OB/GYN Flashcards
ACOG prenatal care
first visit: 8-10 weeks
every four weeks for next seven months (28 weeks)
Every 2 – 3 weeks until 36 weeks gestation.
Every week after 36 weeks gestation
QUAD screen
maternal blood screen -16-18 weeks
o AFP: alpha-fetoprotein is a protein that is produced by the fetus
• High levels of AFP = neural tube defect such as spina bifida or anencephaly. However, the most common reason for elevated AFP levels is inaccurate dating of the pregnancy.
• Low levels of AFP and abnormal levels of hCG and estriol may indicate that the developing baby has Trisomy 21(Down syndrome), Trisomy 18 (Edwards Syndrome) or another type of chromosome abnormality.
o hCG: human chorionic gonadotropin is a hormone produced within the placenta
o Estriol: estriol is an estrogen produced by both the fetus and the placenta
o Inhibin-A: inhibin-A is a protein produced by the placenta and ovaries
Trisomy 21:
- US may show increased nuchal translucency
- On quad screen
- Decreased=AFP, estriol
- Increased=b-HCG, inhibin A
• Flat facies, epicanthial folds (eyelid fold), duodenal atresia, congenital heart defects, increased risk of Alzheimers and leukemias
Trisomy 18:
- Aka Edward’ Syndrome, 1:8,000 pregnancies
- On quad screen
- Decreased=AFP, b-HCG, estriol
- Normal=inhibinA
- Severe mental retardation, rocker bottom feet, micrognathia, low set ears, clenched hands, prominent occiput
- 50% of babies die within the first week life
Trisomy 13:
• Aka Patau’s Syndrome. 1:15,000 pregnancies
• US may show increased nuchal translucency
• On screening
• Most often this is normal
• Sometimes b-HCG will be decreased
Severe mental retardation, rocker bottom feet, microcephaly, cleft lip, cleft palate, holoprosencephaly, polydactly
Median survival is 2.5 days
normal FHR
Bradycardia: Mean FHR < 110 BPM
Tachycardia: Mean FHR>160 BPM
types of variability in FHR
o Absent variability = Amplitude range undetectable
o Minimal = < 5 BPM
o Moderate = 6 to 25 BPM
o Marked = > 25 BPM
• **Persistently minimal or absent FHR variability appears to be the most significant intrapartum sign of fetal compromise. On the other hand the presence of good FHR variability may not always be predictive of a good outcome.
- Etiologies of decreased variability: Fetal metabolic acidosis, CNS depressants, fetal sleep cycles[10], congenital anomalies, prematurity, fetal tachycardia, preexisting neurologic abnormality, normal, betamethasone.\
- NOTE: absent variations = greatest indicator for bad!! – means placenta isn’t giving baby enough O2, and baby isn’t tolerating labor well (could be d/t metabolic acidosis, CNS depression, mother’s pain meds, sleep, prematurity)
Accelerations:
• = abrupt increase in FHR above baseline with onset to peak of the acceleration less than < 30 seconds and less than 2 minutes in duration.
• Adequate accelerations are defined as:
o 15 BPM above baseline for > 15 seconds.
• Prolonged acceleration: Increase in heart rate lasts for 2 to 10 minutes
• The absence of accelerations for more than 80 minutes correlates with increased neonatal morbidity.
• Fetal scalp stimulation can be used to induce accelerations. There is about a 50% chance of acidosis in the fetus who fails to respond to stimulation in the presence of a nonreassuring pattern
gradual vs. abrupt deceleration
o Gradual decrease and return to baseline with time from onset of the deceleration to nadir >30 seconds.
o Abrupt decrease in FHR of > 15 beats per minute with onset of deceleration to nadir < 30 seconds.
early decleration
o Gradual decrease in FHR with onset of deceleration to nadir >30 seconds. The nadir occurs with the peak of a contraction
**think head contraction
late deceleration
o Gradual decrease in FHR with onset of deceleration to nadir >30 seconds. Onset of the decleration occurs after the beginning of the contraction, and the nadir of the contraction occurs after the peak of the contraction.
- *uteroplacental insufficiency **
- excessive contractions, maternal hypotension, maternal hypoxemia
late deceleration with beat to beat variety:
- fetal hypoxia –> chemoreceptors to stimulate alpha receptors –> increased constriction of vessels –> HTN –> slowing of fetal heart rate
late decelerations w/ no variability: (should delivery baby soon if persists!)
- hypoxia –> lactic acidosis
Deliver baby if pH <7.2!!!
• Variable deceleration:
o Abrupt decrease in FHR of > 15 beats per minute measured from the most recently determined baseline rate. The onset of deceleration to nadir is less than 30 seconds. The deceleration lasts > 15 seconds and less than 2 minutes. A shoulder, if present, is not included as part of the deceleration.
- partial cord compression
- decreased O2 –> increased vessel constriction –> HTN –> decreased HR
• Recurrent decelerations ( variable, early, or late ):
Decelerations occur with > 50% of uterine contractions in any 20 minute segment.
• Prolonged deceleration
A decrease in FHR of > 15 beats per minute measured from the most recently determined baseline rate. The deceleration lasts >= 2 minutes but less than 10 minutes.
o Etiologies: Maternal hypotension, uterine hyperactivity, cord prolapse, cord compression, abruption, artifact (maternal heart rate) , maternal seizure.
o Although umbilical cord compression is often responsible for a prolonged deceleration a pelvic examination should be performed to rule out umbilical cord prolapse or rapid descent of the fetal head.
HELP VC
- early deceleration (onset before contraction) = head contraction (these are normal!)
- late deceleration (decrease in HR after contraction) = uteroplacental insufficiency – think hypoxia
- variable deceleration: think cord compression
- no variability = worrisome
lacerations
• First-degree vaginal tears are the least severe, involving only the skin around the vaginal opening. Although the patient might experience some mild burning or stinging with urination, first-degrees tears aren’t severely painful and heal on their own within a few weeks.
• Second-degree vaginal tears involve vaginal tissue and the perineal muscles — the muscles between the vagina and anus that help support the uterus, bladder and rectum. Second-degree tears typically require closure and heal within a few weeks.
• Third-degree vaginal tears involve the posterior vaginal tissues, perineal muscles AND the capsule of the anal sphincter.
• Fourth-degree vaginal tears are the most severe. They involve the perineal muscles and anal sphincter as well as the tissue lining the rectum. Fourth-degree tears require repair, sometimes in an operative setting.
o Complications such as fecal incontinence and painful intercourse are possible.
When to induce labor?
- risks are greater than that of induction
- At 41+ weeks
- Within 96 hrs of ruptured membranes at term
- For pre eclampsia at term
- For maternal diabetes at term
How to induce labor?
• For prolonged pregnancy first sweep/strip the membranes: separation of amniotic sac from wall of uterus
• For ruptured membranes:
o Oxytocin by IV infusion
o Although wait-and-see and vaginal PG’s are acceptable
• For all other patients (except those with a uterine scar)…
o Vaginal prostaglandins
o Regardless of the state of the cervix or the parity of the patient
o Amniotomy followed by oxytocin infusion 3 – 12 hours later is likely to be the most cost effective when the cervix is ripe
C sections
Vaginal birth after one lower segment C-sections:
• For spontaneous labor the risk of scar rupture is 1:200
• With oxytocin infusion the risk is 1:100
• With prostaglandins the risk is 1:40
• Maternal risk of death ~2 for every 10,000
• scar rupture
Risks of Caesarean birth:
• C sections: increased hospital stay, increased IC, increased eath (2-10x), bladder/ureter damage, future hysterectomy risk, increased thromboembolism, increased future placenta previa and stillbirth in next pregnancy
• no difference in postpartum hemorrhage, endometritis, genital tract injury, fecal incontinence, depression, back pain, dyspareunia
• vaginal birth: more likely to have perineal pain, urinary incontinence and uterovagianl prolapse with vaginal birth
when to consult during prolonged labor?
o a Nullipara whose delivery is not imminent after 2 hours
o And 1 hour in a previously parous patient
o Reassess all patients with an epidural who do not push within 1 hour after fully dilated
G5P4113
gravida, TPAL (term, premature, abortions, living children)
• Gravida means number of pregnancies (5)
• Parity means number of births/viable offsprings (4)
PROM
• testing?
o nitrazine test – blue means that vagina is alkaline – positive result!
o microscopic examination: amniotic fluid shows “ferning”
Premature Rupture of Membranes (PROM): Spontaneous rupture of membranes prior to onset of labor
Preterm PROM (PPROM): PROM before 37 weeks gestation
Risks:
• About 1/3 of women with PPROM develop potentially serious intrauterine infections
• increased risk of: placental abruption, umbilical cord prolapse, pulmonary hypoplasia
Risk Factors:
• Genital tract infections ** most common cause **
• Previous PPROM
• Antepartum bleeding
• Cigarette smoking
• Mechanical Stress
• Most patients have no identifiable risk factors
Management:
• delivery of patients >34 weeks gestation
• tx: expeditious delivery!!!
• corticosteroids given to help fetal lung maturity: Betamethasone
• Give antibiotic prophylaxis
• maternal and fetal monitoring
chorioamnionitis?
Organism:
• most commonly: ureaplasma urealyticum, gram – anaerobes, mycoplasma hominis, bacteriods bivius, gardnerella vaginalis Group B strep
Risk factors: • prolonged labor • prolonged membrane rupture • multiple digital vaginal examinations (especially with ruptured membranes) • nulliparity • previous IAI • meconium-stained amniotic fluid • internal fetal or uterine monitoring • presence of genital tract pathogens • alcohol or tobacco • PROM
Clinical Presentation: • Fever** • Uterine tenderness • Maternal tachycardia (>100/min) • Fetal tachycardia (>160/min) • Purulent or foul amniotic fluid • Maternal leukocytosis (variously defined as white blood cell [WBC] count >12,000/mm3 or >15,000/mm) o 70 to 90 percent of cases
How do diagnose?
• ***FEVER and
o Maternal leukocytosis (greater than 15,000 cells/mm3)
o Maternal tachycardia (greater than 100 beats/minute)
o Fetal tachycardia (greater than 160 beats/minute)
o Uterine tenderness
o Foul odor of the amniotic fluid
Management?
• standard treatment: ampicillin 2 g intravenously every six hours plus gentamicin 1.5 mg/kg every eight hours for patients with normal renal function
• other options: ampicillin-sublactam, ticarcillin-clavulanate, cefoxitin
uterine rupture
uncommon in developed countries
1/56 chance in resource poor areas!
Placenta Previa
placental tissue over or adjacent to the cervical os
• Suspected with painless antepartum bleeding after 20wks
- Total placenta previa- internal os completely covered
- Partial- internal os partially covered
- Marginal- Edge of placenta is at the margin of the internal os
- Low-lying placenta- placenta is implanted in the lower uterine segment does not reach the interal os, but is at close proximity
- Vasa Previa- fetal vessels present at cervical os
risk factors:
previous experience, previous Csection, multiparity, advanced maternal age, maternal smoking, cocaine
• male fetus, non-white race
Treatment?
• Asymptomatic previa: monitor placental position with ultrasound examination as an outpatient. Avoid strenuous exercise. Planned C-section for delivery
• Bleeding Previa: Potential emergency. Hospitalize for maternal and fetal monitoring. Emergency C-section if life threatening maternal hemorrhage. If stable patient can be monitored on an outpatient basis with continuous US examination.
• Vaginal delivery: May be attempted if the placental edge is >10mm from the internal os due to the lower risk of hemorrhage during labor.
• C-Section: Due to risk of hemorrhage from placental tear a C-section is the preferred method of delivery for patients who present with placenta previa.
Post partum hemorrhage:
• Blood Loss occurs in 4% of deliveries
o >500 ml vaginal delivery
o >1000ml during C-section
“ The Four T’s”: Tone, Trauma, Tissue, Thrombus
• Tone: (uterine atony) no contraction → spiral arterioles and decidual veins to continue to bleed
o this is the reason for 75% of PPH
o treatment: massage, pitocine/cytotec, methergine (caution for HTN) or hemabate (caution for asthma)
o predisposing factors: over distention of uterus, multiple gestations, polyhydramnios, prolonged labor, fetal macrosomia (increased birth weight), oxytotic augmentation of labor, multiparity (>5), precipitous labor (lasting <3 hours), chorioamnionitis, uterine leiomyomas
• Trauma: second most common cause of PPH
o d/t lacerations – esp. with the use of forceps/extractors
o uterine inversion: seen in 1 in 20,000 pregnancies – d/t improper management of third stage of labor (placenta fails to detach and uterus comes through the vagina)
• Tissue: uterus is unable to contract and involute around the retained placental tissue mass
o tx: manual removal after 30 minutes has passed to allow for spontaneous delivery, followed by D&C
• Thrombus:
o rare
o ITP: abnormal platelet fn
o amniotic fluid embolus- thromboplastin in amniotic fluid leaks into mothers vascular system → consumptive coagulopathy
o VW disease
o tx: coagulation studies
preecclampsia
HTN after 20 weeks gestation w/ associated proteinuria and edema
o Leading cause of maternal and prenatal morbidity and mortality worldwide
o Increased 25% in US during last 20 years
o Risk factor for future Cardiovascular disease and Metabolic disorders
Risk factors:
o nulliparity, age >40, <18, family hx, chronic HTN, CRD, DM, black, woman too small
difft. criteria for preeclampsia
Criteria for ddx of Preeclampsia 1:
o Systolic blood pressure >140 mmHg or diastolic blood pressure >90 mmHg on two occasions at least 4 hours apart after 20 weeks of gestation in a previously normotensive patient
o If systolic blood pressure is >160 mmHg or diastolic blood pressure is 0.3 grams in a 24-hour urine specimen or protein (mg/dl)/creatinine (mg/dl) ratio >0.3
o Dipstick 1+ if a quantitative measurement is unavailable
Criteria for ddx of preeclampsia-2:
o new onset hypertension without proteinuria, the new onset of any of the following is diagnostic of preeclampsia:
o Platelet count 1.1mg/dL or doubling of serum creatinine in the absence of other renal disease
o Liver transaminases at least twice the normal concentrations
o Pulmonary edema
o Cerebral or visual symptoms
Criteria for ddx of preeclampsia-3: SEVERE preeclamptic disease
o CNS dysfunction: cerebral/visual distrubances, (h/a, altered mental status, vision changes)
o hepatic abnormality: severe RUQ or epigastric pain
o severe BP elevation >160 or >110 diastolic
Criteria for ddx of preeclampsia-4:
o Thrombocytopenia: 1.1)
o pulmonary edema
Criteria for mild preeclampsia:
o BP elevated on two occasions >140/90 – normotensive before 20 weeks
o >.3 g protein in urine sample or 3+ proteinuria
o no end organ damage
Early onset vs. Late onset preeclampsia:
o Early onset (34 weeks)
o Early-onset preeclampsia was significantly associated with a high risk for fetal death (adjusted odds ratio [AOR], 5.8), but late-onset preeclampsia was not (
o However, the AOR for perinatal death/severe neonatal morbidity was significant for both early-onset and late-onset
Preeclampsia indications for delivery:
o poor fetal heart status, ruptured membrane, uncontrollable BP, oligohydramnios (AFI 1.5, pulmonary edema,
***SOB or c/p w/ pulse ox <94%, h/a that is persistent/severe, RUQ tenderness, HELLP syndrome
clinical sx of preeclampsia
o Mild Preeclampsia- can have a milder HTN, Proteinuria, but may not have other SX
o Severe Preeclampsia- needs urgent delivery:
o Severe hypertension (SBP>160mmHg or DBP>110mmHg (2 occasions at least 4hrs. Apart or 1X if treated)
o Persistent and/or severe headache
o Visual abnormalities (scotomata, photopsia, photophobia, blurred vision, or temporary blindness)
o Upper abdominal or epigastric pain
o Nausea, vomiting
o Dyspnea, retrosternal chest pain
o AMS
• Laboratory abnormalities:
• MAHA (Schistocytes, elevated bilirubin/LDH, or low serum haptoglobin levels U/L)
• Thrombocytopenia (1.1mg/dL)
• Elevated liver enzymes (twice the upper limit of normal)
Diagnosis
• Meeting the criteria for:
• New onset HTN and either Proteinuria OR end organ dysfunction
• Post diagnosis evaluation includes-determination of severity and assesment of fetal well being
Symptoms of severe disease? o Severe headache o Blurred vision/other vision disturbances o Upper abdominal pain (RUQ, epigastric) o Nausea/vomiting o SOB, chest pain o Altered mental status Maternal complications: o placental abruption, ARF, cerebral hemorrhage, hepatic failure, PE, DIC, progression to eclampsia
HELLP
HELLP: hemolysis, elevated liver enzymes, low platelet count
• Occurs <100,000
• Liver function test (especially AST)
• Peripheral smear w/schistocytes & bilirubin (Tennessee classification)
• If not all laboratory abnormalities are met = partial HELLP syndrome, which may progress to complete HELLP
Treatment:
• Only cure/effective treatment is delivery
• Antihypertensive as needed for HTN
• Platelet transfusion for actively bleeding patients or possible C-section
Prevention:
• daily ASA starting late 1st trimester
• w/l and increased exercise
Prognosis:
• Early detection and treatment decreases risk of serious complications
• Risk correlates with increased severity of symptoms and lab abnormalities
• Death rate among babies born to mothers with HELLP depends on birth weight and organ development
o Many are born prematurely
• Recurrence rate 2-6%
o Partial HELLP = 24-27%
o Preeclampsia = 20-50% (higher recurrence if 2nd tri HELLP)
Eclampsia:
• One or more generalized convulsions or comma in the setting of preeclampsia and without another neurological condition
• 2-3% of women with severe preeclampsia
• Risk factors same as preeclampsia
• can occur antepartum, intrapartum and post partum
o post partum eclampsia is often missed: present with h/a, SOB, blurry vision
• tx: tx seizures, control BP, deliver fetus
Posterior Reversible encephalopathy syndrome (PRES)
= h/a, confusion, seizures, visual loss—see edema in the brain
• Cerebral edema, ischemia/hemorrhages in posterior hemispheres
• Changes seen on MRI/CT
• Findings are due to HTN causing: Vasospasm, Hypoperfusion, Cerebral edema or loss in autoregualtion, Hypoperfusion, Cerebral edema
• Risk Factors – Eclampsia, HTN (acute/severe). Immunosuppression
• Clinical Manifestations:
o HA, AMS, Visual disturbances, Seizures
• Treatment:
o Control HTN (no more than 25% in 6 hrs)
o Control Seizures (Eclampsia responds to MgS04 better than Phenytoin/Diazepam
o Decrease cytotoxic drug
o Manage comorbid conditions (sepsis, fluid overload, electrolyte abnormalities)
• Prognosis:
o Most recover within 2 weeks
o Not always reversible, can lead to neurological deficits
o Can cause death from cerebral edema, hemorrhage
Pre-Gestational Diabetes Mellitus
(Diabetic before pregnancy):
• Pre-existing type 1 or 2 diabetes in a pregnant woman (~4% in US)
• diabetic pt. who gets pregnant, need to evaluate eyes, kidneys, neuropathy, heart and HBA1C levels
Type I Diabetes:
• Caused by destruction of the beta cells of the pancreas, which leads to an absolute insulin deficiency
• Accounts for 5-10% of all diabetes
• 1% of diabetes in pregnancy
• have growth restricted babies and don’t have chubby babies
Type II Diabetes
• Most form of diabetes, accounting for 90-95% of cases (CDC, 2008)
• Characterized by insulin resistance and relative insulin deficiency
• Can be managed through lifestyle modification, diet, exercise and pharmacologically
Gestation Diabetes Mellitus (GDM
Diabetes during pregnancy
• Any degree of glucose intolerance with onset or first recognition during pregnancy (~7% in US)
• GDM is a condition in which a hormone (hPL) made by the placenta prevents the body from using insulin effectively. Glucose builds up in the blood instead of being absorbed by the cells.
o Not caused by a lack of insulin, but by other hormones causing insulin resistance!
• GDM is a risk factor for subsequent diabetes (50-70%)
• Pancreas cannot secrete enough insulin, which increases glucose, glucose crosses placenta and is stored as energy/fat by the fetus. It also results in fetus producing high amounts of insulin.
Epidemiology of GDM:
• Increasing maternal age and weight
• Previous GDM – if had LGA baby
• Previous macrosomic infant
• Family history of diabetes among first-degree relatives
• Ethnic background with a high prevalence of diabetes
• Hispanic, black, American indian, Asian/pacific islander
Risks of uncontrolled diabetes in pregnancy:
• diabetic can result in congenital malformations:
o heart anomalies, spina bifida, renal anomalies, situs inversus
• Pregnancies complicated by diabetes are at increased risk of perinatal morbidity and mortality.
For mothers w/ preexisting DM:
• Hypertension
• Preeclampsia (RR increased x4) – severe HTN, proteinuria, severe edema
• SAB (RR ~3)
• Worsening of diabetic complications – risk of developing type 2 DM
• If Vasculopathy is present, fetal growth restriction
• Ketoacidosis or Severe hypoglycemia
For Baby:
• Macrosomia (birth weight > 4kg)
• Hypoglycemia at birth
• Hyperbilirubinemia
• Low calcium and magnesium
• Respiratory distress syndrome – lungs don’t mature properly
• Polycythemia
• Hyperviscosity
• Increased risk for childhood and adult obesity
• Increased risk of type 2 diabetes later in life
Preterm labor complications:
• incidence of preterm birth is increased
• Vascular disease, hypertensive disorders and obesity contribute to the increased risk of preterm birth in women with diabetes.
Perinatal implications:
• increased risk of RDS!
Metabolic changes during pregnancy:
• During the first trimester, fasting blood glucose decreases because of insulin production, and sensitivity slightly increases
o in early pregnancy see decreased glucose, increased insulin secretion, and glycogen storage along with increased peripheral glucose utilization (d/t baby using up glucose)
o before 20 weeks see decreased maternal glucose, production of FFAs and ketones and continued insulin in response to elevated glucose
o towards end have risk of becoming hypoglycemic!
• By the end of the first trimester, insulin sensitivity decreases, with a responding increase in insulin production; this change creates the diabetogenic state of pregnancy. (d/t hPL)
o increase in hormones allows for ample glucose available to fetus
• increased hCS (hPL) → “diabetogenic” decreased glucose tolerance
• increased PRL → insulin resistance
• increased cortisol → hepatic glucose production
• Euglycemia is maintained in pregnancy because the pancreatic beta cells produce enough insulin to counteract increasing insulin resistance
• In pregnant women, hepatic glucose production is 1.3 times higher than it is in non-pregnant women
maternal hyperglycemia → fetal hyperglycemia → fetal nyperinsulinemia (Bcell hypertrophy/hyperplasia) → excessive fetal growth (macrosomia, increased need for C-sections, maternal HTN)
HcG levels
- normal – HCG should double every 48 hours
* abnormal – HCG can stay the same, decrease (miscariage), or increase minimally (preg. outside of uterus)
spontaneous abortion
Risk factors for spontaneous abortion:
• Age 20 to 30 years (9 to 17 percent), age 35 years (20 percent), age 40 years (40 percent), and age 45 years (80 percent)
• Previous spontaneous abortion
• prolonged time to conception/implantation interval
• smoking, EtOH, cocaine, NSAIDS, caffeine, low folate
• weight extremes: obesity or thin
• fever during pregnancy, celiac disease
Fetal etiology of spontaneous abortions:
• Chromosomal abnormalities**
o 50% of all spontaneous abortions
• Trisomy 16 is most common, almost always lethal
• Congenital abnormalities**
• Trauma
sx of spontaneous abortion
- Vaginal bleeding
- Pelvic pain
- Absence of fetal movement (rate, as usually before movement is perceived)
- Incidental finding on US/hand-held Doppler
Criteria for ddx?
• Ultrasound:
o A gestational sac >25mm in mean diameter that does not contain a yolk sac or embryo
o An embryo with a crown rump length (CRL) >7 mm that does not have cardiac activity
o After a pelvic ultrasound showed a gestational sac without a yolk sac, absence of an embryo with heartbeat in >2 weeks
o After a pelvic ultrasound showed a gestational sac with a yolk sac, absence of an embryo with a heartbeat in >11 days
