliferative trophoblastic abnormalities that can be benign or malignant |
complete moles | 46XX (paternally derived) |
imcomplete moles | 69XXY |
presentation of Gestational trophoblastic disease (moles) | first trimester uterine bleeding, hyperemesis gravidarum, preeclampsia/eclampsia at <24 wks, and uterine size greater than dates. no fetal heart beat, enlarged ovaries or expulsion of grapelike mol |
risk factors for gestational trophoblastic disease | risk factors include extremes of age (<20 or >40), a diet deficient in folate or beta carotene and blood group. |
diagnosis of gestational trophoblastic disease | markedly increased serum beta-hCG (usually >100,000 mIU/mL). and a snowstorm appearance on pelvic US with no gestational sac/fetus present. CXR may show lung metastases; D&C reveals culsters of grapes tissue. |
treatment of gestational trophoblastic disease | type and screen is critical; folow beta-hCG closely and prevent pregnancy for one year. treat maligant disease with chemo - mthotrexate and dactinomycin; and residual uterine disease w/ hysterectomy; chemo & |
complications of molar preganncy | maglignancy, invasive moles and choriocarcinoma with pulmonary or CNS mets. trophoblastic pulmonary emboli may also be seen. |
treatment of multiple gestations | multifetal reduction and selective fetal termination; antepartum fetal surveillance for IUGR. management by a high risk specialist is recommended. |
maternal complications of multiple gestations | 6X more likely to be hospitalized with complications |
fetal complications in multiple gestations | complications include twin to twin transfusion syndrome, IUGR, preterm labor, and an increased risk for a major longterm handicap such as cerebral palsy (patients have a nearly threefold greater risk of cerebral palsy) |
fist stage, protraction or arrest in dystocia | labor that failes to produce adequate rates of progressive cervical change |
complications of failure to progress in labor | fetal infection, pneumonia, bacteremia |
definition of latent first stage of labor failure to progress | failure to have progressive cervical change (>20 hours in a prima, >14 hours in a multi. |
treatment of latent first stage failure to progress | therapeutic rest via parenteral analgesia; oxytocin; amniotomy; cervical ripening |
definition of failure to progress in active first stage of labor | failure to have progressive cervical change after reaching 3-4 cm |
treatment of failure to progress in active first stage of labor | amniotomy; oxytocin; C-section if previous interventions are ineffective. |
definition of failure to pregressin 2nd stage of labor | >3 hours in prima, greater than 2 hours in a multi |
treatment of failure to progress in 2nd stage of labor | close observation with a decrease in epidural rate and continued oxytocin; assisted vaginal delivery; C-section |
premature rupture of membranes = | spontaneous ROM >1 hr before onset of labor (due to vaginal/cervical infections, abnormal membrane physiology, or cervical incompetence. Preterm PROM occurs at <37 wks gestation. Prolonged ROM is defined as rupture >18 ho |
risk factors for PROM | Low SES, young maternal age, smoking, STIs |
suggestive of PROM? | gush of clear or blood tinged amniotic fluid suggests PROM |
how do you diagnosie PROM? | sterile speculum exam revealing pooling of amniotic fluid in vaginal vault, a + nitrazine paper test, and a positive fern test (shape of the glass slide) |
management of PROM | bedrest with close observation <32 wks. 34+ wks deliver?; give antibiotics to prevent infection; antenatal corticosteroids to promote fetal lung maturity in teh absence of intramniotic ifnection prior to 32 weeks of GA. |
complications of PROM | preterm labor and delivery, chorioamnionitis, placental abruption, cord prolapse |
what is preterm labor? | onset of labor b/t 20-37 weeks, occurs in 10% of all U.S. pregnancies and is the 1' cause of neonatal morbidity and mortality. Risk factors include multiple gestation, infection, PROM, uterine anomalies, most patients have no id'd e |
definition of preterm labor | >3 contractions of 30 seconds each over a 30 min period, and concurrent cervical change at <37 wks of gestation. |
management of preterm labor | assess for CI to tocolysis, perform a sterile speculum exam, obtain US, hydration, bed rest, tocolytic therapy and give steroids. Give penicillin or ampicillin for GBS prophylaxis if preterm delivery is likely. |
complications of preterm delivery | RDS, intraventricular hemorrhage, PDA, necrotizing enterocolitis, retinopathy of prematurity, bronchopulmonary dysplasia, death. |
fetal malpresentation = | any presentation other than vertex; risk factors include prematurity, prior breech, uterine anomalies, poly or oligohydramnios, multiple gestations, PPROM, hydrocephalus, anencephaly, and placenta previa. Breech presentations are |
frank breech | thighs are flexed and knees are extended |
footling breech | one or both legs are extended below the buttocks |
complete breech | thighs and knees are flexed |
external version | technique used to turn breech fetus to vertex position by pushing on the abdomen on the outside; risks are placental abruption and cord compression, so be prepared for emergency C-section |
trial of breech vaginal delivery | only if imminent, otherwise contraindicated (complications include cord prolapse and or head entrapment) |
elective C-section for breech pregnancies | standard of care iin many hospitals, but has not been show to improve coutcomes |
episiotomy | surgical extension of the vaginal opening, performed in 1/3 of vaginal births. |
how many types of episiotomy are there? | 2 - median and mediolateral |
complications of episiotomy | extension into the anal sphincter, bleeding, infection, dyspareunia and rectovaginal fistula formation/maternal death |
should u routinely do episiotomies? | NO |
what are the maternal factors that indicate for C-section | prior classical C-section, active genital herpes infection, cervical carcinoma, maternal trauma/demise |
fetal and maternal factors that are indications for C-secton | cephalopelvic disproportion, placenta previa/abruption, failed operative vaginal delivery, post-term pregnancy (relative indication) |
fetal factors that indicate C-section | fetal malposition (e.g. posterior chin, transverse lie, shoulder presentation); fetal distress; cord compression; erythroblastosis fetalis (Rh incompatibility). |
post partum hemorrhage = | loss of >.5 L of blood for vaginal delivery; >1L for C-section |
complications of postpartum hemorrhage | acute blood loss, anemia, sheehan's syndrome |
common causes of postpartum hemorrhage include | uterine atony, genital tract trauma, retained placental tissue |
risk factors for uterine atony include | uterine overdistension, exhausted myometrium, uterine infection, conditions interfering with contraction (anaesthesia, myomas, MgSO4) |
risk factors for genital tract trauma | precipitous labor, operative vaginal delivery (forceps, vaccum), large infant, inadequate episiotomy repair |
risk factors for retained placental tissue | placenta accreta/increta/percreta/previa; uterine leiomyomas, preterm delivery, previous C-section/curettage. |
the most common cause of postpartum hemorrhage is | uterine atony |
palpation of a soft, enlarged, "boggy" uterus suggests | uterine atony or if not pregnant, adenomyosis |
treatment of uterine atony | bimanual uterine massage, oxytocin infusion, methergine if not hypertensie, prostin if not asthmatic |
laceration >2cm in lower genital tract suggests | genital tract trauma |
treatment for genital tract trauma | surgical repair of the physical defect |
treatment of retained placental tissue | manual removal of remaining placental tissue, curettage with suctioning (take care not to perforate the uterine fundus |
manual and visual inspection of the placenta and uterine cavity revieals missing cotyledons (lobules of placenta) | suggestive of retained placental tissue; US can be used to inspect the uterus |
what is a postpartum infection | genital tract infection with T>38C for at least 2 of the first ten postpartum days. endometrial infection is most common. Risk factors include emergent C-section, PROM, prolonged labor, multiple intrapartum vaginal exams and |
treatment for endometritis | hospitalize and give broad specturm empiric IV antibiotics (clindamycin and gentamicin) until patients have been afebrile for 48 hours; add ampicillin for complicated cases |
7 Ws of post partum fever | womb, wind, water, walk, wound, weaning, wonder drugs |
sheehan's syndrome | pituitary ischemia nd necrosis --> anterior pituitary insufficiency 2' to massive obstetric hemorrhage and shock, the primary cause of ant. pit. insufficiency in adult females. |
most common presenting symptoms in sheehan's | failure to lactate; other symptoms include weakness, lethargy, cold insensitivity, genital atrophy, and menstrual disorders. |
what is colostrom | early breast milk, contains protein, fat, IgA and minerals. |
spontaneous abortion | loss of the fetus prior to the 20th week of pregnancy. some 75% of cases occur before the 16th week, with 75% of these occuring before the 8th week. approximately 1/5 clinically recognized pregnancies terminate in SAB. |
risk factors for SAb | history of incompetent cervix, cervical conization, or loop electrosurgical excision procedure, cervical injury, DES exposure, anatomical abnormalities of the cervix. |
Elective Termination of pregnancy | 50% of all pregnancies are unintended, 25% of pregnancies end in elective abortion. Options for elective abortion depend on gestational age and patient preferences. |
complete spontaneous abortion = | all products of conception expelled; pain ceases, but spotting may persist |
incomplete spontaneous abortion | mild cramping and bleeding; some Products of conception expelled. visible tissue in teh vagina or endocervical canal. |
treatened sponteaneous abortion | no products of conception expelled; membranes remain intact. uterine bleeding is present; abdominal pain may be present. teh fetus is still viable. |
inevitable spontaneous abortion | no products of conception expelled, but considered inevitable. uterine bleeding and cramps. |
missed spontaneous abortion. | pregnancy has ceased to develop, no POC is expelled; fetal tissue is retained; no uterine bleeding; symptoms of pregnancy disappear; brownish vaginal discharge. no fetal cardiac actiivty. |
spetic spontaneous abortion | infection with abortion, endometritis --> septicemia. maternal mortality si 10-15%. |
recurrent spontaneous abortion or a total of 3 SABs in 1 year suggests | if early on, karyotype abnormalities --> karyotype parents; incompetent cervix if late (b/t 18-32 wks). |
intrauterine fetal demise = | absence of fetal cardiac activity. |
what is medical management of first trimester elective termination of pregnancy | oral mifepristone (low dose) + oral or vaginal misoprostol. Im/oral methotrexate + oral/vaginal misoprostol. Vaginal misoprostol at high doeses repeated up to 3 times. |
timing of 1st trimester elective termination of pregnancy? | 49 days - 56 days fo GA for medical management, up to 13 wks for surgical managemnet. |
how do you treat spontaneous abortion? | remove remaining products of conception with D&C, prostaglandin suppositories, etc. |