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In the Name of God

Obstetrics Study Guide 3

Mitra Ahmad Soltani 2008

References

Iranian Council for graduate Medical Education. Board and pre-board Exam questions for OBS and Gyn .2001-2006 Panda S . IUGR. Department of Obstetrics & Gynecology Medical College of India 2002 Pritchard JA, MacDonald PC, Gant NF. Williams Obstetrics. 22nd ed. New York, NY: McGraw-Hill; 2005. Tan T and Yeo G. IUGR. Current Opinion in Obstetrics and Gynecology 2005, 17: 135142

emedicine e-journal:
Butler J. postterm delivery. emedicine. June 19. 2006 Gaufberg S. Abruptio placenta. emedicine. Aug 29. 2006 Gibson P. HTN in Pregnancy. emedicine. DEC 13 2007 Hernandez E . GTN. emedicine. Jan 26, 2007 Marinnan G. Placenta Previa. emedicine. Aug 26. 2005 Ross M. preterm. emedicine. 31 may 2007

Pictures and material of multiple pregnancy are adapted with permission from:
Zach T. multiple pregnancy.emedicine. Oct 2. 2007

HTN in Pregnancy

classification
Hypertension is the most common medical problem encountered during pregnancy, complicating 2-3% of pregnancies. HTN is classified into 4 categories 1) chronic hypertension, 2) preeclampsia-eclampsia, 3) preeclampsia superimposed on chronic hypertension 4) gestational hypertension (transient hypertension of pregnancy or chronic hypertension identified in the latter half of pregnancy).

Chronic HTN
blood pressure exceeding 140/90 mm Hg before pregnancy or before 20 weeks' gestation. It persists after 12 wks postpartum.

Gestational Age
New-onset or worsening hypertension after 20 weeks' gestation should lead to a careful evaluation for manifestations of preeclampsia. The diagnosis of severe hypertension or preeclampsia in the first or early second trimester necessitates exclusion of GTD and/or molar pregnancy.

Maternal Risk factors


First pregnancy New partner/paternity Age younger than 18 or older than 35 years History of preeclampsia Family history of preeclampsia in a firstdegree relative Black race Obesity (BMI >35) Interpregnancy interval less than 2 years or more than 10 years Chronic hypertension Preexisting diabetes (type 1 or type 2) Renal disease SLE Obesity Thrombophilia

Placental Risk factor


Multiple gestations Hydrops fetalis Gestational trophoblastic disease Triploidy

BP measurement
Blood pressure should be measured in the sitting position, with the cuff at the level of the heart. Women should be allowed to sit quietly for 5-10 minutes before each blood pressure measurement. Korotkoff sounds I (the first sound) and V (the disappearance of sound) should be used to denote the systolic blood pressure (SBP) and DBP, respectively.

Indications of preg. termination


Mild Diastolic blood pressure Proteinuria Headache Visual disturbances Upper abdominal pain Oliguria Convulsion Serum Cr thrombocytopenia Liver enzyme elevation <100mmhg Trace to 1+ Absent Absent Absent Absent Absent Normal Absent Minimal Severe 110 mmhg or higher Persistent 2+ or more present present Present Present Present Elevated Present Marked

IUGR
Pulmonary edema

Absent
Absent

Present
present

CBC
Platelet counts less than 100,000/L suggest preeclampsia or ITP. Hemoglobin levels greater than 13 g/dL suggest hemoconcentration. Low Hbg levels may be due to microangiopathic hemolysis or iron deficiency.

Proteinurea
Trace levels to +1 proteinuria are acceptable, but levels of +2 or greater are abnormal and should be quantified with a 24-hour urine collection or spot urine protein:creatinine ratio. In a 24-hour urine collection, the reference range for protein excretion in pregnancy is up to 300 mg/d.

Protein:Cr ratio
Creatinine clearance increases approximately 50% during pregnancy, and levels less than 100 mL/min suggest renal dysfunction that is either chronic or due to preeclampsia.
protein:Cr ratios appear to be more accurate than urinalysis, although an abnormal result should still be confirmed with a 24-hour urine collection.

Coagulation tests
LDH, bilirubin, haptoglobin, fibrinogen, D-dimers If: PT/INR/aPTT results are abnormal, thrombocytopenia is present, the hemoglobin level is dropping

Fetal Monitoring Alternate a biophysical profile with a fetal NST twice each week. Ask for Serial fetal ultrasound starting at 18 weeks.

Methyldopa (Aldomet)

Centrally acting antihypertensive agent widely considered the first-line agent for treatment of hypertension during pregnancy.

250 mg PO bid/tid; increase q2d prn; not to exceed 3 g/d

Hydralazine (Apresoline) Intravenous form is useful when treating severe hypertension due to preeclampsia/eclampsia.

10-20 mg/dose IV q4-6h prn initial; increase to 40 mg per dose prn BP >170/110 mm Hg: 0.1-0.2 mg/kg/dose IV q4-6h prn; not to exceed 20 mg or 1.7-3.5 mg/kg/d IV divided q4-6h

Life-threatening complications in preeclampsia


Seizures Cerebral hemorrhage Pulmonary edema Acute renal failure DIC HELLP syndrome Hepatic infarction/rupture and subcapsular hematoma

IMP: mild preeclampsia


General: condition/position/diet =low salt,high prot Lab: CBC ,BG, Rh, U/A,24hr urine (prot,cr,vol), BUN/Cr, PT,PTT,Fib, ALT,AST,Al P, Bil (T, D) reserve of 2 units of PC IV :Ringer at heparin lock OTHER: Control of vital sign q4hrs, control of FHR, FAD chart , NST, sono OB, daily weight inform if BP>160/110, blurred vision, head ache, epigastric pain, seizure

IMP: Severe preeclampsia


General: condition/position/diet =NPO Lab: CBC ,BG, Rh, BUN/Cr, PT, PTT,Fib ,ALT,AST,Al P, Bil (T, D) prep 2 units of PC IV :Ringer 1000cc +10 u of oxytocin if BP>160/110,blurred vision, head ache, epigastric pain, seizure then amp hydralazine 5 mg iv prn

MgSO4 (4 gr) in 200cc DW5% in 20 min then 10 gr(1/2) im in each buttock then 5 gr im q4h If platelet is below 100000 then 20 gr in 1000cc infused in 100cc/hrs (check of I/O, RR, DTR, prep CPR set with 2 gr 20% MgSO4 ready) +Amp Dexa 6 mg bid for 4 doses OTHER: Control of vital sign q15 min , control of FHR, fix foley,

Preterm Pregnancy

Definition
Preterm labor is defined as the presence of uterine contractions of sufficient frequency and intensity to effect progressive effacement and dilation of the cervix prior to term gestation (between 20 and 37 wk). It is the leading cause of neonatal mortality.

Causes of preterm Labor


decidual hemorrhage, (eg, abruption, mechanical factors such as uterine overdistension from multiple gestation or polyhydramnios), cervical incompetence (eg, trauma, cone biopsy), uterine distortion (eg, mllerian duct abnormalities, fibroid uterus), cervical inflammation (bacterial vaginosis [BV], trichomonas), maternal inflammation/fever (eg, urinary tract infection), hormonal changes (eg, mediated by maternal or fetal stress), Uteroplacental insufficiency (eg, hypertension, insulindependent diabetes, drug abuse, smoking, alcohol).

Risk factors of preterm birth


Demographic factors for preterm labor include nonwhite race, extremes of maternal age (<17 y or >35 y), low socioeconomic status, and low prepregnancy weight. Preterm labor and birth can be associated with stressful life situations (eg, domestic violence; close family death; insecurity over food, home, or partner; work and home environment) Previous preterm delivery

Methods for predicting preterm birth


home uterine activity monitoring (HUAM)

salivary estriol : DHEA increases before the onset of labor. This results in an increase of maternal estriol.
FFN is a basement membrane protein that helps bind placental membranes to the decidua. FFN has a predictive value in identifying patients who will or will not deliver within the subsequent 1-2 weeks.

A short cervical length in the early or late second trimester has been associated with a markedly increased risk of preterm labor and delivery.

Contraindication to tocolysis
1-Fetal growth restriction 2-Oligohydramnios 3-Nonreactive NST,Positive CST 4-Absent or reversed diastolic flow upon Doppler examination of umbilical blood flow 5-Repetitive severe variable decelerations 6-Significant vaginal bleeding consistent with abruption.

Definition of IAI (Intra Amniotic Infection)


A temperature greater than 38.0C (100.0F) and 2 of the 5 following signs: 1-WBC > 15,000 cells/mm3 2-Maternal HR> 100 (bpm) 3- Fetal HR> 160 bpm 4-Tender uterus 5-Foul-smelling discharge

Chorioamnionitis Order
General: condition/position/diet=NPO Lab: CBC diff, MP, WW, B/C X2, U/A , U/C,CXR,BUN/Cr IV : 1000cc Ringer +10 units of oxytocin start at 2 drops /min, add 2 drops every 15 min if FHR and contractions are normal
Amp ampicillin 2gr iv qid +gentamicin im 80mg stat then 60 mg TDS AMP clindamycin 900 mg iv TDS for allergic women to penicillin(continue antibiotics after delivery until the mother is a febrile

OTHER: Control of vital sign hourly

IMP:PLP before 37 weeks out patient:


(contractions 4 in 20 min or 8 in 60 min +progressive change in cervix cervical dilation of more than one cervical effacement of more than 80 % or greater)

if: Check of contractions:+ U/A, U/C: Fern:Then: Hydrate and sedate

Stop of contractions: discharge With:isoxsuprine 10 mg TDS for 10 days

Contractions persist: hospitalize Next slide

IMP:PLP before 37 weeks, hospitalized


General: condition/position/diet Lab: CBC, BG, Rh, U/A, U/C, fern, reserve of 2 units of PC IV : 1-1000cc Ringer free 2-MgSO4 (4 gr) in 200cc DW5% in 20 min then 20 gr in 1000cc infused in 100cc/hrs (check of I/O, RR,DTR, prep CPR set- I/O with measure) 3-Amp pethidine 25 mg iv 25 mg im 4-Amp ampicillin 2 gr IV qid 5-Amp erythromicin 400 mg QID 6- Amp betamethasone 12 mg im, repeat after 24 hrs for GA below 34 wks

OTHER: Control of vital sign q4hrs, Inform if LP, leakage, VB, ab VS or FHR

Contraindication for beta mimetics


Maternal cardiac disease Diabetes Thyrotoxicosis HTN

Contraindication for MgSO4


Hypocalcemia Myasthenia gravis Renal failure

Dosage of Ritodrine or Terbutaline for tocolysis


50-100 mcg/min increase by 50 mcg/min every 10 min max dose:350mcg/min If labor is arrested continue the infusion for at least 12 hrs SC: 250 mcg q3-4 hrs

Length of GA with multiple fetuses


Twin=36 wks Triplets=33.5 wks Quadruplets=31 wks

Postterm

Definition of postterm
Postterm pregnancies define pregnancies extending up to or after 42 weeks. The reported frequency is 3-12%.

Cause of postterm P.
The most frequent cause of postterm pregnancy is inaccurate dating criteria primiparity, prior postterm pregnancy, male gender of the fetus, genetic factors

Risks of postterm P
Macrosomia complications like shoulder dystocia, CPD and Maternal risks like an increase in labor dystocia, perineal injuries, and cesarean deliveries. dysmaturity syndrome: affects 20% of postterm fetuses and is thought to be caused by chronic uteroplacental insufficiency resulting in oligohydramnios, meconium aspiration, and reversible neonatal complications.

surveillance
NST and AFI 2 times per week for pregnancies continuing past 41 weeks.

Intra Uterine Growth Retardation

Definition
Intrauterine growth restriction (IUGR)
occurs when the unborn baby is at or below the 10th weight percentile for his or her age (in weeks). The fetus is affected by a pathologic restriction in its ability to grow.

Low birth weight (LBW) means a baby


with a birth weight of less than 2500Gms, which could be due to IUGR or Prematurity

Classification
Symmetricl
the baby's head and body are proportionately small. may occur when the fetus experiences a problem during early development.

Asymmetrical
baby's brain is abnormally large when compared to the liver. may occur when the fetus experiences a problem during later development

Etiology of IUGR
Idiopathic- In a majority of cases (40%)

Maternal Risk Factors


Has had a previous baby with IUGR Extremes of age Small mothers (Ht & Wt) poor weight gain and malnutrition during preg. socially deprived Substance abuse (like tobacco,narcotics, alcohol) low total blood volume during early pregnancy

Maternal Risk Factors


Multiple pregnancy Living in High altitude locations Drugs like anticoagulants, anticonvulsants Cardio-vascular disease:preeclampsia, HTN, cyanotic heart disease, cardiac disease Gr III & IV, diabetic vascular lesions Chronic kidney disease Chronic infection- UTI, Malaria, TB, genital infections Antibody abnormality like antiphospholipid antibody syndrome, SLE

Fetal Risk Factors


Intrauterine infection:German measles (rubella),
cytomegalovirus, herpes simplex, tuberculosis, syphilis, or toxoplasmosis, TB, Malaria, Parvo virus B19.

Birth defect (cardiovascular, renal, anencephally, limb defect, etc). Chromosome defect(trisomy-18 (Edwards
syndrome),21(Downs syndrome), 16, 13, xo (turners syndrome.)

Primary disorder of bone or cartilage. Chronic lack of oxygen during development (hypoxia). Developed outside of the uterus. Placenta or umbilical cord defects.

Placental Factors
Uteroplacental insufficiency: Improper / inadequate trophoblastic invasion and placentation in the first trimester. Lateral insertion of placenta. Reduced maternal blood flow to the placental bed.

Fetoplacetal insufficiency due to:


Vascular anomalies of placenta and cord Decreased placental functioning mass:

Small placenta, abruptio placenta, placenta previa, post term pregnancy.

Screening:
US fetal biometry: HC- BPD- AC

Uterine Doppler studies (Doppler Velocimetry): bilateral notches and a mean resistance index of at least 0.55 Or Unilateral notches and a mean resistance index of at least 0.65 at 20 weeks. Biochemistry: CRH level at 33 weeks

Neonatal Diagnosis
Low ponderal index (Wt./Fl). Decreased subcutaneous fat. Presence / appearance of
Hypoglycemia, Hyperbilirubinemia, Necrotizing enterocolitis, Hyper viscosity syndrome

Prevention
Strong evidence of benefit only for the following interventions:
balanced protein/energy supplementation, strategies to reduce maternal smoking, antibiotic administration to prevent urinary tract infections antimalarial prophylaxis.

Surveillance
Non-Stress Test, Amniotic Fluid Index, Doppler of the Umbilical Artery Biophysical Profile

Surveillance

Amniotic Fluid Index (AFI)

The current recommendations are that if the AFI decreases below 5 after 35 weeks, then delivery should occur.

Treatment
Bed rest Aspirin before 20 wk GA Nutritional supplementation: zinc , fish oil, hormones Oxygen therapy.

For cases termination is indicated:


Corticosteroids with a delay in delivery for 2.4 days Mode of delivery depends on the bishop score and IUGR severity For dichorionic twins : injection of KCl into the heart of the weaker fetus ( in most cases management is expectant)

For monochorionic twins photocoagulation of anastomoses or diathermy in cases of TTTS and AAA

Short Term Risks of IUGR for the neonate


Meconium Aspiration Syndrome, infection, hypoglycemia, hypothermia, Sudden Infant Death Syndrome,

Long term Prognosis


Fetal Death low blood sugar low body temperature abnormal development of the nervous system Adulthood aftermath : CAD HTN Diabetes II Dyslipidemia Stroke Depression Suicide attempts

abruptio

Definition
Abruptio placentae (ie, placental abruption) refers to separation of the normally located placenta after the 20th week of gestation. Abruptio placentae occurs in about 1% of all pregnancies.

Symptoms and signs


Vaginal bleeding - 80% Abdominal or back pain and uterine tenderness 70% Fetal distress - 60% Abnormal uterine contractions (eg, hypertonic, high frequency) - 35% Idiopathic premature labor - 25% Fetal death - 15%

Classification of abruptio
extent of separation (ie, partial vs complete) location of separation (ie, marginal vs central) Clinical

classification
Class VB Uterus BP-HR coagulopathy tenderness Fetal distress

0 1 2(I=27%)

mild mild Mild-mod

--------mild Modsevere

NL NL Tilt +

--------------------------------------Hypofibrinogene present mia (ie, 50-250 mg/dL)


death

3(I=24%)

Mildsevere

tetanic

shock Fib<150 mg/dl

Causes1
Maternal HTN(44% of all cases) Maternal trauma Cigarette smoking Alcohol consumption Cocaine use Advanced maternal age

causes2
Short umbilical cord Sudden decompression of the uterus (eg, PROM, delivery of first twin) Retroplacental fibromyoma postamniocentesis Idiopathic (probable abnormalities of uterine blood vessels and decidua)

Imaging Studies
Ultrasonography is not very useful in diagnosing placental abruption.
Retroplacental hematoma may be recognized in 225% of all abruptions. Recognition of retroplacental hematoma depends on the degree of hematoma and on the operator's skill level.

IMP: R/O abruption


Condition/position/diet:NPO Lab: CBD-BG-Rh-U/A-U/C-PT-PTT-Fib-FDP-D-DimerPrep 4 units of crossmatched packed red blood cells Prep 5 units of platelets, prep 10 units of FFP Continuous high-flow supplemental oxygen One or 2 large-bore IV lines with normal saline (NS) or lactated Ringer (LR) solution+10 units of oxytocin in 1 lit of ringer start at 2 drops/min add 2 drops every 15 min if fetal heart rate and uterine contractions are favorable. perform amniotomy Closely observe the patient. Monitor vital signs and urine output, fetal heart rate and uterine height measurement. Prepare OR for emergent C/S

Placenta Previa

subtypes
(1) complete or total: the placenta covers 360 of the internal cervical os; (2) incomplete or partial: 0-360 of the internal cervical os is covered by placental tissue; (3) marginal: the placental tissue does not cover the internal cervical os; (4) low lying: the edge of the placenta lies abnormally close to but does not abut the internal cervical os.

Risk factors
prior placenta previa, prior cesarean delivery, increased maternal age, large placentae (eg, multiple gestations or erythroblastosis), maternal history of smoking.

Frequency
1 in 200 deliveries

Vaginal Bleeding
painless vaginal bleeding during the second half of pregnancy (70%). It can occur without an inciting cause, although pelvic examination, intercourse, or labor may provoke it. The average gestational age at presentation is 32 weeks. Hemorrhage recurs, and, in nearly all cases, it is more severe the second time.

management
Patients are treated expectantly, with: volume replacement, transfusions, tocolytics, emergent cesarean delivery Without endangering the life of the mother, all attempts are made to delay delivery until the fetal lungs mature.

Preferred Examination
Physical examination should be performed only with a fetus that has achieved pulmonary maturity and only in a fully staffed operating room.

Preferred examination
TA sonography is the test of choice to confirm placenta previa. When the internal cervical os cannot be visualized or when the results are inconclusive, transperineal or transvaginal sonography is recommended as an adjunct. No increased risk of hemorrhage has been associated with transvaginal or transperineal sonography in this clinical setting.

Blood loss classifications

Class 1 Blood Loss Volume (mls) in adult Blood Loss % Circ. blood volume Systolic Blood Pressure Diastolic Blood Pressure

Class 2

Class 3

Class 4

750mls

800 - 1500mls

1500 - 2000mls

>2000mls

<15%

15 - 30%

30 - 40%

>40%

No change

Normal

Reduced

Very low Very low / Unrecordable

No change

Raised

Reduced

Pulse (beats /min)

Slight tachycardia Normal Normal >30

100 - 120

120 (thready)

>120 (very thready)

Capillary Refill Respiratory Rate Urine Flow (mls/hr)

Slow (>2s) Normal 20 med-ed-online - 30 2007

Slow (>2s) Raised (>20/min) 10 - 20

Undetectable Raised (>20/min) 0 - 10

Estimated blood loss

Suitable fluid regimes

1000 mls

3000 mls crystalloid

o r

1000 mls colloid

1500 mls

1500 mls crystalloid & 1000mls colloid

o r

4500 mls crystalloid

2000 mls

1000 mls crystalloid, 1000mls colloid & 2 units blood


med-ed-online 2007

o r

3000 mls crystalloid & 2 units blood

Multiple pregnancy
Pictures and material of multiple pregnancy are adapted from: Zach T. multiple pregnancy. emedicine. Oct 2. 2007 with permission

pathophysiology1
Dizygotic twins(fraternal) are produced when 2 sperm fertilize 2 ova. Separate amnions, chorions, and placentas are formed in dizygotic twins. The placentas in dizygotic twins may fuse if the implantation sites are proximate. The fused placentas can be easily separated after birth. Monozygotic twins (Identical)develop when a single fertilized ovum splits during the first 2 weeks after conception. An early splitting (ie, within the first 2 d after fertilization-30%) of monozygotic twins produces separate chorions and amnions. These dichorionic twins have different placentas that can be separate or fused.

Diamniotic/dichorionic placentation

pathophysiology2
Later splitting (ie, 3-8 d after fertilization) results in monochorionic/diamniotic placentation . Approximately 70% of monozygotic twins are monochorionic/diamniotic.

Diamniotic/monochorionic placentation

pathophysiology3
If splitting occurs even later (ie, during 9-12 d after fertilization), monochorionic/monoamniotic placentation occurs . Monochorionic/monoamniotic twins are rare; only 1% of monozygotic twins have this form of placentation.

Monoamniotic/monoamniotic placentation

pathophysiology4
Monochorionic/monoamniotic twins have a common placenta with vascular communications between the 2 circulations.

pathophysiology5
Trizygotic triplets occur when 3 sperm fertilize 3 ova. Dizygotic triplets develop from one set of monozygotic cotriplets and a third cotriplet derived from a different zygote. Finally, 2 consecutive zygotic splittings with one split results in a vanished fetus and monozygotic triplets.

Frequency
The birth rate of monozygotic twins is constant worldwide (approximately 4 per 1000 births). Birth rates of dizygotic twins vary by race. (Highest in Africans and lowerest in Asians)

mortality
low birth weight infants( due to prematurity and (IUGR) congenital anomalies, placenta previa, abruptio placenta, preeclampsia, cord accidents, malpresentations, asphyxia/perinatal depression, group B streptococcal (GBS) infections, hyaline membrane disease (HMD), TTTS.

History
excessive weight gain, hyperemesis gravidarum, sensation of more than one moving fetus use of ovulation-inducing drugs family history of dizygotic twins

Neonatal Lab Studies


CBC count: In TTTS, the donor twin is frequently anemic at birth. The recipient twin is polycythemic at birth. Calcium level: Hypocalcemia is common in premature infants, especially the donor twin in TTTS. Glucose level: Hypoglycemia is common in premature infants, especially if TTTS is present. Bilirubin level: Hyperbilirubinemia due to TTTS may develop in polycythemic infants.

TRAP
Twin reversed arterial perfusion (TRAP) sequence occurs when an acardiac twin receives all of the blood supply from the normal "pump" twin. This only occurs in monochorionic twins.

TTTS
Occurs in monochorionic/monoamniotic or monochorionic/diamniotic twins. Vascular anastomoses in the monochorionic placenta result in transfusion of blood from one twin (ie, donor) to the other twin (ie, recipient). Polyhydramnios develops in the sac of the recipient twin and oligohydramnios develops in the sac of the donor twin.

Conjoined twins
Incomplete late division of monozygotic twins produces conjoined twins. Classification:
Thoracopagus - Joined at chest (40%) Xiphopagus/omphalopagus - Joined at abdomen (34%) Pygopagus - Joined at buttocks (18%) Ischiopagus - Joined at ischium (6%) Craniopagus - Joined at head (2%)

Discordant
. Birth weight discrepancies of more than 20-25% are considered discordant. Discordant birth weights occur in 10% of twins.

Gestational Trophoblastic Neoplasia

classification
hydatidiform mole : is the most common form of gestational trophoblastic neoplasia it can behave in a malignant or benign fashion, invasive mole (chorioadenoma destruens), choriocarcinoma, and placental site trophoblastic tumor (PSTT).

Clinical course
In 80% of patients with a benign hydatidiform mole, serum HCG titers steadily drop to normal within 8-12 weeks after evacuation of the molar pregnancy. In the other 20% of patients with a malignant hydatidiform mole, serum HCG titers either rise or plateau.

staging
Stage I Confined to the uterus Stage II Limited to the genital structures Stage III Lung metastases Stage IV Other metastases

WHO prognostic criteria1


Age 40 years or older = 1 point Antecedent pregnancy terminated in abortion = 1 point Antecedent full-term pregnancy = 2 points Interval of 4 months to less than 7 months between antecedent pregnancy and start of chemotherapy = 1 point Interval of 7-12 months between antecedent pregnancy and start of chemotherapy = 2 points Interval of more than 12 months between antecedent pregnancy and start of chemotherapy = 4 points

WHO prognostic criteria 2


Beta-HCG level in serum is 1000 mIU/mL but less than 10,000 mIU/mL = 1 point Beta-HCG level in serum is 10,000 mIU/mL but less than 100,000 mIU/mL = 2 points Beta-HCG level in serum is 100,000 mIU/mL or greater = 4 points Largest tumor is 3 cm but less than 5 cm = 1 point Largest tumor is 5 cm or greater = 2 points Site of metastases is spleen or kidney = 1 point

WHO prognostic criteria3


Site of metastases is gastrointestinal tract = 2 points Site of metastases is brain or liver = 4 points Number of metastases is 1-4 = 1 point Number of metastases is 5-8 = 2 points Number of metastases is more than 8 = 4 points Prior chemotherapy with single drug = 2 points Prior chemotherapy with multiple drugs = 4 points

Sign and Symptoms


Patients with a hydatidiform mole present with signs and symptoms of pregnancy.
The most frequent symptom of gestational trophoblastic neoplasia (GTN) is abnormal uterine bleeding. Patients have a history of amenorrhea. Occasionally, the typical hydatid vesicles (edematous villi) are passed through the vagina.

Sign and Symptoms


Prolonged hyperemesis gravidarum preeclampsia Hyperthyroidism signs and symptoms associated with the metastatic disease, such as hematuria, hemoptysis, abdominal pain, and neurologic symptoms

Physical Exam
a positive pregnancy test result occurs in the absence of a fetus. vesicles in the vagina is diagnostic Enlarged ovaries secondary to theca lutein cysts are found in up to 20% of cases.
The cysts regress after evacuation of the hydatidiform mole for 12 weeks.

Cause
A hydatidiform mole occurs when a haploid sperm fertilizes an egg that has no maternal chromosomes and then duplicates its chromosomal complement.
Most complete hydatidiform moles are 46,XX, and all the chromosomes come from the male. Of hydatidiform moles, 10-15% are 46,XY. This occurs when 2 sperm, 1 carrying an X and the other carrying a Y, fertilize an "empty" egg.

Partial moles are 69,XXY, and 2 sets of chromosomes are of paternal origin.

Medical care1
Emergency department care involves : starting intravenous (IV) fluids (crystalloids) sending blood for type and antibody screen Rh-negative patients should receive antiRhD immune globulin, such as RhoGAM, if not already immunized

Medical Care2
Patients with benign do not require medical therapy. observing patients with weekly serum HCG titers. Only patients with rising or plateauing titers should be treated with chemotherapy.

Medical care3
Patients with malignant nonmetastatic or metastatic lowrisk GTN are treated with single-agent chemotherapy like MTX or actinomycin D in patients with poor liver function During treatment, the serum HCG titers are monitored every week. One additional course of chemotherapy is administered after a normal serum HCG titer. After 3-4 normal serum HCG titers, the titers are followed once per month for 1 year. A switch from MTX to actinomycin D is made if the patient receiving MTX for nonmetastatic or metastatic low-risk GTN develops rising or plateauing serum HCG titers.

Medical care4
Patients with high-risk metastatic are subdivided into 2 groups:
In patients with a WHO score of less than 8, a combination of MTX, actinomycin D, and cyclophosphamide can be used. This is known as the MAC regimen. This chemotherapeutic regimen is administered every 19-21 days (from day 1 of the previous chemotherapy cycle) until the serum HCG titers normalize.

Medical Care5
Patients with WHO scores of 8 or higher are treated with a combination of etoposide, MTX, and actinomycin D administered in the first week of a 2-week cycle and cyclophosphamide and vincristine (Oncovin) administered in the second week. This is known as the EMA-CO regimen. Two additional courses of EMA-CO or EMA-CE are administered after a normal serum HCG titer in very high-risk patients.

Medical care6
Patients with metastasis to the brain receive whole brain irradiation (3000 cGy) in combination with chemotherapy. Corticosteroids (Decadron) with systemic effect are administered to reduce brain edema. Patients with liver metastasis are considered for liver irradiation (2000 cGy).

Surgical care
The treatment of a hydatidiform mole is evacuation of the uterus by suction and sharp curettage.
To avoid excessive bleeding, oxytocin is administered intravenously at the initiation of the suctioning of the uterine contents. The largest possible suction curet is used, usually a 10F or 12F.

Further Care
Obtain follow-up serum HCG titers : once per week until 3-4 normal values are obtained. Then, obtain them once per month for 6 months. Have patients use reliable contraception, such as oral contraceptives or depot progesterone injections, during the period of follow-up care.

Prognosis1
Nonmetastatic GTN has a cure rate with chemotherapy of close to 100%. Metastatic low-risk gestational trophoblastic neoplasia has a cure rate with chemotherapy of close to 100%. Metastatic high-risk gestational trophoblastic neoplasia has a cure rate with chemotherapy of approximately 75%. After 12 months of normal HCG titers, less than 1% of patients with malignant gestational trophoblastic neoplasia have recurrences.

Prognosis2
The rate of occurrence of a repeat molar pregnancy is approximately 1-2%. The rate of occurrence of a repeat molar pregnancy in a patient with a history of 2 previous hydatidiform moles is approximately 10-20%. The pregnancy rate after chemotherapy with MTX and cyclophosphamide is 80%. Of women treated with EMA-CO, 46% have had at least 1 live birth after chemotherapy. Patients who become pregnant after treatment for GTN should have a pelvic ultrasound early during the pregnancy to confirm that the pregnancy is normal.

PREGNANT DIABETICS

ADAPTATION TO PREGNANCY
In early pregnancy Estrogen and Progesterone stimulate beta cell hyperplasia and increased insulin secretion Glycogenolyis and peripheral utilization increase The net result is relative hypoglycemia

GLUCOSE LEVELS IN NORMAL PREGNANCY

Fasting levels decline by 10 11 mg/dl Postprandial levels rarely exceed 120-140 mg/dl Glucose excursions with meals 30 35 mg/dl Marked increase in insulin levels with feeding

CHO METABOLISM 20- 24 WEEKS

Increased human placental lactogen diabetogenic Increased prolactin insulin resistance Increased cortisol decreased glycogen storage

OTHER METABOLIC CHANGES


Stable amounts of FFA Increased cholesterol and TG Reduced amino acid levels

MATERNAL COMPLICATIONS
Retinopathy Nephropathy Chronic hypertension Preeclampsia

RETINOPATHY
Remains the leading cause of blindness in women ages 24-64 Every patient with pre-gestational diabetes should have a retinal examination in early pregnancy Laser therapy is safe and effective during pregnancy Has a variable course during pregnancy

NEPHROPATHY
Accounts for 1/3 of the deaths in diabetics < 31 Renal findings are present as early as 1-2 years after diagnosis Creatinine clearance may improve in pregnancy due to increased renal blood flow Proteinuria may increase substantially

CHRONIC RENAL FAILURE


Pregnancy is possible even in patients requiring hemodialysis Reliable contraception is advised Fertility and successful pregnancy outcomes are reduced with serum Cr > 2.0

CHRONIC HYPERTENSION
Should be aggressively controlled ACE inhibitors are contraindicated Calcium channel blockers are probably a reasonable alternative and are safe during pregnancy Increases the incidence of fetal growth restriction and superimposed preeclampsia

PREECLAMPSIA
BP > 140/90 Proteinuria > 300 mg/24 hours or increase in baseline May be difficult to diagnose in the presence of renal disease and chronic HTN 25% incidence of superimposed disease with CHTN

SEVERE PREECLAMPSIA
BP > 180/110 Proteinuria > 5 g/24 hours Lab: elevated LFTs. thrombocytopenia Sxs: headache, epigastric pain, blurred vision Oliguria, pulmonary edema, fetal growth restriction

PREGNANCY COMPLICATIONS
Hydramnios Spontaneous abortions Congenital malformations Macrosomia Diabetic ketoacidosis Neonatal metabolic complications

HYDRAMNIOS
1-2 % in normals and 18% of diabetics Fetal osmotic diuresis is etiologic May also be due to fetal cardiac CNS malformations May be associated with preterm labor ?Associated with level of glycemic control

SPONTANEOUS ABORTIONS
In well controlled patients the rate is similar to the non-diabetic Glycosylated hemoglobin levels are higher in women who have a SAB Higher rates of spontaneous abortion in diabetics with vascular disease

CONGENITAL MALFORMATIONS

Associated with periconceptual glucose control In general the rate is 2-3 x that of the nondiabetic gravida No increase when the father is diabetic Fuel mediated teratogenesis

TYPES OF CONGENITAL MALFORMATIONS

Fetal cardiac anomalies may be complex CNS Spina Bifida, Anencephaly Caudal regression syndrome Must consider family history of other malformations that are unrelated to DM

GLYCOSYLATED HGB AND MALFORMATIONS


HBA1C <8.5% , 3.4% malformations HBA1C > 8.5% , 22.4 % malformations Reflects glucose control over the preceeding 60 90 days

MACROSOMIA
Seen more frequently with GDM and IDDM without vascular complications Related to level of 3rd trimester glucose control May occur in up to 25% of diabetics

DIABETIC KETOACIDOSIS
Seen in type I DM Infection, fever, beta agonists are frequent predisposing factors Suspected with +serum ketones and blood glucose levels above 300 Fetal distress is common

NEONATAL METABOLIC COMPLICATIONS Hypoglycemia Hypocalcemia Hypothermia Hypomagnesemia Hyyperbilirubinemia

PRECONCEPTION COUNSELING

Tight periconceptual control is essential The diabetes should be stable Multidisciplinary team maybe helpful Diabetic education Dietary counseling Assessment of renal function Retinal exam

PRECONCEPTION GLUCOSE CONTROL

Fasting blood glucose < 100 mg/dl Pre-meal levels <110 mg/dl Post-meal levels <140 150 mg/dl Avoid wide swings in control Normalize hemoglobin A1C

PREVENTION OF MALFORMATIONS

Normal glucose levels Folic acid supplementation Dose: 4 mg/day from 1 month pre-pregnancy to 12 weeks

FOLIC ACID
All women of reproductive age should consume at least 0.4 mg of folic acid High risk women should consume 4 mg/day This reduces the risk of neural tube defects Newer evidence suggests a lower risk of facial clefting and congenital heart disease as well

INDICATIONS FOR HOSPITALIZATION

Persistent nausea and vomiting Significant maternal infection DKA Poor control/compliance Preterm labor

ASSESSMENT OF FETAL WELL-BEING


Daily fetal movement counting Twice weekly NST by 32 weeks At least weekly assessment of AFV OR Weekly biophysical profiles With more advanced disease, earlier testing is recommended

FIRST PRENATAL VISIT


Routine prenatal lab Baseline 24 hour UA for protein and Cr Clearance Baseline retinal exam EKG Thyroid function tests in Type 1 Diabetics Hemoglobin A1C Schedule 10-12 week USN

EARLY PREGNANCY CARE


Diabetic education and dietary instruction Multi-disciplinary care is helpful Calibrate reflectance meters Adjust caloric needs for pregnancy and lactation Review benefits of physical activity

TIMING OF DELIVERY
Well controlled IDDM: at term Poorly controlled: after documentation of fetal lung maturity If fetal surveillance reassuring, delivery before 39 weeks should be unusual

INTRAPARTUM GLUCOSE CONTROL

No breakfast the morning of induction Establish IV with D5/.45% NaCl at 125 cc/hour Capillary blood glucose levels every 1 2 hours Begin continuous infusion of insulin with levels above 120 mg/dl Avoid fluid boluses with D5

SHOULDER DYSTOCIA
BW (g) < 4000 4000-4499 No diabetes(%) 0.1-1.1 1.1-10.0 Diabetes(%) 0.6-3.7 4.9-23.1

> 4500

4.1-22.6

20.0-50.0

NERVE INJURY
Rate varies from 4-40% following shoulder dystocia Most (90%) resolve without sequelae Can occur with EFW < 4000 g Can occur in utero and therefore not preventable by cesarean

POSTPARTUM GLUCOSE CONTROL

Insulin requirements may fall 50% in the 1st 24 hours Little need for treatment if under 200 mg/dl

CONTRACEPTION
Reliable contraception should be offered Low-dose combination OCPs do not significantly impair carbohydrate metabolism Progestin only oral contraceptives appear to accelerate the development of Type 2 DM in women with gestational diabetes Barrier methods and even IUD may be acceptable

ACOG Low Risk


Age < 25 Not a member of an at risk ethnic group (Hispanic, African, Native American, South or East Asian, Pacific Islanders) BMI < 25 (non-obese) No history of abnormal glucose tolerance or FH No adverse outcomes

Screening
If FBS is 110-126: Then 1 hr 50 gr or 3 hrs 100 gr remember 105 195165---145

Summary
Every practice should adopt a screening strategy, either by historical or laboratory means Screening best between 24-28 weeks Remember to screen post delivery

Some diabetic cases

Bita Hazrati
A PLP case complicated by HTN and GD
24 yrs old G2 P1 L0 D1/ first fetal loss due to preterm c/s delivery ( because of placenta previa) GA on admission 32-33 w CC: LP ( contractions mild/20 seconds D/ 2 in a 10- minute interval) WB: Intact ROM: - ( detected by Fern test) Reduced fetal movement: -

Ph E: PR= 86/min RR:16/min T:36 BP= 140/90 mmHg BS: FBS=112 /10am=134 /4pm=145 /8pm=163

20-30 units total : 2/3 intermediate 1/3 regular Morning: 10 units of NPH- 4 units of regular Afternoon: 4 units of NPH 4 units of regular

FBS is used to adjust evening NPH 2-hr PP (10 am) is used to adjust morning Regular Afternon preprandial (4 pm) is used to adjust morning NPH 2hr PP is used to adjust evening Regular

What is your management of this combined case of : 1- preeclampsia 2- GD 3- PLP

Answer: Mg so4 Ampicillin+ Erythro Isoxsuprine Sedation

FBS-BS NST-FAD-OB US (AFI and GA) Insulin

Which is true about gestational diabetes?

A-This happens during pregnancy with FBS less than 105 mg/dl. Its treatment is insulin. B-It is a kind of type 2 diabetes. C- All cases will develop overt diabetes within 20 years. D- It happens because of reduced pancreas b cell function. Ans:B

Which is an independent cause of IUFD in diabetes?

A-hydramnios B-abruptio C-oligohydramnios D-oxygen and metabolites transportation Ans:D

Which is not a good method of contraception in a diabetic woman?

A-LD OCP B-medroxy progesterone acetate C- HD OCP D-norplant Ans:C

What is the test for a 30 year old 10 wk pregnant woman whose FBS is 85/ 2hr PP is 125?

A- 3 hr GTT B-Repeat of FBS and 2hr PP next week. C-Repeat of FBS and 2hr PP in 24-28 wk. D-Repeat of FBS and 2hr PP in 34 wk. Ans: C

Which is not a cause of PIH for a diabetic pregnant woman?

A-poor blood glucose control B-albuminurea C-high creatinine D-chronic HTN Ans: A

What is the most common cause of perinatal mortality in diabetic pregnancies?

A- malformations B- RDS C-metabolic errors D- IUFD Ans:A

What is one stage screening test for diabetes in pregnancy?

A-100 grs oral glucose in 24-28 wk. B-50 grs oral glucose in 20-22 wk. C-75 grs oral glucose in 18-20 wk. D-25 grs oral glucose in 30-32 wk. Ans:A

What is your plan for a 35 wk diabetic pregnant woman whose BP is 140/90 mmHg/ is on 60 units of insulin /FBS=120 mg/dl?

A-increasing the insulin dose B- no treatment C-hospitalization and adjusting insulin dose D-termination of pregnancy Ans:C

What is your management of a 30 yr old 35 wk pregnant woman class R diabetic with severe retinopathy?

A-termination of pregnancy B-Laser photocoagulation C- high dose steroids D-No action is needed now.

Ans:B

Which is not among the complications of type A2 diabetes in pregnancy?

A- macrosomia B-increased C/S C- still birth D-malformations Ans:D

A woman with a history of gestation diabetes is asking for follow-up management after her delivery. Her FBS is 108 mg/dl and 2hr PP 135 mg/dl. What do you suggest?

A-repeat of FBS and 2hr PP a year after delivery. B- repeat of FBS and 2hr PP 3 yrs after delivery. C-GTT with 100 grs glucose. D-HbA1C 6 months after delivery. Ans:B

In a woman with overt diabetes , BS is reported to be 130 mg/dl . What do you suggest for her IV infusion?

A- RL and DW5% B-RL and DW5% +insulin 1 unit/hr C-NS +insulin 1.5 units/hr D- NS+insulin 2 units/hr Ans:B

Points to remember about diabetic labor:

BS below 100 mg/dl : no insulin is needed 100-140 mg/dl:1 unit insulin 140-180 mg/dl:1.5 units insulin 180-220 mg/dl:2 units insulin More than 220 mg/dl:2.5 units insulin

BS more than 140 mg/dl needs NS as IV infusion

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