Endo Repro Last Flashcards
Early pregnancy loss, ectopic and Rh isoimmunization
Ok
First trimester
First day of last period (FDLMP)-13+6 weeks
Second trimester
14-27+6 weeks
Third trimester
28-42
Estimate date of confinement
40 weeks after FDLMP
Abortion
<20 weeks
Preterm delivery
20-36+6 weeks
Full term
37-42 weeks
Postdates
> 42 weeks
What percent of pregnant women have vagina bleeding in early preg
40%
What d if girl present with vaginal bleeding
Pregnancy test
What is a negative hCG
<5 mIU/L
HCG level at time of expected menstruation
100 IU/L
HCG ___ every __ days
Doubles
2
What hCG level can we see gestational sac? :Discriminatory level”
1500-2000 mIU/L
Fetal pole seen what hCG
5200, 5 weeks
What is abnormal rise in hCG of less then 53% in 48 hours
Abnormal IUP or ectopic
Spontaneous abortion percent
10-15%
Biochemical pregnancy
Refers to the presence of hCG 7-10 days after ovulation but in whom menstruation occurs when expected
-when both clincial biochemical pregnancies are considered evidence suggests that 50% of all conventions end in abortions
Abortus
Loss before 20 weeks or less than 500 grams
Most common cause of first trimester SAB
Chromosomal abnormalities
45 CO most common abnormality
Trisomy 16 most commontrisomy
Threatened abortion
Vaginal bleeding and closed cervic
25-50% result in lsos
Treatment is expected management
Inevitable abortion
Vaginal bleeding and the cervic is partially dilated
Loss inevitable
Incomplete abortion
Vaginal bleeding, cramping lower abdominal pain with dilated cervix
Passage of some but not all products
Treat with suction D and C
Complete abortion
Passage of all with closed cervic
With resolution of pain, bleeding and pregnancy symptoms
No treatment needed
Missed abortion
Fetus has expired and remains int he uterus
Usually no symptoms
Coagulation problems may develop, check fibrinogen levels weekly until SAB occurs or proceed with suction D and C
Expectant management vs misoprostol vs D and C
Septic abortion
Fever, uterine and cervical motion tenderness, purulent discharge, hemorrhage, and renal failure
Retained infected products
Treat septic abortion
IV antibiotics and D and C
Blighted ovum
Anembryonic gestation
Gestational sac to large to not have embryo >25 mm
Induced or elective abortion
Roe v wade 1971
Suction D and C is most common in first trimester
Anembryoinc gestation (blighted ovum)
Fertilized egg develops a placenta but no embryo
How see anembryonic gestation
US reveals empty gestational sac
Treat anembryonic gestation
Expectant management
Medical management -misoprostol
D and C
Suction D and C
Uses suction to remove products of conception
Surgical D and C is a more successful primary therapy then medical or expectant management
Recurrent abortions
Defined as three successive SAB
Excluding ectopic and molar pregnancies
1% of pregnant women
Often no identifiable cause can be found
Recurrent abortions: infection
Mycoplasma, chlamydia, listeria, or toxoplasmosis rarely identified
Can be treated with antibiotics
Recurrent abortions: smoking and etoh
Increase SABS
4 fold increase risk. If smoke 20 cigarettes a day and consume 7 alcoholic beverages per week
Recurrent abortions: medical disorders
DM, Hypothyroidism, SLE< antiphospholipid ab syndrome and hypercoagulability sources
Factor V Leiden defiency, antithrombin III, protein C and S, prothrombin G20210A, ANA, anticardiolipin antibody, methylene tetrahydrofolate reductase
Recurrent abortion maternal age
> 40 lots 56%
Increase with maternal age
Recurrent abnortions: uterine abnormalities
Congenital anomalies (DES)
Submucosal fibroids, uterine septum
Intrauterine synechiae (asherman)
Recurrent abortion: cervical incompetence
Second trimester loss
Painless dilation and delivery
Risk factors cervical incompetenance
Uterine anomalies,previous trauma, and history of conization
Treat cervical incompetence
Cervical circulate
Recurrent abortions chromosomal abnormalities
45 XO most common
Trisomy 16 most common trisomy
Recurrent abortio karyotype gets
Recommended for both parents bc 3% chance that one parent is an asymptomatic carrier of a genetically balanced chromosomal translocation
Detect balanced reciprocal or robertsonian translocations that could be passed on
Recurrent abortions antiphospholipid syndrome
Most common
Has been associated with recurrent fetal loss, preeclampsia, venous and arterial thromboembolism and stroke
Tests for immunological factors
Lupus anticoagulant
Anticardiolipin antibodies IggIgm
Anti B2 glycoproteins 1 antibodies iggigm
Treat immunological
Prophylactic dose of heparin and low dose asprin
Ectopic pregnancy
Fallopian tubes, abdomen, cervix, ovary, uterine cornua
% ectopic
1.5%
How ectopic pregnancy happen
Trophoblastic implant into the mucosa of the Fallopian tube and rapidly erode through to underlying blood vessels
-if the bleeding is extensive it can create a pressure necrosis of the overlying tubal serosa resulting in acute rupture and significant hemoperitoneum
Leading cause maternal death 1st trimester
Ectopic pregnancy
Natural vs art locations
Natural-tubal
Art-some tubal more ampullae and cornual
Also get ovarian /abdominal (heterotopic more), more cervical
But both most tubal
Risk factors ectopic pregnancy
History tubal infection (G or chlamydia)
Previous ectopic
Previous tubal reconstructive surgery or sterilizaiotns
DES
IUD preg
IVF or ART
Smoking
Differential ectopic
Threatened or incomplete abortion
Ruptured hemorrhagic corpus luteum cyst
Acute PID
Adnexal torsion
Degenerating leiomyoma
Nongynecological ectopic pregnancy
Acute appendicitis
Pyelonephritis, renal calculi
Pancreatitis
Triad ectopic pregnancy
Prior missed menses
Vaginal bleeding
Lower abdominal pain
Ectopic pregnancy signs
Usually 1 visit before diagnosis
-follow hcg and TVUS
Ab pain, spotting, bleeding
PE ectopic: possible
Uterus soft and normal size
May not feel any adnexal mass
US-thickened endometrial stripe (arias Stella reaction)
Rarely do you see the ectopic preg)
Symptoms probable ectopic pregnancy
Lower ab pain vag spotting
Abdominal adnexal tenderness or cervical motion tenderness
US-variable amounts of fluid in cul de sac
May see ectopic
Acutely ruptured ectopic pregnancy
Severe abdominal pain and dizziness from intraperitoneal preg
Distended and acute tender abdomen , cervical motion tenderness, sign of hemodynamically instability
US-empty uterus with free fluid
Hcg Doubles every 48 hours
Indicates a normal IUP
Some 66%
Slowest is 53%
<53% rise in hCG
Consistent with ectopic pregnancy or nonviable IUP
Can an ectopic pregnancy have normal rising HcG
Yup
Falling hCG
Most likely blighted ovum, spontaneously resolving ectopic ,abnormal pregnancy
Discriminatory zone
1500-2000 IU/L should see an intrauterine great sac
What see with transvaginal US
IUP
Extrauterine preg
Nondiagnostic-follows with hCG a
When repeat US
Hcg in discriminatory zone
Manage ectopic preg
Methotrexate-folic acid antagonist whihc inhibits DNA synthesis and cell replication
Follow up methotrexate
Check hCG levels day 4 and 7
-if 15% continue to follow weekly until negative
If plateau or fall slow, give another dose
Increase-surgical intervention
What avoid when on methotrexate
Folate containing vitamins
Success rate methotrexate
70-90%
Absolute contraindications methotrexate
IUP, breastfeeding, immunodeficiency, alcoholism, liver disease, hepatic renal failure
Relative contraindicatiosn mtx
Gestational sac>3.5 cm
Embryonic cardiac motion
HCG>6000
Expectant management
Stable and symptoms are resolving
Follow hCG and give strong ectopicprecaution
A lot of ectopic with hCG< 1000
Not rupture and resolve spontaneously
Laparotomy
Preferred for hemodynamically unstable
Laparoscopy
Stable patient
Salpingectomy
Entire Fallopian tube when damage
Salpingostomy
Incision is made parallel to the axis of the tube over the site of implantation and incision is left open to heal by secondary intention
Most studies reveal salpingostomy results in better long term tubal fcuntion
Salpingostomy
Incision is sutured
What do after surgery
Repeat hCG 3-7 days post op
Salpingostomy risk
20% risk residual trophoblastic tissue
Thesis isoimmunization
Rh negative women with RH positive fetus
Rh complex
C,D,E,c,d,e
> 905 of cases of Rh isoimmunization
Antibodies to D antigens
Who most common Rh D negative
Caucasion>african American> Asian an Native American
Rh sensitization
IgM initially then igg that cross placenta and into fetus
Bind fetal rbc and hemolysis
Mild hemolysis
Fine bc increase erythropoietin
Severe hemolysis
Resulting in hydrops fetalis from congestive heart failure and intrauterine fetal deat
RhoGAM
Prophylactic Rh immune globulin prevent maternal production of antibodies
Fetomaternal hemorrhage that can lead to isoimmunization
Most commonly occur during routine uncomplicated vaginal deliveries
Factors that can increase the volume of fetomaternal hemorrhage
-c section, placenta previa or abrupton and manual extraction of placenta
1-2% of Rh isoimmunization occur in the antepartum period
Abortion, abdominal trauma, ectopic preg, obstetrical procedures
Prevent rh isoimmunization
Rhogam decrease availability to RHD to maternal immune system
Prevent Rh isoimmunization
More than 1 dose in some populations
-do kleinhauer-betke test which identifies fetal rbc in maternal blood and will determine if rhogam is necessary
All pregnant women wha test
ABO blood group, Rh D type and antibody screen
What is women rh neg and anti d antibody tigers are positive (sensitized)
Test father for antigen status
If he is rhd negative, no further workup or treatment is necessary bc the fetus will be rh negative
If positive for rh d
- homozygous, all with be rh +
- heterozygous-50% will be
Fetal rhd status determined by cell free fetal DNA in maternal plasma or invasively with the fetal antigen testing
Maternal rh antibody tigers
Screening tool to estimate the severity of fetal hemolysis in rh disease
Titers less than 1:8
Usually indicate the fetus is not in serious jeopardize
Recheck titers in 4 weeks
Titers>1:16
Further evaluation
Detailed US to detect hydrops and Doppler studies of the idle cerebral artery
US fetal hydrops
Ascites, pleural effusion, pericardial effusion, skin scalp edema, polyhydramnios
US isoimmunization
Doppler assessment of peak systolic velocity in the fetal mca most valuable
Do ever 1-2 weeks from 18-35
Fetal MCA
Value peak systolic velocity >1.5 MOM for gestational age
Predictive of moderate to severe fetal anemia
Need to proceed with percutaneous umbilical blood sampling to assess true hemoglobin concentration
Intrauterine transfusion if indicated
Amniotic fluid in isoimmunization
Before MCA Doppler
Find bilirubin analysis with spectral analysts 450nm which correlated with cord blood hemoglobin of newborn at birth
Issue of amniotic fluid spectrophotometer in isoimmunization
Amniocentesis can increase the severity of fetomaternal transfusion and worsen the disease
Manage severe fetal anemia: what is it
HCT below 30% or 2 Sd below mean for gestational age
Teat severe fetal anemia
Intrauterine transfusions between 18-35 weeks
Use group O Rh neg packed rbc
- <20 weeks intraperitoneal transfusion
- IV transfusion into umbilical vein are preferred secondary to therapeutic effects are more rapid and reliable
- repeat transfusion 1-3 weeks
Survival rate after transfusion
85%
Antepartum testing
Twice weekly non stress test or biophysical profiles
Serial growth scans q 3-4 weeks
After 35 weeks
The risk of intrauterine transfusions may be greater then that of a preterm 35 week
Consider delivery and transfuse
Each subsequent pregnancy after the first affected pregnancy is likely to manifest more severe fetal/neonatal hemolytic disease and at an earlier gestation
-90% risk of hydrops
Ok
Visit by all patient who are considering pregnancy
Risk assessment(smoking cessation, etoh ,illicit drugs)
Health promotion (nutrition, folic acid, weight)
Medical intervention(DM management)
Psycosocial intervention (stress reduced, 10% are abused during preg)
When start folic acid
At least 1 month before
Why manage glucose
SAB, morbidity, fetal malformation, fetal macrosomia, IUFD
G1p1002
Given birth 1 set of twins both alive
G4p1123
One term infant, one set of preterm twins and 1 miscarriage and 1 ectopic
2 living kids
Systolic murmur, splitting and S3, palmar erythema, spider angiomatosis, linea nigra, striae gravidarum, Chadwick’s sign
Normal in preg
What get for prenatal labs at 1st visit
Cbc, type and screen rubella immunity (cavvinate post partum if not0, syphilis, hepatitis B surface ag, HIV, cervical cytology and gonorrhea, DM, urine culture
Albumin, calcium, glucose, cr, protein, na, urea nitrogen, folic acid blood
Decrease
Fibrinogen
Increase
Urine
Cr no chance, protein increase, cr clearance decreased
Amy last
Increased
Alt ast
No chance
Hematocrit, leukocyte factors 7-10
Increase
Platelets hemoglobin
Decrease
Gestational ae
Number of weeks elapsed since first day of LMP and date of delivery
Serum hcg value preg
<5 no
Above 25 positive
100-time of next menses
First 20 days hcg
Doubles every 2 days
When see gestational sac
5 weeks, hcg 15000-2000
Fetal pole when seen
6 weeks, hcg 5200
Cardiac activity
7 weeks, 17500
Naegels rule
LMP minus 3 months and add 7 days-but only in 28 day cycle ppl
How use US to determine date of delivery
Crown rump length (CRL) between 6-11 weeks can determine due date within 7 days
At 12-20 weeks measuring femur length, biparietal diameter and abdominal circumference can determine due date within 10 days
Third trimester due date can be off up to +/- 3 weeks
How PE estimate exam
Size of uterus
Who needs genetic counseling
Over 35
Previous child.family history of birth defects or known genetic disorder
Previous birth mental retarded
Previous dead baby
Multiple fetal lossses
Abnormal serum marker
Consanguinity
Maternal conditions
Exposure to teratogens
Abnormal US
Genetic disorder
Down’s syndrome
Meiosis nondisjucntion 47 chromosome extra 21
If have a Down’s syndrome have 1% cance of another
Chromosomal studies (karyotype) on couples after 3 or more spontaneous abortions
3-5% will have balanced translocation
Should get counseling on having kid with an unbalanced translocation and therefore be offered prenatal diagnosis (chorionic villus sampling/amniocentesis)
Most common class of spontaneous abortion
Autosomal trisomy (16)
Most common single chromosomal abnormality in SAB
45 xo
AD dosirders
Tuberous sclerosis, neurofibromatosis, achondroplasia, craniofacial synstosis, adult onset POCS, muscular dystrophy
AR
Ray sachs, sickle cell, alpha and beta thalassemia, cystic fibrosis
Who is offered CF screen
1/25 ppl carry the AR tait
15% undiagnosed
All preg women
Sex linked
Duchene muscular dystrophy, fragile x
Fragile x
Most common inherited mental retardation
Second most common mental retardation a fter Down’s syndrome
How get x linked disorder
No male male transmission
Unaffected females carry
Effect males
Multifactorial inherited
Cleft lips, heart defects, pylorus stenosus, neural tube
Neural tube defects
Folic acid
When screen and uploads
1st and 2nd
1st trimester screening
Maternal age, fetal nuchal translucency (NT) thickness (echo free area at back of neck between 10 and 14 weeks-high thickness chromosomal and congenital abnormalities)
Hcg
Pregnancy associated plasma protein a PAPPA
Elevated bhcg and low pappa
Down’s syndrome
Increased nuchal translucency
Also downs
Second trimester triple screen
Bhcg, estriol, alpha fetoprotein
Detect trisomy 21
Second trimester quadruple screen
Bhcg, estriol, afp, inhibiton a
Trisomy 21
Combined 1st and 2nd trimester screening
Report results after 2nd trimester
Improve detection rate
Cell free fetal dna
9-10 weeks
Tests cell free fetal dna, thought to be from apoptosis of trophoblastic cells that have entered the maternal circulation
What cell free dna good for
Trisomy 21
Trisomy 18
Trisomy 13
Sex chromosome
NOT NEURAL FETAL DEFECTS LIKE NT
Who cell cell free dna
High risk
-old, prior trisomy preg, family history chromosomal abnormalities, US abnormal, positive fist trimester screen
If positive
Anniocenteisis or Chorionis villi sampling
Amniocentesis
16-20 weeks
.3% miscarriage
Chorionic villi sampling
11 weeks
1% miscarriage
Teratology
Study abnormal fetal development
Thalidomide
Phocomelia
Pregnancy and lactation labeling rule
PLLR
Removed letters changed content and format for information to assist health care provides in assessing benefit vs risk
PLRR
Pregnancy subsections 8.1-preg
Pregnancy subsection 8.1 breastfeeding
Females and male reproductive potential 8.3
Fetal susceptibility to teratology
Genetic make up of mom and fetus and environment
Multifactorial
Low dose
Fine
Intermediate dose
Organ malformation
High dose
Abortion
Most vulnerable time
17-56 days during organogenesis
4 th month and after
Growth delay and not malformation
Organogenesis
Malformation
Most common teratogen
Alcohol
Fetal alcohol syndrome
Antianxiety
Meprobamate or chlordiazepoxide
Congenital anomalies
Antineopalstic
Aminopterin and methotrexate are both folic acid antagonists
=before 40 lethal
Later UIGR, craniofacial, mental retard
FAS
Growth restriction
Facial abnormalities(low ears, smoot philitrum, thin upper lip, short palpebral tissues, flat midface)
CNS dysfunction
-microcephalic, mental retardation and behavior disorders
Alkalyating
Iugr, fetal death, cleft lip, microphthalmia, limb reduction, poorly developed external genetalia
Anticoagulatnts
Coumadin cross placenta, heparin doesnt
Coumadin
SAB, IUGR, CNS mental retardation, stillbirth, craniofacial features, fetal warfarin syndrome
Anticonvulsants
Usually epileptic women benefits of seizure prevention weighed against teratogenicity of the drug
Diphenylhydantoin
Fetal hydantoin syndrome
-craniofacial , limb reduction, FHS, mental defiency, cardiovascular anomalies
Valproic acid
Spina bifida
Cardiac, skeleton, craniofacial abnormalities
Carbamazepine
Spina bifida, craniofacial defects, fingernail hypoplasia
Phenobarbital
Neonatal withdrawal and neonatal hemorrhage
Estrogen and progesterone
Masculinization of female external genetalia
DES
Treat threatened abortion
Risk cervical and uterine issue
Cancer
Male-testicular abnormalities, infertility and malignancy
T uterus
Retinoids
CNS
CVD
Craniofacial defects
SAB, congenital malformations 50%
Tobacco smoke
low birth weight IUGR
SAB, fetal death, neonatal death and prematurity
Illicit drugs
Opiate-experience withdrawal
Infectious agents virus bacteria
Congenital malformations, growth restriction, fetal death, mental retardation
CMV
Proposes, depressed nasal bridge, triangular mouth
Radiation
Dose dependent
2-6 weeks
Before 2 lethal or none
Less than 5 rads of exposure no risk
How deal with n/v
Small frequent meals Avoid greasy fried food Room temp soda and saltnines Acupuncture Medes
Heartburn
From relaxation of esophageal sphincter by progesterone
-donut lie down after meals, elevate head of bed, small frequent meals, antacids, H2O blockers
Constipation
Decrease in colonic activity
Increase water, fiber, fruits, and vegetables, stool softened
Hemorrhoids
Increase in venous pressure in rectum
Rest, sti bath, stool softener, elevat legs, avoid cnstipation
Leg crams
Last half preg, calves at night
Massage stretch
Backache
Avoid weight gain, exercise/stretch, comfortable shoes, pillows, heat massage
How often go to doctor
Every 4 weeks until 28 then ever 2 weeks tilll 36 and weekly until delivery
What get at routine visit
Bp, weight, urine protein, uterine size, fetal heart rate (Doppler)
Quickening
First sensation of miovement 20 weeks
Near term
Evaluate fetal lie and fetal position
20 weeks
Fetal survey ultrasound
28 weeks
Gestational diabetes and repeat hemoglobin and hematocrit
Rhogam injection to Rh negative patients
Tdap give between 27-36 weeks
35 week
Screening for group b step carrier with vaginal culture-treat in labor if positive
Kick counting
Monitor how often
Nonstress test
Reactive-2 accelerations of at least 15 beats above baseline lasting at least 15 seconds during 20 minutes of monitoring
Contractions tress test
Give oxytocin to establish at least 3 contractions in a 10 min period. If late decelerations are noted with the majority of contractions the test is positive and delivery is warranted
8-10
Reassuring
6
Deliver if at term
4 or less
Onreassuring consider delivery
Still birth reactive non stress test
2/1000
Negative contraction stress test still birth
.3/1000
Biophysical profile
.8/1000
Normal labor and delivery
Gynecoid
Gynecoid
Round at inlet
Wide transverse diameter
Wide suprapubic arch
Head into the occiput anterior position
Good for deliver
Android
Males and 30% females
Wides transverse diameter closer to scrum
Prominent ischial spines
Narrow pubic arch
Fetal head to occiput posterior position
Arrest of descent common
Bar prognosis for delivery
Anthropoid
Ape pelvis 20%
Larger AP then transverse Creasy long narrow oval with narrow pubic arch
Fetal head anterioposterior diameter
Usually in OP position
Good delivery
Platypelloid
Flat gynecoid pelvis 3% of females
Short AP and wide transverse diameter
Wide bispinous diameter
Wide suprapubic arch
Fetal head has to engage in transverse diameter
Poor prognosis for delivery
Diagonal conjugate
Inferior pubic symphysis to sacral promontory
>11.5 ok
Obstetric conjugate
Diagonal-2 cm
Narrowest fixed distance through which the fetal head must pass through during a vaginal delivery
What palpate
Sacral and iscial spine
Pelvic outlet
Measure ischial tuberosities and pubic arch
Iscial tuberosities distance between
8.5 cm distance ok
Infrapubic angle
Place thumb next to each inferior pubic ramus and estimate the angle at which they meet
>90 good
Radiographically MRI CT
Rare only do if history or clincial indication of pelvic abnormalities or pelvic trauma
Initial evaluation
Review prenatal records, identify complications, confirm gestational age, review labs, history, PE
Focused history
Frequency contractions, loss fluid, vaginal bleeding
Fetal lie
Reference to maternal spine
Longitudinal, transverse, oblique
Fetal presentation
Vertex, breech, transverse, or compound
Leopoldo maneuver
- Palpate fundus
- Palpate or spine and fetal small parts
- Palpate what is presenting in the pelvis with suprapubic palpation
- Palpate for cephalic prominence
Dilation
Check at internal os
Effacement
Thinning cervix occurs and is reported as % change in length
Normal 3-5 cm
Thick 100% effaced
Station
Degree of descent of the presenting part of fetus
Measured in cm from presenting part to ischial spines
When the bony portion of the head reaches the level of the ischial spines the station is zero
-5 to 5 cm
First stage labor
Onset labor to complete cervical dilation
Latent and active
Second stage
Complete cervical dilation to delivery
Third stage
Delivery of infant to delivery of placenta
Fourth stage
Delivery of placenta to stabilization of patient
Phases of first stage
Latent active
Latent
Onset of labor and slow cervical dilation
Active
Faster rate of dilation and usually begins when cervix is dilated to 4 cm
Admit for labor
Duration 1st stage primiparas and multiparas
6-18 hrs
2-10 hours
Rate cervical dilation primiparas and multiparas
1.5 cm per hour
When may patient ambulated
Head engaged and reassuring monitoring is noted
I in bed be left lateral recumbent
Fluids
IV to hydrate give meds if need
Labs
Cbc and t ands
Maternal monitoring
Vitals q 1-2 hours
External fetal monitoring
Continuous
Intermittent if uncomplicated or complicated differs
Monitor uncomplicated
Q 30 min in active phase of first stage
Q 15 min in second stage of labor
Monitoring if complicated
Q15 min in active phase
Q15 min during the second stage
How get most accurate tracing
Internal monitoring
How get uterine activity
External tocodynamometer
Internal pressure catheter
Can get strength of contractions and help xyytocin augmentation
Vaginal exam
Active phase q2 hrs record dilation, effacement, station
Amniotomy
Augment labor, allows assessment of meconium status
Risk cord prolapse, prolonged rupture is associated with chorioamnionitis
Second stage
Descent of the presenting part through the maternal pelvis and culminates in delivery
Increase in bloody show and desire to bear down with contractions
Duration second stage
Primiparas without epidural 2 hours
With 3 hours
Multiparas without epidural 1 hour
Multiparas 2 hours
Engagement
Presenting part at zero station
Descent
Brought about by the force of uterine contractions and maternal valsava efforts
Flexion
OA baby’s chin to chest thus changing the presenting part from occipitofrontl to the smaller suboccipitobregmativ
Internal rotation
At ischial spines
Fetal head enters pelvis int ransverse diameter, rotates so the occiput turns anteriorly or posteriorly toward the pubic symphysis
Extension
Crowning occurs when the largest diameter of the fetal head is encircled by the vaginal introitus
+5
Head is born by rapid extension
External rotation
Delivered head now returns to its original positiona t the time fo engagement to align itself with the fetal back and shoulders
Expulsion
Anterior shoulder then delivers under the pubic symphysis, followed by the posterior shoulder and the remainder of the body
Maternal position second stage
Avoid supine
Dorsal lithotomy
Bearing down second stage
With each contraction, the mother should hold her breath and bear down with expulsion efforts
2nd stage fetal monitoring
Continuous
Q15 with no risk factors
Q5 minutes during seconds tage with risk
Vaginal exam 2nd stage
Access descent and confirm position
Delivery head
2 nurses and physician
Antiseptic soap vulva
Episiotomy
Facilitate with modified rotten maneuver
Head out bulb suction oral cavity and use index finger to assess nuchal cord
-if loose can manually reduce over the infants head if tight clamp and cut
How deliver shoulder
Anterior shoulder with gentle downward traction on fetal head
Posterior shoulder by elevating the head
Support head, bulb suction, dry and stimulate
Cord
Clamp x2 and cut
Obtain cord blood specimen
Deliver placenta
Third stage then inspec and repair
Indications episiotomy
Likelihood of spontaneous laceration seems high
To expedite delivery by enlarging the vaginal outlet
Midline episiotomy
Common
Risk of extension 3rd or 4th degree
Less postpartum pain
Meidolateral episotomy
Greater blood loss
More difficult to repair
More postpartum pain
Increase risk of dyspareunia
Rotten maneuver
Fingers of the right hand are used to extend the head while counterpressure is applied to the occiput by the left hand to allow for a more controlled delivery
Or just support perineum
FIRST DEGREE LACERATION
SUPERFICIAL LACERATION INVOLVING THE VAGINAL MUCOSA AND OR PERINEAL SKIN
SECOND DEGREE
LACERATION EXTENDING INTO THE MSUCLES OF THE PERINEAL BODY BUT DOES NOT INVOLVE THE ANAL SPHINCTER
THIRD DEGREE
LACERATION EXTENDS INTO OR COMPLETELY through the anal sphincter but not into the rectal UC osa
Fourth degree
Involves the rectal mucosa
Third stage
Interval between delivery of the infant and delivery of placenta
Retained placenta
Placenta not delivered in 30 minutes
Signs placental separation
Gush of blood from vagina
Lengthening of umbilical cord
Fundus of uterus rises up
Change in shape of the uterine fundus from discoid to globular
What do
Apply counter pessure between symphysis and fundus
Do not pull cord until classic signs noted
Inappropriate pulling cord
Uterine inversion
Fourth stage
Monitor patient
Vitals
Uterine fundal checks and assess for vaginal bleeding
Postpartum hemorrhage commonl occurs during this time
-uterine stony, retained placenta, unprepared vaginal or cervical laceration
Cervical ripening
Do before labor
Augmentation
Artificial stimulation of labor which already began
Vs induction of labor
Indication induction
Abruptio placenta, chorioamnionitis, fetal demise, preeclampsia, eclampsia, gestational HTN, prom, postterm pregnancy, maternal medical conditions, fetal compromise
Contraindications induction
Unstable fetal Acute fetal distress Placenta previa or vasa previa Previous classical c section or transfundal uterin surgery HIV high viral load, active herpes
Bishop score
Cervical dilation, cervical effacement, station, cervical consistency cervical position
Biochip<6
Unfavorable
Bishop>8
Probability of vaginal delivery after labor induction is similar to that of spontaneous labor
Cervical dinoprostone
E2 vaginal insert
Not in previous c section
Misoprostol cytotoxicity
E1
Oral or vaginal
Can’t be removed
Not in previous c section
Mechanical dilators
Foley bulb catheter
Laminara japonicum
Pitocin infusion
Synthetic oxytocin stimulate contraction
IV
Induction and augmentation
In normal saline IV and stopped if fetal distress
1-30 mu/min
Uterine tachysystole
More than 5 contractions in 10 min
Side effect
Antidiuretic effect
Pitocin ADH has effect can lead to increase water reabsorption
-convulsion and coma
Uterine muscle fatigue
Prolonged pitocin increase risk
-post partum hemorrhage secondary to uterine stony
Obstetric anesthesia
Pain relied sage for baby
Maternal mortality due to anesthesia
1:500000
Uterine blood flow
Blood flow to uterus may decrease To uterus with anesthesia from hypotension
Need adequate hydration
What do if hypotension anesthesia
Vasopressor
Pain uterine contractions
Visceral pain t10-t12 through l1
Perineum pain
Somatic s2-4
Regional anesthesia
Low of pain below t10
Epidural, spinal
Local
Perineum, pudendal block
Early labor anesthesia
Morphine, fentanyl, meperidine nalbuphine
Not for labor pain women work bc moa is sedation
Opoids cross placenta
Regional
T8-t10 and below
Local anesthesia and narcotic
Epidural
Most effective catheter in epidural space l2-l3 , l3-l4, l4-L5 then placed over needle
Spinal
Single shot analgesia which provide excellen pain relief for limited procedures
Limited use in labor since a single shot
Regional ae
Hypotension , spinal HA, fever, spinal hematoma, abscess
Contraindications regional
Coagulopathy, heparin within 12 horus, bacteremia, ICP, skin infection
Local
1-2% lidocaine for 20-40 min
Before episiotomy or laceration repair
AE local
Hypotension, seizures, cardiac arrhythmias
Pudendal ae
Intravascular injection, hematoma infection
General
Propofol
Loss of consciousness need airway management
16 fold increase maternal mortality
All inhaled anesthetics
Cross placenta and associated with neonatal respiratory depression
When do general
Emergent cases
Regional anesthesia
Fetal heart rate monitoring
To look for for patterns that may be frequently associated with delivery of infant with poor outcomes
For benefit
No increase operative deliveries and c section no change in neuro damage
Who do for
Reassurance
Would have to get nurse
Still goor warning of potential problems
External monitoring vs internal
Internal Rome accurate
External
Doppler US< pressure sensiiive tacodynanmometer
Doppler US
On maternal abdomen overlying fetal heart
Records reflected sound waves fromt he fetal heart back to transducer
Pressure sensitive tocosynanmometer transducer
Detects and records contractions
Useful for measuring the frequency of contractions but not the strength
Internal
Fetal scalp electrode
Intrauterine pressure catheter
Fetal scalp electrode
R wave peaks of the fetal echocardiogram
Maternal and fetal movement will not alter the quality of signal
Rare cases of fetal pustules
Not for HIV
Intrauterine pressure catheter
Soft plastic catheter placed transcervically
Gives precsise measurement of the intensity of uterine contractions in millimeters of mercury
What does internal require
Membranes to be ruptured
Fetal oxygen reserve is only enough to meet its metabolic needs for ___
1-2 min
When is blood flow from maternal circulation stopped
Every contraction
Can tolerate without hypoxia bc adequate oxygen exchange occurs still between contractions
A fetus who is marginal
Can’t tolerate stress of contractions and will become hypoxic
Hypoxia in fetus
Chemoreceptors and baroreceptors in the peripheral arterial circulation of the fetus influence the FHR by giving rise in contraction related or periodic FHR changes
Anaerobic metabolism, Peruvian and lactic acid and fetal acidosis
PH fetal scal normal and acidosis
7.25-7.3
<7.2
How do uterine contractions effect HR
Blood flow ceases
Increase or decrease
Decrease
Normal uterine activity
5 contractions or less in 10 minutes over 30 minutes
Tachysystole
> 5 in 10 min over 30 min
Presence or absence FHR decelerations
How measure contractions
Peak to peak
Normal contractions
3 in 8 minutes
Occurring 2-3 mintues
MVU
> 200 Montevideo units (sum of the contractions in a 10 minute period) for at least 2 hours
Baseline FHR
Increments of 5 bpm during 10 minute
Assess between contractions
Normal
110-160 bpm
Tachycardia
Baseline>160 bpm
Bradycardia
<110 bpm
Tachycardia
> 160
Bradycardia
<110
Causes tachycardia
Fetal hypoxia Meds-oxytocin Arrhythmias Prematurity Maternal fever Fetal infection-chorioamnionitis most common cause1
Bradycardia
Fetal hypoxia, obstetric anesthesia, pitocin, maternal hypotension, prolapsed or prolonged compression of the umbilical cord, heart block
Chemoreceptors tachycardia
In response to hypoxia
Baroreceptors
Vagus in response to changes in fetal bp
Absent
Amplitude undetected
Minimal
<5 bpm
Moderate
6-25 bpm
Marked
Amplitude>25 bpm
Decreased variability
Indicators of fetal stress
Persistent late decelerations
Hypoxia and acidemia
-lack of oxygen and the build up acid in the fetus depresses the fetal heart rate and cns
Decreased variability
Prematurity, sleep, maternal fever, fetal tachycardia, fetal congenital anomalies, maternal hyperthyroidism, drugs
Accelerations
Abrupt increase in the FhR and is a normal reassuring response
>32 weeks HE>15 bpm above baseline for 15 sec or more
<32 weeks HR>10 bpm above baseline for 10 sec or more
Prolonged acceleration
> 2 min
Change in baseline
If acceleration lasts >10 min
Cause accelerations
Spontaneous fetal movement
Vaginal exam
Deceleratiosn
FHR decreases in response to uterine contractions
Early, variable, late
Early deccelerations
Head compression-fetal autonomic response to increased ICP caused by transient compression of the fetal head
Not associated with fetal distress
The nadir of the deceleration occurs at the same time as the peak fo the contraction and thi s. Amirror image
Cause early deceleration
Pressure on fetal skull increase ICP->decrease cerebral blood flow->activates central vagus nerve-> produces decrase in HR->recovering occurring as pressure is relieved
Variable decelerations
Secondary to umbilical cord compression
Abrupt decrease in FHR-can occur before, during or after contraction starts
Decrease in FHR >15 bpm lasting >15 sec and <2 min in duration
Onset depth and duration an vary with successive uterine contractions
Variable decelerations abuse
Cord compression
Slight cord compression
Obstruct umbilical vein which returns re oxygenated blood to fetal heart
Response to cord comrpession
Shoulder
Slight fhr decrase followed by major drop
Late decelerations
Uterine placental insuffiency
Most ominous deceleration-repetitive late decelerations usually indicate fetal metabolis acidosis and low arterial pH
Nadir of the deceleration occcurs after the pea of contraction
Cause late deceleration
Excessiveuterine activity
Maternal supne hypotension
Prolonged deceleration
Decrease in FHR from baseline that is >15 bpm >2 min but <10 min
Disruption of oxygen transfer from the environment to the fetus at one or more points along the oxygen pathways
Maternal pushing
Change in baseline prolonged decelaeration
> 10 min
Sinusoidal pattern
Smooth sine wave like undulating pattern in fhr
Fetal anemia
Category 1
Baseline 110-160 bpm
Moderate variability no late or variable decelerations
May have acccelerations and early decelerations
Tracing category 1
Normal
Manage category 1
Intermittent CEFM
Category II
Intermittent: variable decelerations <50% of contractions
Recurrent variable decelerations >50% of contractions
Category II intermittent
Normal outcome
Category II recurrent variable
Umbilical cord compression with acidemia impending
Moderate variability and or accelerations suggest fetus is not acidemia
Manage intermittent category II
No intervention required
Treat recurrent category II
Alleviate cord comrpession repositioning amnoiinfusion
Modify pushing efforts push with every other ctx
Amnioinfusion
Instillation of normal saline can alleviate cord compression
250-1000 cc infused 15 cc/min
Continuous infusion of 100-200 cc/hour
How infuse amnioinfusion
Transcervical IUPC
Category iI
Minimal or absent variability
Recurrent late decelerations
Prolonged decelerations
Tachycardia, bradycardia
Variable late or prolonged decelerations occurring with maternal pushing efforts
Etiology category II
Fetal sleep, meds, acidemia, UPI:hypotension, tachysystole, maternal hypoxia
Rapid fetal descent , cord comrpession, tachysystole
Prematurity , chorioamnionitis, epidural , cord prolapse, cord comrpession UPI
Manage categor II
Promote fetal oxygenation
Decrease oxytocin
Tachysystole category II
Spontaneous labor, induction or augmentation
Goals tachysystole
Reduce uterine activity
Lateral positioning, IV bolus, decrease oxytocin, tocolytic (tertbutaline)
Absent baseline variability(recurrent late decelerations, recurrent variable decelerations, bradycardia0
Sinusoidal pattern
Increased risk of fetal acidemia
Increased risk of hypoxemia and acidemia
Manage
Prepare for delivery
Fetal scalp stimulation
Fetal scalp stimulation
Poke it with finder
If an acceleration of 15 bpm lasting 15 seconds occurs the fetal pH value almost always is 7.33 or greater
How fetal scalp stimulation show difference between fetal sleep from acidosis
When teal tracing shows reduced variability but no decelerations
Category III
How many minutes is standard of care to deliver this infant
Idk
Operative delivery with category II tracing
Get consent, get team, assess transit time and location for operative deliver, ensure IV access, review labs, assemble neonatal resuscitation personnel
Normal FHR good?
98% fetal wellbeing
Does electronic fetal monitoring result in reduction of cerebral palsy
False positive >99%
Abnormal patterns or non reassuring FHR can occur into e absence of fetal distress
False positive rate is 80%
Do most patient sithe nonreassuring FHR give birth to healthy infants
Yup
Watch end for reading
Please
Medical conditions in pregnancy
Ok
Geational DM
7% get glucose intolerance
Screen GDM when
24-48 weeks
50 gm on hour glucose challenge (>130-140 abnormal)
May perform an earlier screen if risk
If abnormal 50 gm one hour oral gloat glucose challenge (>130-140)
Follow 3 hour 100 gm oral load glucose tolerance test
-fail three hour with 2 or more abnormal values
Risk factors for development of GDM
Obesity, history, family history DM, glucose intolerance
Maternal complications
Increase risk of gestational HTN
Increase risk preeclampsia
Greater risk of c delivery
Increase risk Dm later in life
Fetal complication GDM
Macrosomia, neonatal hypoglycemia, hyperbilirubinemia, operate delivery, shoulder dystocia, birth trauma
Antepartum management
Diabetic teaching, blood glucose monitoring, fetal testing, US for fetal weight get c section is over 4500 gm
When can u wait for spontaneous labor or estimated due date
Testing, growth, glycemic control are good
Diet controlled
No treat
Medication control intrapartum
Hourly glucose monitoring
Need between 80-120
Continuous fetal monitoring in labor
Increasing glycosylated hemoglobin levels HgBA1C in period of embryogenesis, sixfold increase risk of congenital anomalies
Birth defects
Maternal complications
Worsening nephropathy and retinopathy, increased risk of developing preeclampsia, greater risk of diabetic ketoacidosis
Fetal complications
Increase risk of spontaneous abortions, anatomic birth defects, fetal growth restriction and prematurity
White classification
Class a1 and a2
A1
Gestational diabetes, diet controlled
A2
Gestational diabetes; insulin or oral meds controlled
What want fasting glucose
Less than 95 mg/dl
Two hour postprandial
Less than 120
Exercise after meals
Half an hour
Antepartum maternal evaluation
Renal-24 hour urine collections every trimester
Cardiac ekg
Ophthalmic detailed eye exam in first trimester
Glycemic control (dail finger stick blood glucose and hgba1c0
Fetal evaluation antepartum
Early dating US
Detailed fetal anatomy US and echo
Biochemical testing for congenital malformations in first trimester 11-13 weeks or quad screen at 16-21 weeks
Fetal growth US every 2-4 weeks
Fetal testing every weeks tarting 32 weeks
Postpartum management
Insulin requirements drop significantly after delivery of placenta
Insulin dependent patients typically require about 2/3 of pregnancy dose of insulin
GDM frequently do not need further treatment
With GDM-need 2 hour glucose tolerance 6 to 12 weeks postpartum to look for preexisting disease
Hyperthyroidms
Similar to preg so hard to see symtpoms
Diagnose hyperthyroidism
T4 up and TSH down
Treat maternal hyperthyroidism
Radioactive iodine contraindicated
PTU and methimazole in 2 or 3 (aplasia cutis in 1st)
PTU-liver toxicity so only 1st
Fetal effects hyperthyroidism
Meds cross placenta and fetal hypothyroid an goiter an come
Risk of prematurity, IUGR, preeclampsia and stillbirth
Thyroid storm trigger
Infection, labor, c secretion, noncompliance with medication
Symptoms thyroid storm
Hyperthermia, tachycardia, perspiration, high output cardiac failure,
Maternal mortality thyroid storm
25%
Treat thyroid storm
Beta blockers-propranolol
Sodium iodide
PTU
Dexamththasone
Replace fluid
Bring t down
Hypothyroidism
Normal preg
Untreated hypothyroidism
Spontaneous abortion, preeclampsia, abruption, low birth weight infants, still birth, lower intelligence leees (cretinism)
Treat hypothyroidism
Levothyroxine
Monitor tsh and free t3/t4
Neonatal thyrotoxicosis
Due to transplacental transfer of thyroid stimulating antibodies
Transient
Mortality 16%
Neonatal hypothyroidism
Defiency results in generalized development retardation causes
-thyroid dysgenesis
Inborn error of thyroid function
Drug induced
Rheumatic heart disease
Mitral stenosis
High risk of developing heart failure, subacute bacterial endocarditis and thromboembolic disease
Congenital heart disease
Atrial and ventricular septal defects, primary pulmonary htn, t of fallout, transposition of great vessels
-if corrected in childhood no consequences
Primary pulmonary htn
Contraindications to pregnancy due to decompensation during pregnancy and a high mortality rate, epidural anesthesia is preferred and vaginal delivery ma be an option for these patients
Cardiac arrhythmias
Most frequently supraventricular tachycardia
Benign
A fib.flutter more worrisome for underlying cardiac disease
Postpartum cardiomyopathy
No underlying cardiac disease
Develops typically within last weeks of pregnancy or within 6 months postpartum
Women with preeclampsia, htn and poor nutrition
Mortality rate postpartum cardiomyopathy
10%
Prenatal manage cardiac disease
Co managed with cardiologist!!!!!
Ekg, echo, avoid na, left lateral position, no strenuous, prevent anemia, avoid infection, fetal echo
Delivery cardiac disease
Vaginalis unless obstetric indications
Antibiotic prophylaxis for endocarditis in high risk patients
Acute cardiac decompensation with congestive heart failure is managed as a medical emergency
Immune idiopathic thrombocytopenia
Immunoglobulins attach to maternal platelets
Treat immune idiopathic thrombocytopenia
Begun after platelets from to 50000 Prednisone IV immunoglobulin if severe Platelet transfusion Splectomy
Baby risk immune idiopathic thrombocytopenia
Neonatal thrombocytopenia can occur due to placental transfer of antiplatelet antibodies
SLE
1/3 improve 1/3 same , 1/3 worse
Treat sle flares
Prednisone
Fetal complications sle
Preterm delivery restrictions
Still birth
Miscarriage
10% risk for neonatal lupus passive transfer of anti ro.ssa or anti la/SBS
SLE
Antiphospholipid syndrome
Presence of lupus anticoagulatn and or anticardiolipin antibody
Associated with arterial or venous thrombosis
Pregnancy complications antiphospholipid syndrome
Increase risk of miscarriage
Risk for developing preeclampsia
Fetal growth restriction
Treated during pregnancy with heparin/low olecular weight heparin and low dose asprin
If history of thrombosis-full anticoagulation
Acute renal failure
Due to rpeexisting renal disease or pregnancy induced
Three types acute renal failure
Pre renal renal post renal
Pre renal
Acute blood or fluid loss
Renal
Usually preexisting disease or hypercoagulable state
Post renal
Rare, urologic obstructive lesions
What do if renal pro
Urine output, BUN:Cr, fractional excretion of Na, uring osmolality
Cvs study-in labor need swan gang catheter
Urologic-foley catheter, renal us to diagnose obstructive source
Treat pre renal
Retort volume
Electrolytes, diuretic, flus restriction, hemodialysis
Post renal treat
Mechanics to remove the obstruction
Left lateral position, urethral catheter, possible surgical intervention to remove stone
Chronic renal failure
Bad outcome
Cr>1.5-2 worsens prognosis
Treat chronic renal failrue
Monitor renal function with 24 hour urine collections for protein and cr clearance , manage htn, fetal surveillance with growth us and nonstress tests/biophysical profiles
Post renal transplant
Not recommended
May lose graft function or experience rejection; best candidates are 1-2 years post transplant with stable cr and proteinuria without severe htn
Fetal complications post renal
Steroid induced adrenal and hepatic insuffiency, prematurity, intrauterine growth restriction
Asymptomatic bacteriuria
More likely to lead to cystitis and pyelonephritis in pregnant women
From urinary stasis and glucosuria
Initial asymptomatic bacteriuria
Urine culture at initial prenatal visit
Most common Asymptomatic Bacteruria
E. coli
Treat asymptomatic bacteriuria
Antibiotic (3 or more if recurrent)
Pyelonephritis signs
Fever, costovertebral tender, malaise, WBC up
Issue pyelonephritis
Increase uterine activity and preterm labor
Result in adult respiratory distress syndrome
Treat pyelonephritis
IV hydration Antibiotics Antipyretic Tocolytics Suppression remainder pregnancy
N/v in pred
8-12 weeks not known why
Treat n/v preg
Symptomatic
Hyperemeis gravidarum
Persistent nausea and vomiting >5% loss of pre preg weight, ketonuria, dehydration
Who get hyperemesis gravidarum
Occurs more frequently in first pregnancy, multiple pregnancies, trophblastic disease
Treatment hyperemesis gravidarum
Outpatient management fails then may need hospitalization for IV fluids, electrolytes, glucose, vitamins and Anti-emetic
Severe-may need nasogastric feeding or parental nutrition
Gerd common how treat
Small meals, avoid lying down after meals, elevate head when sleeping, antacids, H2O blocs
Peptic ulcer
Preg may improve
Diagnose symptoms, and only endoscopy if severe or signs of gi bleeding
Treat peptic ulcer
No caffeine, alchol tobacco, spicy foods
Antacids, H2O blockers/proton pump
Treat H pylori
Mendelsons syndrome
Acid aspiration syndrome
Preg women get from delayed gastric emptying and icnreased intrabadominal intra gastris pressure
Treat mendelsons
Supplemental o2, maintain airway, treat for acute respiratory failure
Prevent mendelsons
Decrease acid ins tomach
Do not feed in labor
Ibd
Fine in pred, IC more active
If bowel disease active at time of conception may increase miscarriage
Treat ibd preg
Acute exacerbation is same as non preg
Intrahepatic cholestasis of pregnancy
Cholestasis and pruritis is second half ofpregnancy
ICP associated
Can recur with each pregnancy
Association with oral contraceptives and multiple gestation
Benign course for maternal consequences
Increase risk of meconium strained amniotic fluid and fetal demise
Symptoms ICP
Itching without abdominal pain r rash
Labs reveal elevated serum bile acids and occasionally elevated liver enzymes
Treat icp
Local treatment cold baths, bicarbonate washes
Use ursodeocycholic acid
Fetal surveillance and delivery at early term
Acute fatty liver of pregnancy
Scary!
Diffuse fatty infiltration of liver resulting in hepatic failure
1 per 14000 pregnancies
Symptoms scute fatty liver
Ab pain, nv, jaundice , irritability, polydipsia/pseudodiabetes insipidus, HTN.proteinuria in 50% of cases
Lab finding acute fatty liver
Increase prothrombin time and partial thrombophlebitis time, elevated bilirubin, ammonia and uric acid and elevation of liver transaminase
Treat acute fatty liver
Termination pregnancy
Supportive care-IV fluids with 10% glucose, FFP and cryoprecipitate
Maternal fetal mortality acute fatty liver
Yup both about 10-20%
If survive acute fatty liver
Full recovery
Anemia
Physiology decreas in hgb/hematocrit during pregnancy
Hematocrit less than 30% or a HgB concentration less than 10 g/dL
Most common reason for iron defiency
Screened at initial prenatal visit and again 26-28 weeks
Treat iron supplementation-oral or IV
Preg is hypercoagulably
5 fold increase in venous thrombosis and greatest risk is fist 5 weeks postpartum
Superficial thrombophlebitis
Most common in patients with varicose gains, obesity and little physical activity
Most common in calf, will not result in pulmonary emboli
Symptoms hpercoagulable
Most common in patients with varicose veins, obesityand littlen physical activity
Most common in calf, will not result in pulmonary emboli
Symptoms hypercoagulable state
Swelling, ternderness
Treat pregnancy hypercoagulable
Bed rest , pain medication, local heat, no need for anticoagulants, wear support hose
Dvt
1/2000 antepartum 1/700 antepartum
Symptoms dvt
More common in the left leg than the right
Pain in the calf with dorsiflexion
May also have dulla Che, tingling or pain with walking
Diagnose dvt
50% asymptomatic
compression US with Doppler
MRI suspect pelvic thrombosis
Treat dvt
Anticoagulation
Low molecular weight or unfractioned heparin
-PTT values with heparin and factor Xa values with lovenox
Coumadin for 6 weeks postpartum nut not during preg
Pulmonary embolism
Maternal mortliaity -80% untreated treated 1%
From dvt
Symptoms pulmonary embolism
Pleuritic chest pain, shortness of air, air hunger, palpitations, hemoptysis
Signs pulmonary embolism
Tachypnea, tachycardia, low grade fever, pleural friction rub, chest splinting, pulmonary rales, accentuated pulmonic valve second heart sound
Pulmonary embolism
Ekg, chest x ray, arterial blood gas, ventilation perfusion scan, helical computed tomography
Treat pulmonary embolism
Anticoagulation
Thrombophlebitis work up for dvt or pulmonary emboli
Lupus anticoagulatnts, anticardiolipin antibody, factor v Leiden, protein c and s, antithrombin III, prothrombin G20210A
All patients with history of thromboembolism need what
Prophylactic anticoagulant
Asthma
Most common pregn pulmonary disease!
1.3 better 1.3 same 1/2 worse
Severe asthma problem
Miscarriage, preeclampsia, intrauterine fetal demise, intrauterine fetal growth restriction, preterm delivery
Treat asthma
Mile-SABA Mild persistence-low dose inhaled CS Moderate persistent0saily inhaled corticosteroid combined with long acting inhaled beta agonist Severe persistent-add systemic CS Maternal monitoring
Fetal monitoring asthma
Serial growth US, NST.biophyscial profiles, deliver for fetal growth restriction or maternal deterioration
Labor and delivery asthma
Stress dose of IV steroids if using daily inhaled or high potency oral for more than 3 weeks
Tension HA
Most common
Give acetaminophen
Migraines
Highes prevenalce in childbearing years
Improve preg
Neurology can be helpful
Multiple sclerosis
Diagnose at 30
Fewer and less severe pregnancy but may exacerbate post partum
Increased risk LBW, C section
Seizure rate in preg
Not alter
Treat seizure
If seizure fre 2 years propr to conception may stop
Monotherapy at lowest dose
Med for seizure
Alt eratogen
Valproate
Noooooooooooo
Most common preg ant seizure
Dilatin phenobarbital
What give women on anti epileptics
1-4 mg of folic acid
Anti epileptic complications preg
Preeclampsia, placental abruption, hyperemesis, premature labor, intrauterine fetal demise, congenital cleft lip and palate and cardiac anomalies
Depression
Arise and recur postpartum in 10%
Risk factors post partum depression
Personal or family history depression
History of abuse
Drug use
History of personality disorder
Treat post partum depression and anxiety
Counseling
Antidepressants -not 1st trimester and if 3rd may get neonatal withdrawal
Post partum depression
70-80% from hormonal fluctuations get maternal blues
10-15 depression
Treat post partum
Counseling an medication
Risk post partum depression
Depression during pregnancy
Younger women
Operative
Non spontaneous
Vaginal forceps assisted, vacuum extracted /c section
Operative vaginal delivery
Direct traction with vacuum extractor or forceps
Maternal indications for operative vaginal
Maternal exhaustion/lack of expulsion effort
Inability to have expulsive effort
-spinal cord injuries, neuromuscular disorders
Need to avoid maternal expulsive efforts-certain cardiac conditions, cerebrovascular disease
Fetal indications for operative vaginal delivery
Non reassuring fetal status (bradycardia, repetitive heart rate decelerations)
Other indications operative vaginal delivery
Prolonged second stage of labor
Nulliparous>2 hours without regional anesthesia or>3 hours with regional anesthesia
Multiparous >1 hour without regional anesthsia or> 2 hours with regional anesthesia
Prerequisites for maternal vaginal delivery
Adequate analgesia, lithotomy position, bladder empty, verbal or written consent
Fetal prerequisites for operative vaginal delivery
Vertex presentation, fetal head must be engaged (biparietal diameter at 0 station), position fothe fetal head must be known with certainty, station fo hte fetal head must be> 2
Ureteroplacentla criteria prerequisites for operative vaginal delivery
Cervix fully dilated, membranes ruptured, no placenta previa
Outlet operative vaginal delivery
Scalp visible without labia separation
Fetal skull reached the pelvic floor
Sagittal suture is in the anteroposterior diameter or right or left occiput anterior or posterior position
Fetal AED at perineum
Rotation not exceed 45 degrees
Low operative vaginal delivery
Leading potent of the fetal head is at +2 station or more and is not on the pelvic floor
Midpelvis and high forceps operative vaginal delivery
Fetal skill is above +2
Not ever indicated today
If you aren’t positive of position
Don’t do forceps
If they don’t articulations easily-reapply. If they still don’t articulate well
Don’t apply
Always
Make sure no vaginalis tissues or the cervic are caught in the forceps
Blades should dit the fetal head evenly, should lie against the fetal head so that they cover the space between the orbits and ears
Traction is applied into e plane of least resistance and follows the pelvic cord-if not come early
Stop
Maternal complications forceps
Lacration of vagina/cervic, episiotomy extension, pelvic hematoma, urethral and bladder injuries, uterine rupture
Fetal complications forceps
Facial laceration, forcep marks, brachial plexus injur, skull fracture, intracranial hemorrhage, seizures
Vacuum
Indications requirements exactly same
Advantage-little maternal analgesia
Contraindications vacuum
Gestational age less than 34 weeks
Suspected fetal coagulation disorder
Suspected fetal macrosomia
Breech
How do vacuum assisted vaginal delivery
Applied to fetal head with a mechanical pump
Steady traction
No rocking or torque on the device
No rocking or torque on the device
Incidence of serious complication is about 5%
3 checks for forceps
No material tissue trapped int he cup, cup should be placed int he midline of the sagittal suture, the vacuum port of the suction cup should point toward hte occiput
What o with vacuum between contractions
Release suction
How many pop offs ok
No more than 2
How long can we vacuum
No mroe than 20 minutes
Can u turn or twist device
No
Complication vacuum vs forceps
More failures deliveries
Fewer perineal injuries
Icnreased incidence of delta cephalohematoma
More scalp lacerations and bruising
C section
Delivery of a fetus through a surgical incision of the anterior uterine wall
Rate is climbing
Fetal indication c sectio
Nnonreassuring fetal heart rate
Reach presentation/transverse presentation
Very low birth weight
Active herpes
Immune theomocytopenia purpura
Congenital anomalies
Maternal fetal indications c section
Cephalopelvic disproportion
Failure to progress
Placental abruption
Placenta previa
Maternal indications c section
Obstructive benign and malignant tumors
Large vulvar condyloma
Abdominal cervical cerclage
Prior vaginal colporrhaphy
Conjoined twins
Maternal requires
Intraoperative complications c section
Uterine artery lacerations, bladder injuries, urethral injures, GI injury, uterine atony, placenta accretion, c hysterectomy
Post op complications c sectio
Nendoyometritis
Wound-infection, separation, dehiscence
Urinary complications, ileus diarrhea, thromboembolic disorders (pulmonary emboli/dvt), septic pelvic thrombophlebitis
Preterm labor
After 20 weeks before 37
Diagnose preterm labor
Uterine contractions with cervical change or cervical dilation of 2 cm and/or 80% effaced
Leading cause of infant mortality
Prematurity
Socioeconomic factors PTL
African Americans Decreased access prenatal care High stress Poor nutrition Genetics
Medical obstetric PTL risk
Previous History SAB Bleeding 1st trimester UTI/genital infections Multiple gestation Polyhydramnios, Incompetent cervix
Pathways to prevent PTL
Infection
Placental-vascular
Psychosocial
Uterine stretch
Infection
Bacterial vaginosis
Group B strep
Gonorrhea, chlamydia
Treat infection
Antibiotics,
Link between infection and what that is a risk for preterm
Cervical length
Cervical length 3.5 cm or up RR 2.4
Cervical length 2.5 cm RR 6.2
Relative risk of PTL increases as cervical length decreases
How assess cervical length
US
Fetal fibronectin (FFN)-released from the BM of the fetal membranes
Released in response to disruption of the membranes as with uterine activity, cervical shortening or infection
Placental vascular pathway
Immunologic component
Vascular component
Low resistance connection of spiral arteries
Stress strain pathway
Mental and physical stress increase cortisol and catecholamines
Cortisol
From adrenal
Stimulates early placental CRH known to help in labor
Catecholamines
Affect blood flow an can cause uterine contractions
How treat stress strain
Nutrition and stress reduction
Risk factors for uterin stretch
Polyhydramnios
Multiple gestation
Symptoms PTL
Cramps, backache, pelvic pressure, increase in discharge/bloody discharge, uterine contractions
What do when present
Initial-cervical exam to see dilation, effacement and fetal presentation
Look for correctable prob like infection
External monitoring for uterine activity and fetal HR
Oral or IV hydrate
Reevaluate cervic in an hour
Culture for groups strep and gonorrhea and chlamydia (once diagnosis CBC, urinalysis and urine culture)
US
Hydrationa d bed rest
Works 1/5
I f 2 cm an or80 % effaced or made cervical change what do
Tocolysis
Mg sulfate
Nifedipine
Prostagladin synthase inhibitors
Mg sulfate
Yes
Competes with ca for entry into the cell at time of depolarization
IV
NEUROPROTECTIVE (cerebral palsy, )
If less Han 32 weeks
AE MG sulfate mom
Feeling of warmth and flushing NV Respiratory depression -seen with serum levels 12-15 Cardiac conduction
AE fetal mg sulfate
Loss of msucle tone, drowsiness, low APGARs
Nifedipine
Oral suppress preterm labor
Minimal side effects
Inhibits slow, inwar current of ca during the second phase of the action potential
Prostagladin synthetase inhibtiors
Inhibits prostagladin production that induce myometrial contractions
Used on a short term basis
Indomethacin-oral orrectal
AE indomethacin
Oligohydramnios, preterm closure of fetal ductus arteriosus and cause pulmonary HTN
Indomethacin fetal risk
Necrotizing enterocolitis and intracranial hemorrhage
NSADIS
Can decrease uterine activity
Not for primary tratment
When not meet diagnosis preterm labor or after discontinuing mg to decrease prostagladin procuction
When give glucocorticoids for fetal lung maturation
24-34 weeks gestation
Effects last 7 days
Pregnant women between 34 0/7 weeks and 36 6/7 weeks at risk preterm within 7 days and no antenatal corticosteroids
Single course of betamethasone
Vertex presentation PTL
Vaginal delivery preferred
-some recommended c section for very low birt weight
If breech presentation
Increased risk of cord prolapse of compression as well s head entrapment with vaginal delivery therefore most will c section
Prevent PTL
Progesterone IM
Women with previous PTL/PPROM
Smooth msucle relaxant is the thorny
Vaginal progesterone
Used in women with shortened cervix <2.5
Pessary Arabian pessary
Women with short cervix
PROM
Rupture before labor onset at any gestational age
Risk factor PROM
Vaginal/cervical infections
Abdominal membranes
Incompetent cervix
Nutritional defiencies
Diagnose PROM
History! Loss of fluid and amniotic fluid in vagina
Why not check cervix of PROM presumed
Infection
How confirm rupture
Sterile speculum
3 tests to confirm PROM
Pooling
Nitrazine paper
Ferning
False positive nitrazine
Urine, semen, cervical mucous, blood, vaginitis
False negative nitrazine
Remote PROM with no remaining fluid
Minimal leak
Intact amniotic sac
Barrier to infection preventing chirioamniotitis
Maternal risk PPROM
Endomyometritis
Sepsis
Failed induction due to unfavorable cervix
PROM less than 24 weeks
Pulmonary hypoplasia and structural abnormalities from position
Amniotic fluid index less than 5
Oligohydramnios and no fluid is called anhydramnios
Conservative management PPROM
Continue preg until lung mature
Assess lung maturity with vaginal poor of amniotic fluid
Most deliver at 34 weeks
When do most PPROM deliver
34 weeks
Diagnose PROM
Maternal temp 100.4
Fetal maternal tachycardia
Tender uterus
Foul smelling amniotic fluid/purulent discharge
Antibiotic PPROM
IV ampicillin and erythromycin 48 hours
Amoxicillin and erythromycin and amoxicillin 5 days
Tocolytic PPROM
Sure
Steroids PPROM
Reduce risk RDS up to 34 weeks
When type I pneumocytes ok
24 weeks start making surfactant
How tel FLM
Phosphatidylinositol and phosphatidylglycerol from amniocentesis
L/S ration
Greater than 2 is mature
Lecthicin increase rapidly after 35 weeks
What is phosphatidylglycerol is present
Mature lungs
Rapid test FLM
Lamellar body number density assessment
2 hours (6-12 for amniocentesis)
More sensitive and predictive
IUGR
Below the 10% for a given gestational age
Causes IUGR
Maternal, placental, fetal
Maternal IUGR
Poor nutritional intake/maternal low body weight Smoking Drug abuse Alcoholism Cyanosis heart disease Pulmonary insuffiency Antiphospholipid syndrome Hereditary theomvophilias Collagen vascular disease
Placental IUGR
Insufficient substrate transfer through placenta as well defective trophoblast invasion
Conditions that may result in placental insuffiency
HTN, renal disease, placental or cord abnormalities such as velamentous cord, diabetes
Fetal IUGR
Inadequate substrate
-TORCH
Congenital anomalies, multiple gestations, chromosomal abnormalities
Diagnose IUGR
PE fundal height
US biometry
Amniocentesis, percutaneous umbilical blood sampling
Doppler studies
Diagnose IUGR
Serial fundal measurement is primary screening tool
What do if fundal height lags more than 3 cm behind the gestational age then order an
US
US is routinely for high risk conditions that predispose to IUGR
HTN, renal disease, diabetes, drug abuse, antiphospholipid syndrome, lupus
Pre pregnancy IUGR prevent
Optimize disease processes
Antepartum manage IUGR
Decrease modifying factors-improve nutrition, sop smoking, bed rest
Deliver before fetal compromise but after fetal lung maturity monitor:
Non stress test twice weekly, biophysical profile, Doppler studies of umbilical artery
Nonstress test
Patient lateral tilt position, the fetal heart rate is monitored with an external transducer. The tracing is observed for fetal heart rate accelerations that peak at least 15 beats per minute above the baseline and last 15 seconds from baseline to baseline. It may be necessary to continue the tracing for 40 min
When omit nonstress test
All four US components normal
Fetal breathing movements
One or more episodes of rhythmis fetal breathing movements of 30 seconds or more within 30 mintues
Fetal movement
Three or more discrete body or limb movements within 30 minutes
Fetal tone
One or more episodes of extension of a fetal extremity with return to flexion or opening or closing of a hand
Amniotic fluid volume
A single vertical pocket of amniotic fluid exceeding 2 cm is considered evidence of adequate
Each 5 components given score
2
Composite score
8-10
6
Equivocal
4
Abnormal
Doppler study umbilical artery
Vascular impedance
Umbilical flow velocity waveform of normally growing fetuses is characterized by high velocity diastolic flow, whereas with intrauterine growth restriction, there is a dimunition of umbilical artery diastolic flow
What do is suspect IUGR
US-if ok no intervention
US-abnormal intervene
US IUFR and greater than 38-39 weeks
Deliver
US IUFR less than 38-39 weeks
Antenatal testing normal-continue pregnancy
Antenatal testing abnormal -delivery
Antenatal testing normal
Continue preg
Antenatal testing not normal
Deliver
C secretion with IUGR
May benefit
Will need continuous fetal monitor
After birth IUGR
Monitor neonatal blood glucose bc these neonates have less hepatic glycogen stores
Monitor respiratory status as respiratory distress syndrome is more common
Prognosis IUGR
Greater risk DM, HTN, atherosclerosis as adults
Post term preg
Over 42 weeks 10% with a 2-3x high perinatal mortality
Postmaturity syndrome
Related to aging and infarction of the placenta
Loss of subcutaneous fat, long fingernails, dry and peeling skin and abundant hair
Post term also at risk with what
Macrosomia, abnormal labor, shoulder dystocia and c section
Postterm pregnancy etiology
Unsure dates, fetal adrenal hypoplasia, anencephalic fetuses, placental sulfatase defiency, extra uterine pregnancy
41st week
Begin antenatal testing to include twice weekly NST and biophysical profile
If testing abnormal or oligohydramnios induce labor (AFI lesss than 5 cm)
42 week
Induction of labor
Induction of labor at 41 weeks preferred plan
IUFD
Intrauterine fetal demise
Fetal death after 2 weeks but before onset of labor
Most causes IUFD
Unknown
Diagnose IUFD
Suspect if patient complains of absence of fetal movements or if unable to Doppler fetal tones
Confirm by US with lack of fetal activity and absence of fetal cardiac activity
IUFD watchful expectancy
Only up till 28 weeks gestation, spontaneous labor will occur in 2-3 weeks of fetal demise
Manage IUFD
Most will require cervical ripeningwith prostagladin/laminaria/misoprostol/oxytocin
Manage IUFG monitoring of coagulopathy
Patients with IUFD are at risk of disseminated intravascular coagulopathy: need to follow complete blood count, fibrinogen level, PT/PTT/INR
Laminaria
Open up cervix
Follow up IUFD
Look for cause TORCH, parvovirus, listeria, anticardiolipin……
IUFD and future preg
Greater risk reoccurrence
HTN pregnancy
10%
Maternal risk HTN
MI, cardiac failure, cerebral vascular accident, renal failure, hepatic failure
Fetal complications HTN
Fetal growth restriction, preterm birth, placental abruption, stillbirth, neonatal dearth
Normal bp
<120/8-
Stage I
Systolic 130-129 or
Diastolic between 80-89
Stage 2
Systolic at least 140 or diastolic at least 90 mmHg
Chronic
Present before or during 1st half of preg
Gestational htn
After 20 weeks
Preeclampsia
Occurs after 20 weeks gestation and coexists with proteinuria
Eclampsia
New onset seizure activity associated with preeclampsia
Superimposed preeclampsia
Transposed onto chronic HTN
Evaluate chronic HTN
Rule out causes
Look for maternal end organ damage
-CBC, glucose, complete metabolic profile, 24 hour urine collection for total protein, EKG
Assess fetal wellbeing
-US, screening , growth US monthly after 28 weeks, antepartum fetal testing to begin 32-34 weeks gestation
Mild HTN (less than 160/110)
Initiate antihypertensive if reach threshold
Visit every 2-4 weeks until 34-36 weeks and then weekly
Antepartum fetal monitoring
Deliver 39-40 weeks
Severe HTN (greater than 160/110)
Methyldopa, labetalol, nifedipine
When associated with renal disease
24 hr urine collection
Antepartum fetal surveillance
Growth US every 3-4 weeks
Nonstress tests and or biophysical profiles
Severe htn when deliver
38 weeks
HTN without preeclampsia
After 20 weeks gestation
48-72 hrs after delivery
Resolves by 12 weeks
Diagnose preeclampsia
HTN, proteinuria, edema
Symptoms preeclampsia
Scoroma, blurred vision, epigastric and/or right upper quadrant pain, HA
Risk preeclampsia
<20 >35 Primigravid Multiple gestation DM Thyroid HTN chronic Collagen vascular disease Antiphospholipid syndrome Highest of it
Bran preeclampsia
Cerebral edema
Heart preeclampsia
Absence of normal intravascular volume expansion
reduction in circulating blood volume
Lungs preeclampsia
Noncardiogenic pulmonary edema
-changes in colloid osmotic pressure, capillary endothelial integrity, and intravascular hydrostatic vessels
Liver preeclampsia
Sinusoidal fibrin depositio in periportal areas with surrounding hemorrhage and portal capillary thrombi
Subscapularis hematoma-> liver rupture
Stretching of glisson’s capsule results in right upper quadrant pain
Kidney preeclampsia
Swelling and enlargement of glomerular capillary endothelial cells
Narrowing of capillary lumen
Eyes preeclampsia
Retinal vasospasm
Retinal edema
Mild preeclampsia
Proteinuria >300 mg/24 hr uring but less than 5 gm/24 hr or single specimen uring protein: cr ration of .3 mg/dL
Asymptomatic
Severe preeclampsia
Proteinuria 5gm/24 hr or 3+ protein on two random urine dips at least 4 hours apart
Oliguria from renal insuffiency
Symptomatic-cerebral or visual, pulmonary edema, epigastric or right upper quadrant pain, elevated liver enzymes, thrombocytopenia
Oliguria
Renal insuffiency
What do if have preeclampsia
HISTORY of htn or renal disease
Address HA, ab pain, n/vom vaginal bleeding, vision
PE finding preeclampsia
Brisk reflexes, clonus, edema
Lab finding preeclampsia
Increased hematocrit, LD, ALT AST, uric acid
Thrombocytopenia (low paltelet0
Manage severe preeclampsia les than 37 weeks
Bed rest, 1 BPP or twice NST weekly antepartum testing
Fetal growth US every 3-4 weeks
Office visits and laboratory evaluation
Possible hospitalization
Manage severe preeclampsia 37-40 weeks
If favorable cervix induction
If unfavorable cervix use a cervical ripening agent to begin induction
Manage immediate severe features preeclampsia
Immediate hospitalization, delivery if greater than 34weeks
Hydralazine, labetalol, nifedipine
If less than 37 weeks administer corticosteroids and work towards delivery as long as patient and fetus are stable
Intrapartum management
Vaginal delivery
Cervical ripening agents and pitocin as necessary
Mg sulfate for seizure prophylaxis
Pain management as with delivery useless thrombocytopenia then may not be able to receive an epidural
Mg sulfate
Loading dose for preeclampsia 4 gm
Maintenance dose 2 gm/hr
Therapeutic value 5-9 mg/dL
Why not give mg sulfate over 7-8 mg/dL
Loss patellar reflexes, respiratory paralysis, cardiac arrest
How revers mg sulfate
Calcium glucoronate
Fluid restriction with mg sulfate
Prevent overload
Eclampsia
1-3 per 1000 patients
Most seizures 1-2 min and 24 hours before delivery
What do eclampsia
Protect airway is first
First line treatment eclampsia
Mg sulfate
Persistent aclampsia
Lorazepam
HELLP
Hemolysis, elevated liver , low platelets
Severe preeclampsia patients and 50 % eclampsia
Symptoms HELLP
Right upper quad pain, epigastric pain, n/v , HTN, proteinuria
Prevent eclampsia
Asprin
Relaxation uterus
Increase cAMP
Contraction uterus
Increase intracellular Ca
Promote interaction of actin and myosin causing uterine contractions
Two segments of the uterus during labor
Upper segment-actively contracts and retracts to expel the fetus the lower segment-along with cervic becomes thinner and passive
Cervix change in labor
Soft pliable, dilateble structure
-these structural changes from collagenous is, incrase in hyaluronic acid, decrease in dermatan sulfate which favors increased water content
Labor
Regular uterine contraction of sufficient intensity, frequency, and duration to bring about demonstratable effacement and dilation of the cervix
First stage of labor
Onset of contractions to full dilation of cervix
Second stage
Full dilation of cervix to delivery of the infant
Third stage
Delivery of the infant to delivery of placenta
Latent phase
Cervical softening and effacement occurs with minimal dilation
Active phase
Starts when cervix is dilated to 4 cm
This phase of labor includes both cervical dilation and ultimately, descent of the presenting fetal part
Acceleration phase
Deceleration phase
Protraction of a phase of labor
Slower than normal
Arrest disorder of labor
Complete cessation of progress
An arrested latent phase
Labor has not begun
Dysfunctional labor
Rates of dilation and descent exceed times of normal labor
Normal limits of latent phase for nulliparous and multiparous
Up to 20 hrs
Up to 14 hrs
Prolonged latent phase effect
Little
Etiology of prolonged latent phase
Without substantial cervical change
Excessive use of sedatives or analgesics
Fetal malposition
Manage abnormal latent phase
Rest
Morphine
Normal limits of fetal descent nulliparous and multiparous
Nulliparous 1 cm/hr
Multiparous 2 cm/hr
Protraction of fetal descent (active phase)
Less then what is expected
No change in descent has occurred in 1 hr
Arrest has occurred
Risk of perinatal mortality latent vs active phase
No increased risk
Etiology of active phase abnormalities
Inadequate uterine activity
Cephalopelvc disportion
Fetal malposition
Anesthesia
Dystocia
Difficult labor/dysfunctional labor
Three P of active phase of labor
Power, passenger, passage
When not make a diagnosis of dystocia
Not be made before an adequate trial of labor has been tried
Augmentation
Refers to stimulation of uterine contraction when spontaneous contraction have failed to result in progressice cervical dilation or descent of the fetus
When consider augmenting
Contractions less than 3-10 minute period and or intensity is less then 25 mmHg
What give for protraction
Oxytocin
After look at maternal pelvis, fetal position, station, maternal and fetal status
Intrauterine pressure catheter for assessing 3P of active phase
Soft plastic catheter placed transcervically
Gives precise measurement of the intensity of the uterine contractions in mmHg
IUPC requires what
Membranes to be ruptured
Benefits. IUPC
Augment labor, allows assessment of meconium status
Risk IUPC
Cord prolapse, prolonged rupture is associated with chorioamnionitis
Minimal effective uterine activity
3 contractions in a 10 minutes period averaging 25 mmHg abover baseline
Montevideo units (MVU)
Calculated by measuring the peaks of contractions in mmHg in a 10 min period
> 200 MVU
For at least2 hours
Before c section
Document adequate contractions at least for 4 hours
Pitocin
FDA approved medicine for labor stimulation
MOA pitocin
Stimulates uterine contractions
Increase intracellular Ca in
When is uterus most sensitive to pitocin
20-40 weeks
How long for pitocin to take effect
20-30 min
Cephalopelvic disproportion
Disparity between the size of the maternal pelvis and the fetal head that preculdes vaginalis delivery
CPD causes a failure of descent and sometimes engagement of the head
Nulliparous women who present in labor wth an unengaged head indicate an increased likelihood of CPD
Gynecoid and anthropoid pelvis have good prognosis for delivery
Pubis are how>90
Ischial tuberosity>8.5
Diagonal conjugate>11.5
Prominence of ischial spines
Presentation other than ___ are abnormal in labro
Vertex occiput anterior (OA
How get to OA
Fetal head enters and engage the maternal pelvis in occipitotransverse position then rotated to OA
What if no go to AO
Rotate to OP or stay OT
Macrosomia, shoulder dystocia, fetal anomalies
Also dystocia
Persistent OT
No rotate to OA
Caused by CPD, android or platypelloid pelvis, relaxed pelvic flood (epidural
Transverse arrest of descent
Persistent OT position with arrest of descent for a period of 1 hr or more
Why arrest OT
Deflection positions the occipitofrontal diameter 11 cm becomes presenting diameter
+1 +2 stations
Occipitofrontal
11 cm
Head deflected
Seen in OT and OP
Manage OT if pelvis adequate, infant not macrosomia and contractions are inadequate
Oxytocin
Rotation manuallly or keilland forceps
Manage OT if pelvis inadequate or infant macrosomia
C section
Persistent OP position
Most go to OA in labor
OP labor usually normal if not may have prolonged second stage , more back discomfort
Manage OP
Prolonged labor in second stage
Delivery of head often occurs spontaneously
Or operative vaginal delivery -vacuum or forceps
Macrosomia
Over 4500 g
Account for 1.5% of births
Large for gestational age
Birth weight equal to or greater then 90% for a given gestational age
How diagnostic macrosomia
US imprescise
Hydrocephalus
May cause enlargement of the head that makes vaginal delivery impossible
Usually see with US
Fetal ascites or enlargement of fetal organs (liver) can result in a dystocia secondary to enlarged fetal abdomen
Immune. Hydrops Rh isoimmunization is most common
Nonimmune hydrops-caused by congenital infections, chromosomal abnormalities or fetal arrhythmias
Locked twins
Baby a breech, baby b vertex
3 p
Power passage passenger
LGA
Birth weight >90% for gestational age
Macrosomia
> 4500 grams
Risk factors for macrosomia
Maternal diabetes, previous history, maternal pre preg obesity, weight gain, mulitparity, male fetus, >40 weeks, maternal birth weight, maternal height, maternal age <17 years , +50 g glucose screen with a negative 3 hr
Maternal morbidity with macrosomia
C section
Post partum hemorrhage and significant vaginal lacerations
Fetal morbidity and mortality
Shoulder dystocia, fracture clavicle, damage to nerves of brachial plexus (c5, c6) resulting in era duschenne , brachial plexus injuries are rare and majority resolve without any permanent injury
Brachial plexus injuries and macrosomia
Increase 21x
Err duschenne
Upper arm palsy
Most common brachial plexus injury
C5 c6
Klumpke
Lower arm palsy
Damage c8-t1
Paralysis entire arm
All four nerve roots
> 5000 grams non diabetic
>4500 grams diabetic
C section
Shoulder dystocia
Delivery that requires additional obstetric maneuvers following failure of gentle downward traction on the fetal head to effect delivery of the shoulders
Cause of shoulder dystocia
Impaction of the anterior fetal shoulder behind the maternal pubic symphysis or the impaction of the post shoulder on the sacral promontory
Turtle sign
Retraction of the delivered fetal head against the maternal perineum
Antepartum risk factors shoulder dystocia
Fetal macrosomia Maternal diabetes Obesity Post term gestation Short stature Previous history macrosomia Previous history of shoulder dystocia
During labor risk for shoulder dystocia
Labor induction
Epidural analgesia
Prolonged labor
Operative vaginal deliveries
Neonatal risk shoulder dystocia
Erbs most common, klumpke, fractured clavicle or humerus, hypoxic, death
Mcroberts maneuver
Hyperflexion and abduction of the maternal hips
Suprapubic pressure
May dislodge the impacted anterior shoulder
Do not apply fundal pressure
Zavanelli maneuver for shoulder dystocia
Cephalic replacement, last resort, poor prognosis significant risk of fetal morbidity and mortality
Rubin maneuver shoulder dystocia
Place pressure on an accessible shoulder to push it toward the anterior chest wall fo the fetus to decrease the bisacrominal diameter and free the impacted shoulder
Woods corkscrew maneuver
Apply pressure behind the posterior to rotate the infant and dislodge he anterior shoulder
Zavanelli maneuver
Last resort
Fetal head manually returned to its prostitution position
Slowly replaced int he vagina by steady upward pressure
Delivery is by emergent c section
What do with shoudler dystocia
Obstetric emergency
Call for help, team
Can NOT be predicted or prevented and most accurate in absence of macrosomia
Predict shoulder dystonia
Can’t
Initial maneuver shoulder dystocia
Mcroberts and suprapubic
Dizygotic twins
Two separate ova are fertilized by two separate sperm
Distinct pregnancies coexisting in same uterus
Each have own amnion, chorion and placenta
Monozygotic twins
Arise from cleavage of a single fertilized ovum at various stages during embryogenesis
Arrangement of fetal membranes and placentas will depend on the time at which hte embryo divides
Time of cleavage
Scab 0-3 dichorionic dimniotic 4-8 days monochorionic diamniotic 9-12 monochorionic, monoamniotic >13 days conjoined twins
Most monozygotic twins are what
Monochorionic diamniotic
Most serious
Monochorionic monoamniotic
Not separating amnions
Cord entanglement , mortality 50-80%
Craniopagus
Joined at the cranium
Thoracopagus
Joined chest wall most common
Ischiopagus
Joined at the coccyx and sacrum
Dizygotic twins influence
2x more likely after 35
Familyhistory
Most spontaneous twins dizygotic
When suggest multiple gestations
HCG higher than normal
Uterus palpated larger
Pregnancy has occured after ovulation induction or in vitro fertilization
Confirmwith US
Increased risk of what with monozygotic
Congenital anomalies Weight discordance Twin twin transfusion syndrome Neurologic sequelae Preterm delivery Fetal demise
Determination of zygomatic is the most important step after after diagnosing twins
Diagnosing
Dizygotic
Different fetal gender
Visualization of a thick amnion chorion septum
Peak or inverted V sign at the bae of the septum
Monozygotic
Dividing membrane is fairly thin
If US is not definitive in determining zygomatic
Inspect placenta after delivery
DNA analysis
Conjoined twins
Cleavage occurs 13-15 days
1 in 70,000 deliveries (ratio of females to males is 3:10
Mortality rates 50%
C section
Advancement of imaging allows mapping of shared organs and more successful surgical separation procedures
Elective termination if cardiac or cerebral fusion is identified
Interplacental vascular anastomoses
90% occur in monochorionic twins
Most common type is arterial arterial followed by arterial-venous and then venous venous
Vascular communications between the 2 fetuses through the placenta can cause several problems
-abortion polyhydramnios, TTTS, fetal malformations
Twin twin transfusion
Results secondary to uncompensated arterial-venous anastomoses in a monochorionic placenta
-which leads to a net transfer of blood flow going from one twin to the other
Fetal complications donor twin
Hypovolemia, hypotension, anemia, oligohydramnios, growth restriction
Recipient twin TSS
Hyperbole is, polyhydramnios rhomboids, HTN, polycythemia, edema, and cardiomegaly , congestive heart failure
Baby bad twin twin transfusion
Both twins are at risk of demise bc of heart failure
Diagnose TTTS
US
Donor twinUS
Smaller stuck appearance
Oligohydramnios
Recipient twin US
Larger
Polyhydramnios
Ascites
Treat TTTS
Serial amniocentesis with amniotic fluid reduction
Laser photocoagulation of the anastomoses vessels on the placenta
Fetal malformations arterial to arterial anastomosesarterial blood flow fromt he donor twin enters the arterial circulation of hte recipient twin
The reversed blood flow may cause thrombosis within critical organs or atresia due to trophoblastic embolization
Recipient twin being perfused in a reverse direction with poorly oxygenated blood fails to develop normally. It is known as acardiac twin (ACARDIAC)
ACARDIAC twin
Fully formed lower extremities
No anatomic structures cephalic of the abdomen
Umbilical cord abnormalities
Primarily associated with monochorionic twins
Absence of umbilical artery
Velamentous umbilical cord insertions occur more frequently
Absence of umbilical artery
Associated with renal agenesis
Retained dead fetus syndrome
Incidence of single fetal death in utero up to 5%
If gestation is 20 weeks or greater retained dead fetus syndrome can develop
- disseminated intravascular coagulopathy in the mother
- check platelets and fibrinogen levels weekly
Vanishing twin syndrome
Vanishing twin syndrome if gestation is <12 weeks and dead fetus reabsorbed
Maternal polyhydramnios
Polyhydramnios anemia, HTN, preeclampsia, gestational diabetes, preterm labro, c section, postpartum hemorrhage, uterine atony
Fetal complications of multiple gestations
Prematurity, malpresentaiton, placental previa, placental abruption, PROM, umbilical cord prolapse, IUGR, congenital, incrase perinatal morbidity and mortality
Manage first and second trimester
2 week office visits
US cervical length assessments
Third trimester
Cervical length of less than 25 mm at 24-28 weeks doubled the risk for premature birth in twins
Serial US to check for intrauterine growth q 4-6 weeks begin at 24 weeks.
Looking for discordant fetal growth
—defined by a 20% reduction in fetal weight of the smallest fetus compared with the largest
Antepartum testing testing (NSTs or weekly BPPs)
Often patients will be placed on bed rest
Monoamniotic twins should be delivered 32 weeks
Secondary to increase risk for lethal cord entanglement
Hospitalization at 26 weeks, antenatal steroids, and fetal heart rate monitoring several times daily
Most twins deliver when
35-36 weeks
If no complications when deliver twins
38 weeks
What have before intrapartum management
Delivery room equipped for c section
Large IV bore needle, blood products
Capability to monitor fetal heart rates
Anesthesiology
US to determine precise presentations of the twins
Two pediatricians/NICU personnel one for each Abby
Nurses
Vertex vertex presentations
Presenting twin is designated twin a and secondtwin b
After delivery 1st cord clamped and cut
Vaginal exam to assess station of second
-second twin is at increased risk of cor prolapse, placental abruption and malpresentation
Careful attention to fetal monitoring is necessary
After seen twin delivers obtain cord samples and deliver placenta
Be prepared for hemorrhage
Vertex transverse and vertex breech are usually delivered by
C section
Breech breech and breech vertex twins are delivered
C section
High perinatal mortality in singletons
Secondary to prematurity and congenital anomalies
RDS, intracranial hemorrhage
Birth asphyxia-second twin 2 x the perinatal mortality then the first born twin and are 4x more likely then first to die from birth trauma complications
Stillbirths
2x more frequently then in singletones
Cerebral palsy
Most in twins
Size twins
Shorter and lighter until 4 years old
Triplets quadruples
ART,
Prematurity increases
As number of fetus grow
Deliver triplets
C section
Fetal malpresentation most common
Breech
Breech
Fetal butt or lower extremities presents into the maternal pelvis
Most common factor for breech
Prematurity
Diagnoseis breech
US, Leopoldo, pelvic exam
Frank
Most common presentation
Thighs flexed
Lower extremities are extended at knees
Complete breech
Thighs are flexed
Lower extremities are flexed
Incomplete breech
1 or both thighs are extended
1 or both feet are below the bout
External cephalic versio
Applying pressure to moms abdomen to turn the fetus in either a forward or backward somersault to achieve a vertex presentation
Who gets ECV
36 weeks
Contraindication ECV
Placental previa
Non reassuring fetal monitoring
Oligohydramnios
Previous uterine surgery that is contraindication for vaginal delivery
Where do ECV
Hospital equipped for c section
Prepare for ECV
NPO 7 hrs IV access Continuous monitor NST BPP Confirmbreech with US Consider tocolytics
Vaginal delivery breech
Frank or complete >37 weeks 2500-4000 grams Fetal head flexed Adequate maternal pelvis No maternal or fetal contraindications for vag Anesthesia
Standard care breech
All c section
Assisted breech vaginal delivery: two hands
NO aggressive traction can cause deflection of the fetal vertex and increase risk of head entrapment or nuchal arm entrapment
Assisted breech vaginal delivery: after spontaneous expulsion to scapula one hand
YES external rotation of each thigh combined with opposite rotation of the fetal pelvis restyles in flexion of the knee and delivery on the leg
Wrap towel around fetus for better traction
When scapula appears under the symphysis.
The operator reache over the left shoudler , sweeps the arm across the chest and delivers the arm
Delivery head breech
Gentle traction maintain cephalic flexion by applying pressure on fetal maxilla NOT fetal mandible
Forceps for breech
Piper forceps
Breech presentation delivery
C section preferred esp pre term
Don’t want fetal asphyxia
Outcomes breech
Perinatal mortality higher than forvertex fetuses
Lethal congenital anomalies, prematurity, birth trauma and asphyxia are common
Brown presentation
Presenting part of the fetus is between the facial orbits and anterior fontanelle
- presenting diameter is the supraoccipitomental diameter
- frontal bones are te point of designation
Brow presentation change before birth
Usually to a face presentation through extension or vertex presentation throug flexion
Persistent brow
Vaginal delivery impossible CSECTION
Persistent brow
C section
Brown supraoccipitoental diameter vs vertex
- 5
9. 5
Face presntation
Fulle xtension of the fetal head and neck with occiput against upper back
Incidence face
1.500
Can be seen in frequently with fetal malformations
-anencephaly is seenin 1/3 of face presentation
Fetal chin is chosen as point of definition for face
Most present mentum anterior and can deliver vaginally
Can NOT deliver vaginally menum posterior presentation
-will need to proceed with c section
Face trachelobregmatic diameter face vs vertex
12.6 cm
9,5 cm
Face
C section
Compound presentations
Fetal extremity found prolapsed alongside the presenting fetal part (head)
Premature
Compound presentation with failureto progress, cord prolapse, non reassuring fetal status
C section
Initial evaluation antepartum hemorrhage if bleeding profusely
Knowledgeable team for hemodynamically stability and correct cause
2 large bore IV
Access vitals, bleeding, mental status
What history for antepartum hemorrhage
Known bleeding disorders, liver disease, anatomic abnormalities, and abnormal placentation
Labs for profuse post partum hemorrhage
CBC and coagulation profile
Serial H and H
Type and crosmatch
Type and crossmatch 4 units of blood
PRBC
When can you do a digital exam
Avoid until placenta previa has been ruled out by US
Sterile speculum exam
Genital lacerations or cervical lesions
Digital exam
Cervical dilation
How assess entire situation
US-placenta location, rsetnation of fetus
Amount of bleeding, maternal status, gestational age, continuous electronic fetal monitoring
Vaginal bleeding before 20 weeks cause
Abortion ectopic clot
Vaginal bleeding after 20 weeks upper genital tract
Placental abruption
Placenta previa
Uterine rupture
Vasa previa
Vaginal bleeding lower genital tract
Bloody show labor Cervical polyps Infection Trauma Cancer vulvar varicosities Blood dyscrasia
Placenta previa
Implantation of placenta over cervical os
Most common placental prob
Presentation placenta previa
Painless vaginal bleeding
Risk factors placenta previa
Maternal age >35
Multiparity geation
Cocaine smoking
Prior previa, previous c section
Marginal placenta previa
Edge of the placenta extending to the margin of cervical os
But does not cover the os
Partial placenta previa
Partial occlusion of the cervical os by the placenta
Complete placenta previa
Cervical os completely covered by the placenta
Most serious type and is associated with greater blood loss
Classic presentation placenta previa
Painless bleeding at 30 weeks
How diagnose placenta previa
US
What do if have since 4-5% have is at 24 weeks
Repeat US at 30 weeks
Do msot placenta previa resolve
90% by 32-25 weeks by placental migration
Which previa least likely to resolve
Third trimester
Manage preterm preg with placenta previa
Fetal maturation is goal
Manage in hospital and bed rest and if bleeding stops cn go home but 70% recur bleed
Placenta previa. 36-37 weeks
C section if fetal lung maturity
If unstoppable labor and placenta previa, fetal distress, or hemorrhage
C section immediately regardless of gestational age
How stabilize patient with placenta previa
Hospitalize, IV access
2 large bore needles if bleeding profuse
H/H type and cross
PT PTT fibrinogen
RH neg-kleihauer-betke test, give rhogam if need
How prepare for catastrophic hemorrhage
Serial blood draws , NPO statins, type and cross 4 units
Placenta previa prepare for preterm delivery
Prior to 34 weeks give antenatal steroids (betamethasone) tocolysis can be used in stable
Placenta accretion
Abnormal firm attachment to the superficial lining of the myometrium
Most common
Placenta incretins
Invades myometrium
Placenta percreta
Through the myometrium into the uterin serosa
Least common
Previa without prior uterine surgery
Incidence of accreta is 4%
Ok
Risk factors
Previous c section
C hysterectomy
Placenta abruption
Premature separation of the normally implanted placenta
Most common third trimester bldeeding
Painful bleeding, uterine tenderness, uterine hyperactivity, and fetal distress and/or death
Symptoms placenta abruption
Painful bleeding, uterine tenderness, uterine hyperactivity, fetal distress and /or death
Risk factors placental abruption
Maternal HTN*
Cocain
Blunt trauma
Polyhydramnios and multiparity
Previous abruption
Diagnose placenta abruption
Painful vaginal bleeding, uterine tenderness and uterine hyperactivity and fetal distress or death
US can detect, but better for previa
Manage placenta abruption
Monitor fetal and maternal condition s
If both stable
Vaginal delivery—rapid delivery often ensues after abruption
If remote from vaginal delivery with signs of fetal distress or uncontrolled bleeding proceed with c section
Abruption os mst common cause of DIC in pregnancy
Results from the release of thrombophlebitis from the disrupted placenta and subplacental decidua causing consumptive coagulopathy
DIC occurs in 20%
Ok
Stabilize placenta abruption patien
HostpiatIV access
2 large bore 16 guage if bleeding profusely
H/H type and cross
PT PTT fibrinogen, platelets
RH neg consider kleihauer Bette test, give rhogam if indicated
Prepare for catastrophic hemorrhage
Serial blood draws
NPO status
Type and cross 4 units
Prepare for preterm delivery
Prior to 34 weeks give antenatal steroids
Tocolysis can be used to stabilize
Couvelaire uteris with placenta abruption
Extravasation of blood into the uterus
Causing red and purpl discoloration of the serosa
Uterine rupture
Complete separation of the uterine musculature through all layers
Cause uterine rupture
Spontaneous, traumatic ,associated ith previous uterine scar
Uterine rupture sequelae
Fetal mortality or permanent neurologic sequelae
Risk factors uterine rupture
Prior uterine incision
Injudicious use of oxytocin
Trauma
External cehoali version
Multiparity
Diagnose uterine rupture
Rupture associated with sudden onset of intense abdominal pain vaginal bleeding
Abnormal fetal heart rate pattern of cessation of fetal heart tones
Regression
Fetal parts may be easily palpable on abdominal exam
Manage uterine rupture
Immediate laparotomy and delivery of fetus
If feasible repair ruptured site
If large rupture may have to do c section
Uterine rupture and future preg
C section
Recurrence rate! Upper segment recurrent more common than lower though
Fetal bleeding in 3rd trimester causes
Rupture fetal vessel secondary to velamentous insertion of umbilical cord
Most common cause of third trimester bleeding
Rupture of fetal vessel
How does cord insert
At a distance away from the placenta and its vessels must transverse between the chorion and amnion without the protective Wharton’s jelly
Vasa previa
Unprotected vessels pass over the cervical os
Signs vessel rupture
Acute vaginal bleeding with a change in fetal heart rate .
What do if rupture
Diagnose rapidly and proceed to delivery
Define postpartum hemorrhage
> 500 cc following vaginal birth
>1000 cc following a c section
Primary postpartum hemorrhage
In first 24 horus
Secondary to uterine atony
Secondary postpartum hemorrhages
24 hours to 12 weeks
Can occur with subinvolution of the uterus, sloughing of the Escher or retained products
Can core than half of all maternal deaths occur in_
24 hours
Leading cause of maternal death worldwide
Postpartum hemorrhage
Etiology primary postpartum hemorrhage
Uterine atony
Retained placenta espicially accreta
Defects in coagulation
Uterine inversion
Secondary etiology
Subinvolution of placental site
Retained products of conception
Infection
Inherited coagulation defects
Risk factors postpartum hemorrhages
Prolonged labor Augmented labor Precipitous laborhistory of postpartum hemorrhages Placental abruption Placental previa Vag delivery
Uterine atony post partum hemorrhages
Immediately preceding or after delivery of placenta
Most PPH are due to it
Excessive blood loss most commonly result when the uterus fails to contract after delivery of placenta. Palpation-boggy uterus
Risk factor uterine atony
Enlargement of the uterus
Abnormal labor
Conditions which interfere with contraction of the uterus
-leiomyoma and mg sulfate
Effects hemostasis after separation of the placenta is dependent on what
The myometrium to comrpession the severed vessels(spiral arterioles and decidua veins)
Manage uterine atony
Bimanual massage uterus
Oxytocin, methylergovinins, hemabate, dinoprostone, misoprostol
Uterine packing or large volume balloon catheter
Interventional radiology
Surgical measure/hysterectomy
Bimanual massage
Confirms diagnosis
Boggy!
Massage of the uterine corpus can dismiss bleeding, expel blood clots and allow time for other measured to be implemented
Uterine packing
4 inch gauze layer back and forth from one course to other using sponge stick
Large volume balloon
Interventional radiology
Patient has stable vitals and persistent bleeding may be a candidate for arterial embolization
Surgery
Is last resort, if patient desires future fertility may try to lighten uterine arteries
If unstable proceed with total abdominal hysterectomy
Second most common cause of postpartum hemorrhage
Trauma during delivery
What do if genital tract trauma
Inspect for vaginal, perineal, periurethral and cervical lacerations
Repair surgical
Retained placenta
Most of secondary PPH have it
-bleeding is secondary to inability of uterus to maintain a contraction and involuted normally around the placental tissue
Risk factor retained placenta PPH
Previous c section, leiomyoma, prior d and c, and accessory placenta lobe
Treatment retained placenta
Manual removal if bleeding is profuse
+/- uterine curettage with or without US guidance be careful not to perforate
Uterine inversion
Top of fundus descends into the vagina and sometimes through the cervix
-if occurs before placenta is delivered DO NOT remove placenta until inversion is corrected
Iatrogenic uterine inversion
Improper management of third stage
Uterine inversionsymptom
Copiousbleeding and hypovolemia shock
Treat postpartum hemorrhroage
Anesthesiologist
Manually replace the uterus
Once replaced start oxytocin to cause the uterus to contract
Rarely paratotomy
Amniotic fluid embolism
80% mortality rare
Caused by infusion of amniotic fluid into maternal circulation
Characterization amniotic fluid embolism
Respiratory distress, intense bronchospasm, cyanosis, cardiovascular collapse, hemorrhage, coma
Treat amniotic fluid embolism
Respiratory support, correct the hypovolemia shock and replace coagulation factors
Von williebrans
Inherited coagulopathy with prolonged bleeding times
Factor VIII defiency
Treat Von williebrand
Factor VIII concentrate or cryoprecipitate
Idiopathic thrombocytopenia
Platelets function abnormally and have a shortened life span
Causes thrombocytopenia an tendency to bleed
Circulating antiplatelet antibodies of igg type can occasionally cross placenta resulting in fetal and neonatal thrombocytopenia
Treat idiopathic thrombocytopenia
Require platelet concentration infusions
Puerperal sepsis
Following delivery women can develop a febrile morbidity
Febrile morbidity
Temps100.4 or higher that occurs for more than 2 consequetive days during first 10 postpartum das
Most fevers
Endometriosis
After delivery , the pH of the vagina becomes more alkaline
Alkaline pH after birth
Favors growth of aerobic organisms
About 48 hours after delivery the endometrial and placental remnants produce a favorable intrauterine environment for the production of anaerobic bacteria
Most organisms that cause peurperal infection
Anaerobic organisms
Cocci, (peprostrep, peptococcus, streptococcus)
Mixed with abcteriodes fragilis
Aerobic-e coli
Predisposing factors for puerperal sepsis
Poor nutrition and hygiene
Anemia
PROM
Prolonged rupture of membranes
Prolonged labor
Clinical features peurperal sepsis
Postpartum fever and increasing uterine tenderness on postpartum day 2 OT 3 are the key clinical findings
-purulent lochia, child, malaise, anorexia
Diagnose peurperal sepsis
Careful history and physical
Extreapelvic causes of fever should be excluded
Treat peurperal sepsis
Antibiotic treatment
Anaerobic coverage since more scommon
Ampicillin and gentamicin
Major pathogen resistant to this is bacteriodes fragilis, which is sensitive to clindamycin
Septic pelvic thrombophlebitis
Physiologic conditions for the pathogesis of thrombosis
Endothelial damage, venous stasis, hypercoagulable state of preg
Ovarian vein thrombophlebitis
Fever and ab pain within 1 week after delivery or surgery
Clincial ovarian vein thrombophlebitis
Fever, abdominal pain, localized to the side of the affected vein
How see ovarian vein thrombophlebitis
Ovarian vein on radiography
Deep septic pelvic vein theombophlebitis
Unlocalized fever int he first few days that is non responsive to antibiotcs
Clincial deep septic pelvic vein theombophlebitis
So not appear CLINCIALLY ill
See deep septic pelvic vein theombophlebitis
No radiographically evidence of thrombosis
Diagnosis of exclusion
Treat septic pelvic theombophlebitis
Anticoagulation is though to prevent further thrombosis
Unfractioned heparin or low molecular weight heparin
Discontinue after resolution of fever x 48 hrs
If ovarian vein thrombosis is seen radiographicallytrat
Anticoagulatnts 6 weeks
Repeat imaging to evaluate for persistence
