1. Split 1st heart sound
2. Middiastolic murmur
3. Shift of apex beat to 4th ICS and outwards
4. Decr peripheral vascular Resistance.

1. Mitral stenosis
2. Aorti c aneurysm
3. PDA
4. Transposition of great vessels

1. 8 wks
2. 10 wks
3. 14 wks
4. 22 wks

1. Pulmonary stenosis
2. Mitral stenosis
3. VSD
4. ASD

1. NYHA class>3
2. Obstructive lesion of the heart (mitral valve and aortic valve <1 cm²
3. Previous H/O heart failure
4. Ejection fraction <40%.

• P2L2 patient, on the 3rd postoperative day of caesarean develops sudden cardiac failure.
  • – She has weakness, shortness of breath, palpitation, nocturnal dyspnea and cough.
  • – O/E- Tachycardia, arrhythmia, peripheral edema, pulmonary rales are present. S3 is present but no murmur is heard.
  • – She had been a booked patient with regular antenatal check-ups and with no prior heart problem and uneventful prior obstetric history.

 

• Hemoglobin A 1c: 10.8%
• Glucose: 222 mg/dL
• Thyroid-stimulating hormone: 1.0 µU/mL
• Free thyroxine: 1.7 ng/dL
• Creatinine: 1.1 mg/dL.

1. Asymptomatic bacteriuria
   7
2. Preeclampsia
3. Congenital adrenal hyperplasia
4. PPH after delivery
5. Shoulder dystocia

1. Susceptibility for infection
2. Fetal hyperglycemia
3. Congenital malformations in fetus
4. Neonatal hypoglycemia

• 0 (fasting): 90 mg/dL 1 hour: 195 mg/dL
• 2 hours: 155 mg/dL 3 hours: 145 mg/dL
  As a result, she is diagnosed with gestational diabetes. She is counselled to start diet modification and exercise to control her glycemic levels. 3 weeks after her diagnosis, she presents her values:
• Fasting: 95 mg/dL 1hr pp: 185 mg/dL

1. Continue diet modification
2. Start insulin
3. Repeat GTT
4. Start metformin

1. 70 – 100 mg%
2. 100 – 130 mg%
3. 130 – 160 mg%
4. 160 – 190 mg%

 

1. 500 mg
2. 1000 mg
3. 800 mg
4. 300 mg.

• She is suspected to be anemic and her blood sample was ordered for examination which showed.
• Hb 7.4 gm % (12–14 gm%)
• Hct 22 % (36–44%)
• MCV 72 fL (80–97 fL)
• MCH 25 pg (27–33 pg)
• MCHC 30 % (32–36%)
• Peripheral smear shows microcytic hypochromic RBCs with anisopoikilocytosis
• Naked eye single tube red cell osmotic fragility test (NESTROFT) is negative.

1. Thallesemia
2. Iron deficiency anemia
3. Megaloblastic anemia
4. Vit B12 deficiency anemia.

 

1. Wait for 2nd trimester to start ATT
2. Start category 1 ATT in 1st Trimester
3. Start category 1 1 ATT in 1st Trimester
4. Start category 111 ATT in 2nd Trimester

1. Cervical Chlamydia culture
2. Cervical gonorrhea culture
3. Elisa for HIV
4. Rectovaginal grp B streptococcal culture

1. Current symptoms of genital pain and tingling
2. h/o previous cesarean section
3. IVF
4. Maternal colonization with group B streptococci

1. Administer one dose of acyclovir if she has active genital herpes at the time of delivery.
2. Administer prophylaxis with acyclovir from now and uptil delivery whether she has active herpes or not.
3. Perform elective LSCS even if mother is asymptomatic at the time of delivery.
4. Perform elective LSCS only if mother has active herpes at the time of delivery.

1. Nothing needs to be done, chickenpox in children is mild and self limiting.
2. The chance of transmitting the virus of the baby is low and so we treat if symptoms develop.
3. Baby must be treated immediately after birth as chickenpox is serious in newborns
4. Varicella virus is teratogenic and baby might have mild birth defects.

1. Administer high dose acyclovir to the infant at birth.
2. Administer high dose acyclovir to the patient now.
3. Administer varicella immunoglobulin to the infant at birth.
4. Administer varicella immunoglobulin to the patient.

1. Hepatitis B core antigen status is the most sensitive indicator of positive vertical transmission of disease
2. Hepatitis B is the most common form of hepatitis after blood transfusion
3. The proper treatment of infants born to infected mothers includes the administration of hepatitis B Ig as well as vaccine.
4. Patients who develop chronic active hepatitis should undergo MTP.

1. Within 12 hours
2. Within 6 hrs
3. Within 24 hrs
4. Within 48 hrs

1. Despite the potential for fetal infection, she may opt out from the test
2. Early retroviral therapy will absolutely decrease the chances of transmitting infection to the baby.
3. CDC recommends screening only for patients with high risk factors
4. Risk of the test include potential for fetal loss.

 

1. VDRL in mother and baby
2. HbS ag
3. Montoux test
4. ELISA for HIV

1. Erythromycin
2. Azithromycin
3. Penicillin
4. Cephalosporin/ceftriaxone

 

1. Transvaginal usg
2. Follow up after 3 months
3. Quantitative b hcg measurement
4. Rapid urine b hcg measurement
5. Methotrexate inj.

1. Incomplete abortion
2. Missed abortion
3. Threatened abortion
4. Complete abortion
5. Inevitable abortion.

1. Lupus anticoagulant
2. Factor vii
3. Von willebrands disease
4. Hemophilia.

1. Septic abortion
2. Recurrent abortion
3. Consumptive coagulopathy with hypofibrinogenemia
4. Future infertility
5. Ectopic pregnancy

1. B hcg levels will be higher than normal.
2. B hcg levels will be lower than normal
3. uterus will be of normal levels
4. TSH levels will be increased

 

1. Admit to antenatal unit for bed rest and betamethasone.
2. Admit to antenatal unit for bed rest and blood transfusion.
3. Induction of labour
4. Perform emergency cesarean section.

• On examination
• Her PR : 66/min
  15
• B/P : 100/70mm of hg
• RR : 10/min

1. Emergent cesarean section
2. Fetal umbilical blood transfusion
3. Expectant management
4. Induction of labour with prost aglandins

1. DIC
2. IUGR
3. Subarachnoid hemorrhage
4. Vasa previa

1. Disruption of placenta and release of fetal tissue into circulation
   16
2. Liver failure
3. Haemorrhagic shock
4. Release of thromboplastin by damaged placenta
5. Ruptured ectopic

1. Administer a tocolytic
2. Administer a corticosteroid.
3. Administer fresh frozen plasma.
4. Deliver the fetus immediately by LSCS
5. Observe closely.

 

• WBC count: 9000/mm³
• Hemoglobin: 13 g/mL
• Hematocrit: 39%
• Platelet count: 240,000/mm³
  17
• Blood urea nitrogen: 11 mg/Dl
• Creatinine: 1.0 mg/dL
• Aspartate aminotransferase: 20 U/L Alanine aminotransferase: 12 U/L.
• Urinalysis reveals 3+ protein but no blood, bilirubin, bacteria, leukocyte esterase, or nitrites. The patient is sent directly from the clinic for a nonstress test and an ultrasound. Six hours later her blood pressure is rechecked, and it is 162/110 mm Hg.

1. Chronic hypertension
2. Preeclampsia
3. Eclampsia
4. Gestational hypertension
5. Severe preeclampsia

1. Start iv furosemide
2. Induce labor after doing Bischop score
3. Put her on hydralazine
4. Initial inpatient evaluation followed by restricted activity and outpatient management.
5. Start her prepregnancy regime

• FHS regular
• Fetal parts palpable

1. Emergency cesarean section
2. Oral glucose tolerance test
3. I/V mgso4
4. Stabilisation of vital signs and bed rest
5. Follow up after 2 weeks

• She is 168 cms (5’ 6”) tall, weight is 59 kg, B/P = 120/84 mm of hg and fundal ht is 17 cms. Fetal movements are appreciated and FHR = 140/min.
• Results of dipstick are negative.
• Which of the following tests should be preformed:

1. CVS
2. Grp B strepto coccal testing
3. Triple test
4. USG of fetal kidneys

 

• USG shows AF I>21
• Modification of which of the following would most likely have helped to prevent this condition:

1. Folate supplementation
2. Hypertension
   19
3. Rh Isoimmunisation
4. Diabetes
5. Smoking

 

1. Advise against amniocentesis as it will increase the risk of isoimmunisation
2. Follow Rh titres carefully and give Anti D if evidence of isoimmunisation is present.
3. Give Anti D at 28 weeks f pregnancy and after delivery if baby is Rh neg
4. Give Anti D prior to her amniocentesis
5. give rubella vaccine as she is Rubella non immune

1. Schedule an amniocentesis for amniotic fluid bilirubin at 16 weeks
2. Repeat titer in 4 weeks
3. Repeat titer in 28 weeks
4. Schedule PUBS to determine fetal hematocrit at 20 weeks
5. Schedule PUBS as soon as possible to determine fetal blood type

1. After a spontaneous first trimester abortion
2. After treatment for ectopic pregnancy
3. Within 3 days of delivering an Rh–ve fetus
4. At the time of amniocentesis
5. At the time of external cephalic version

 

1. Intense itching
2. SGOT, SGPT less than 60 IU
3. Serum bilirubin > 5 mg/dl
4. Markedly raised levels of alkaline phosphatase

1. 34 weeks
2. 36 weeks
3. 38 weks
4. 40 weeks

1. Immediate delivery
2. Cholecystectomy
3. Intravenous diphenhydramine
4. MgSO₄ therapy
5. Bed rest and supportive measures since this condition is self limiting

 

1. B₂ agonist are contraindicated during pregnancy.
2. Both B₂ agonist and inhaled corticosteroids are both contraindicated in pregnancy.
3. Both B₂ agonist and inhaled corticosteroids are safe in pregnancy
4. B₂ agonist and inhaled corticosteroids are both safe in pregnancy but during 2nd and 3rd trimester only
5. Inhaled corticosteroids are contraindicated in pregnancy.

 

1. Stop taking Thyroxine and switch to methimazole as we would like to control your baby's thyroid levels
2. Thyroxine is safe during pregnancy but it is not absolutely necessary during pregnancy to continue thryo­xine.
3. Thyroxine is not safe during pregnancy and it is better for your baby to be hypothyroid than hyperthyroid
4. Thyroxine is absolutely safe and necessary for you in pregnancy but we would like to decrease your dose as pregnancy is accompanied by mild physiological hyperthyroidism
5. Thyroxine is safe in pregnancy and the dose of thyroxine would be increased during pregnancy to avoid hypothyroidism, which may affect the baby adversely.

 

1. The frequencies of monozygosity and dizygosity are the same
2. Division after formation of the embryonic disk result in conjoined twins
3. The incidence of monozygotic twinning varies with race
4. A dichorionic twin pregnancy always denotes dizygosity
5. Twinning causes no appreciable increase in maternal morbidity and mortality over singleton pregnancies

1. Dichorionic and monoamniotic in dizygotic twins
2. Dichorionic and mooamniotic in monozygotic twins
3. Monochorionic and monoamniotic in dizygotic twins
4. Dichorionic and diamniotic in monozygotic twins

1. CHF
2. Anemia
3. Hydramnios
4. widespread thromboses

 

1. indomethacin
2. Nifedipine
3. MgSO₄
4. Progesterone

1. Atosbian
2. Isoxsuprine
3. Nifedipine
4. Mgso₄

1. IUD
2. Severe preeclampsia at 36 weeks
3. complete placenta accreata
4. Chorioamnionitis
5. Postterm pregnancy

1. Uterine massage
2. Delivery of placenta by controlled cord traction
3. Early cord clamping
4. Injection methergin after delivery of shoulder of baby

1. Preterm delivery
2. Postdated pregnancy
3. Birth asphyxia
4. Maternal diabetes

1. Abduct mothers thigh and apply suprapubic pressure.
2. Apply fundal pressure.
3. Flex mothers thigh against her abdomen.
4. Push infants head back into the uterus and do cesarean section.
5. Do a symphiosotomy.

• Uterus is soft
• Fundal ht ≃ 32weeks
• Contractions present 20-30secs/8mins
• Cephalic presentation
• FHS + Regular

1. Cervical culture for group B streptococci
2. Digital cervical examination and assessment of dilation and effacement.
3. Quantification of strength and timing of contraction with external tocometer.
4. Speculum examination to rule out leaking and usually assess cervical dilatation and effacement.
5. USG examination of the fetus.

1. Sedate the patient and wait
2. LSCS
3. Amniotomy
4. Induction with membrane rupture

1. do LSCS
2. encourage the patient to push after a short period of rest.
3. attempt forceps delivery
4. apply fundal pressure

• O/E – P/R = 95/min
• B/P = 135/8 o mmof hg
• R/R – 15/min
• P/A – fetus lie-long, presentation cephalic
• Tocometer detcts contractions every 8 mins
• Fetal heart rate tracing show baseline FHS 140/min, beat to beat variability is present, occasional heart rate acceleration of 160/min for 15–20 secs. There are also decelarations to 115–120/min with the onset of contractions.

1. Augment contractions wid oxytocin
2. Monitor and follow labor on partogram
3. Obtain immediate consent for LSCS
4. Send the patient for BPS
5. Perform urgent aminoinfusion

1. Emergency CS
2. IV MgSO4 and induce labor with with pitocin
3. Overnight cervix ripening with PGE2 and induction with Pitocin in morning
4. Admission and CS after 12 hrs of NPO
5. Induce labor with misoprostil

1. Admission and immidiate CS
2. Admission and Pitocin induction
3. Schedule a CS in one week if she has not undergone spontaneous labor in the mean time
4. She should continue to monitor kick count and return to you after a week to reassess the situation

1. wait and watch
2. repeat scalp ph after 15 mins
3. midforceps rotation
4. LSCS

1. incr rate of oxytocin infusion
2. Perform sterile vaginal examination
3. perform immediate LSCS
4. Perform mc roberts manouvre
5. stimulate fetal scalp

1. Fetal viabilty
   27
2. Fetal maturity
3. Fetal weight
4. Cervical dilatation

1. Fetal distress during active stage of labor.
2. Labor complicated by shoulder dystocia.
3. Prolonged active stage of labor due to inadequate uterine contraction strength.
4. Prolonged latent stage of labor due to inadequate uterine contraction strength.
5. Prolonged second stage of labor due to adequate uterine contraction strength.

1. Fetus should be vertex prestation or face presentation with mentoanterior
2. The saggital plane should be less than 15 degree from anterioposterior plane
3. There should be no caput saccedenum
4. It should be at station zero (AIIMS Nov 2011)

1. mentovertical
2. suboccipitobregmatic
3. occipitofrontal
4. occipitomental

1. High forceps
2. Mid cavity forceps
3. Low forceps
4. Outlet forceps

1. Breech presentation
2. Face presentation
3. Transverse position
4. Occiput posterior
5. Occiput anterior

1. Allow the pt to undergo a vaginal breech delivery whenever she goes into labor
2. Send the pt to labor and delivery immidiately for an emergent CS
3. Schedule a CS at or after 39 weeks gestation age
4. Schedule an ext cephalic version in next few days

 

1. immediately after delivery
2. 24 hrs after delivery
3. 3 weeks after delivery
4. 6 weeks after delivery

1. Immediately after delivery
2. 3 weeks after delivery
3. Only after LSCS
4. During third trimester of pregnancy

1. continue breast feeding from both the breasts
2. breastfeed from unaffected breast only
3. immediately start antibiotics and breastfeed only when antibiotics are discontinued.
4. pump and discard breastmilk till infection is over and then continue breatfedding
5. stop breastfeeding immediately.

1. Amoxicillin
2. Diclocloxacillin
3. Penicillin v
4. Erythromycin
5. Levofloxacilin

1. Patient may continue breast feeding at her own risk.
2. Patient should breast feed her baby only if her INR is at <2.5
3. Patient can breast feed her baby after 6 weeks course of warfarin is over
4. Warfarin is not a contraindication for lactation.
5. Warfarin is absolutely contraindicated during lactation.

1. Currettage
2. oral antibiotics
3. Reassurance
4. Order urinalysis
5. vaginal culture

1. Dilatation and curretage
2. PGF2A
3. Methylergometrine
   31
4. Misoprost
5. Platelet transfusion

 

1. Factor 2
2. Factor 7
3. Factor 10
4. Factor 11

1. 28 wks
2. 32 wks
3. 36 wks
4. Post partum

1. HCG
2. Papp-1
3. Pregnancy specific beta1 glycoprotein
4. Activin

1. Increased GFR (APPG 2011)
2. Increased RBF
3. Hypertrophy of bladder musculature
4. Increased activity of ureters

1. Incr GFR
2. Decr GFR
3. GFR remains the same
4. GFR can incr or decr

1. First two weeks after conception
2. 3 – 8 weeks after conception
   32
3. 8 – 12 weeks after conception
4. 13 – 20 weeks after conception

1. Bimastoid
2. Bitemporal
3. Occito frontal
4. Submento vertical

1. 1st degree
2. 2nd degree
3. 3rd degree
4. 4th degree

 

1. 8-10 weeks
2. 11-13 weeks
3. 14-16 weeks
4. 18-20 weeks

1. Blood test
2. USG
3. Chorionic villi sampling
4. Assure her that there is no chance since she is less than 35 years.

1. Trisomy 21
   33
2. Cleft palate
3. Gauchers disease
4. Phenylketonuria

1. Fetal loss
2. Infections
3. Limb reduction defects
4. Bleeding

1. 500
2. 1000
3. 2000
4. 4000

1. A gestational sac can be first seen 2 weeks after LMP.
2. The accuracy of determining gestational age using ultrasound begins to decrease after first trimester.
3. Yolk sac is the first sign of pregnancy on USG
4. USG can be used to determine the sex of the baby

1. Determination of uterine size on pelvic examination
2. Quantitave serum HCG levels
3. Crown rump length on abdominal or vaginal examination
4. Determination of progesterone level along with serum HCG level

1. Downs syndrome
2. Molar pregnancy
3. Overestimated gestational age
4. Congenital nephrotic syndrome

1. insignificant
2. Occurs in 10% of newborn
3. An indicator of considerably increased incidence of major malformations of the fetus.
4. E qually common in newborn of dibetic and non diabetic mothers

1. Warfarin
2. Phenytoin (AIPG2012)
3. Mifepristone
4. Misoprostol

1. Amphetamines
2. Barbiturates
3. Heroin
4. Methadone
5. Ethyl alcohol

1. Glucose challenge test with 50 gms of glucose
2. culture for Neisseria gonorhhea and Chlamydia trachomatis (normally done at initial visit and in certain high risk grps at 32–36 weeks along wid grp B streptococcal screening)
   35
3. ECV
4. immediate LSCS
5. immediate induction and vaginal delivery

1. decelerations at the beginning of contractions
2. FHR incr to 140 bom several times during 5 mins
3. FHR incr to 170 bpm on 2 occasions and returning to baseline in a pd of 20 mins
4. FHR ranging from 110-120 bpm over a period of 40 mins

1. early decelerations
2. variable decelerations
3. sinusoidal heart rate pattern
4. accelerations.

1. Instruct the patient to go to labor and delivery for a contraction stress test
2. Reassure the patient that one fetal movement per hr is within normal limits and she does not need to worry
3. Counsel the patient that the baby is probably sleeping and that she should continue to monitor fetal kicks. If she continues to experience <5 kicks/hr by morning, she should call you back.
4. Instruct the patient to go to labor and delivery for a nonstress test.

1. The results are equivocal, and should have a repeat BPP within 24 hr
2. The results are abnormal and she should be induced
3. The results are normal and she can go home
4. The results are abnormal, and she should undergo emergent CS
5. The results are abnormal, she should undergo umbilical artery doppler velocimetry

1. Cessation of marijuana
2. Cessation of smoking
3. Taking vitamins before conceiving and continuing them after conceiving
4. Early t/t of chlamydia
   

   Fig. 1:

     

• Pulse Rate increases
• Diastolic B.P decreases
• First heart sound is prominent and split
• Second heart sound–normal
• Third heart sound–normally not heard but in pregnancy it is prominent
• Murmurs-ejection systolic murmur heard normally in aortic or pulmonary area at 10–12 weeks due to expanded intravenous volume.
• Continous murmur heard normally over the tricuspid area in left 2–3rd intercostal space.
• Apex beat is heard in the fourth ICS 2.5 cms left to midclavicular line
• Slight cardiomegaly
• Ecg- left axis deviation

• Systolic murmur greater than grade 3
• Diastolic murmur
• Marked Cardiomegaly
• Sustained arrhythmia
• Persistent split second heart sound

     

• Class I: No limitation of physical activity
• Class II: Slight limitation of physical activity
• Class III: Marked limitation of physical activity

 

• Time of hospitalisation in:
  • – Class I of NYHA – 36 weeks
  • – Class II 28 weeks.
  • – Class III and IV – If seen in the first trimester.

• Intrapartum Management:
  • – Patients should be allowed to go into spontaneous labour, if required induction with vaginal PGE2 may be done (Induction is safe in case of heart disease).
    Ref. Williams Obs. 22/e, p 1021-1022, 23/e, p 962
  • – Trial of labour is contrain dicated in patients of heart disease.
    41
  • – Vaginal delivery is preferred with the use of outlet forceps.
    Note in heart disease patients-even if there is no fetal distress, maternal distress or prolonge second stage of labour still we use forceps, this is called as prophylactic use of forceps.
  • – Heart disease where vaginal delivery is contraindicated /Ceasrean section should be done are all those diseases where Aorta is involved (because in a patient with involved aorta, bearing down can lead to aortic rupture).
  • – Coarctation of aorta
  • – Aortic Aneurysm
  • – Marfans syndrome with aortic involvement.
  • – A patient who is fully anticoagulated with warfarin at the time of labor needs to be counseled for cesarean section because the baby is also anticoagulated and vaginal delivery carries increase risk to the fetus of intracranial hemorrhage.
    Anaesthesia given for LSCS due to heart disese: Epidural anaesthesia.
  • – If cesarean is being done for intracardiac shunts or aortic stenosis, GA is given to prevent hypotension.
    Antibiotic prophylaxis is given for prevention against infective endocarditis:

• The American Heart Association recently updated its guidelines regarding which patients should take a precautionary antibiotic to prevent infective endocarditis (IE).
• Prophylactic antibiotics are no longer recommended for gastrointestinal or genitourinary tract procedures. This recommendation follows from the observation that most cases of IE result from bacteremia caused by routine activities such as chewing food, brushing teeth, and flossing.

• Prosthetic cardiac valve
• Previous IE
• Unrepaired congenital heart disease (including palliative shunts and 42conduits)
• Completely repaired congenital heart defect with prosthetic material or device, during th first 6 months after the procedure.
• Repaired congenital heart disease with residual defects at the site or adjacent to the site of aprosthetic patch or device.
• Cardiac transplantation recipients who develop cardiac valvulopathy.

• Only a few regimens are recommended by the American College of Obstetricians and Gynecologists (2008) 10 for prophylaxis which is given preferably 30-60 minutes before the procedure. Either I.ampicillin, 2 gm, or cefazolin or cef­tria­xone, 1 gm, is given intravenously.
• For penicillin sensitive patients, one of the later regimen is given, or if there is history of anaphylaxis, then clindamycin, 600 mg is given intravenously. The recommended oral regimen is 2 gm of amoxicillin.If Enterococcus infection is of concern, vancomycin is also given.

• Contraception of choice: Temporary–Barrier contraceptives (condoms)
• Contraception to be avoided:
  1. OCPs(can precipiatate thromboembolic event)
  2. Intrauterine devices (can lead to infection)

• If the heart is not well compensated, the patient's husband is advised for vasectomy.^Q
• If heart is well compensated–tubal sterilisdation can be carried out:
  Sterilisation should be considered with the completion of the family at the end of first week in the puerperium under local anaesthesia through abdominal route by minilap technique.

• Best time for cardiac surgery in Mitral Stenosis 14–18 wks
• Surgery of choice Balloon valvuloplasty
• Septic abortion m/c valve affected is tricuspid valve
• M/C fetal complication in heart dis IUGR
• M/C time of heart failure
  Immediate post partum>at the time of delivery>at 30–32 weeks of gestation.

 

1. Cardiac failure within last month of pregnancy or within 5 month postpartum.
2. No determinable cause for failure (may be immunological or nutritional).
3. No previous heart disease.
4. Left ventricular dysfunction (Echocardiography) as evidenced by ejection fraction < 45%
5. Left ventricular end-diastolic dimension > 2.7 cm/m².

• Multiparous
• Young 20-35 years
• Twins pregnancy
• Chronic hypertension pre-eclampsia
• Prolonged tocolytic therapy.

• Chest X-ray: Enlarged heart and pulmonary vascular redistribution.
• Echo: Enlargement of all chambers of the heart (predominantly left heart) with decreased ejection fraction in left ventricle.

     

1. Random plasma glucose >200 mg/dl
2. Fasting blood glucose >125 mg/dl
3. Two or more abnormal values on 100 gm oral glucose tolerance test during pregnancy.

   

• Performed by orally administering 50g of glucose and measuring 47venous plasma glucose 1 hour later irrespective of previous meal.
• Interpretation of result:
  • – Plasma glucose: Interpretation
  • – 140 mg/dl: Further testing by GTT required
  • – 140 mg/dl: Further testing not required.
  • – 200 mg/dl: No further testing required as values > 200 mg/dl confirm the diagnosis of gestational diabetes.
• Time for screening: Between 24 and 30 weeks of gestation (patients at high risk should be screened between 18-22 weeks and if initial screenings is negative it can be repeated between 26 and 30 weeks).Ideally it should be performed in all pregnant females but all those who have average/high risk for diabetes should be screened.
  Average risk:
  • – Members of ethnic group with high prevalence of GDM,
  • – diabetes in first degree relatives
  • – age > 25 years
  • – overweight before pregnancy,
  • – weight high at birth
  High risk:
  • – Marked obesity
  • – strong family history of type 2 DM
  • – previous history of GDM
  • – History of stillbirth
  • – History of delivery of large baby(> 4 kg)
  • – glycosuria
  • – h/o unexplained neonatal death
  • – h/o congenital malformation
  • – polyhydramnios
  • – h/o traumatic delivey with associated neurological disorder in infant
  • – h/o > 3 spontaneous abortions.
  • – Recurrent monoliasis,
  • – age > 30 years
  • – impaired glucose metabolism

• Patients with abnormal screening test are followed by a 3 hour glucose tolerance test (GTT)
• The test is performed with 100gm of glucose. Upper limit of normal for the 3 hour glucose tolerance test during pregnancy:
  • – Fasting: 95 mg/dl
  • – One hour: 180 mg/dl
  • – Two hour: 155 mg/dl
  • – Three hour: 140 mg/dl
• If two or more of these values are abnormal: Gestational diabetes is confirmed.
• If one value is abnormal: Increased risk of complications like macrosomia and preeclampsia - eclampsia. (Though gestational diabetes is not present)
• WHO recommends use of glucose of 75 g GTT and only two samples to be withdrawn viz: The fasting and the 2 hour value.

• Diet: Medical nutrition therapy (MNT): It is the cornerstone of treatment of diabetes in pregnancy. Caloric requirement is 25-35 kcal/kg body weight/ day according to body mass index (Table). It is advisable to take 3 major and 3 minor meals so that there is no intermittent hypoglycemia and still ideal blood sugars are maintained.

  Body mass index(BMI) kg/m2	Calories intake
  18.5-24.9 (Normal)	30 kcal/kg/day
  16.5-18.4 (Underweight)	35 kcal/kg/day
  25-30 (Overweight)	25 kcal/kg/day
  40 (Morbid obesity)	12 kcal/kg/day

  Diet composition should be 50-60% of carbohydrates, 20% proteins and 25-30% fats
• Exercise: Planned physical activity for 30 minutes/day is recommended for all individuals capable of participating. Advising patients to walk briskly or do arm exercises while seated in chair for at least 10 minutes after each meal accomplishes the goal.

• Premeal value- 70-95 mg/dl (Answer 9)
• Post meal (2 hrs post parandial) 120 mg/dl
• HbA1c-6%.
  • – If these goals are not achieved patient should be put on Insulin. (Answer 8).
  • – Oral hypoglycemics are not advised during pregnancy as they can cross the placenta and cause fetal hypo­glycaemia.The only oral hypoglycemic drug approved for use in pregnancy is Glyburide

 

• Low risk patients-wait for spontaneous labor till maximum 41 weeks
• High risk patients-37 completed weeks-induce labor as IUD occurs mostly in last 2 weeks of pregnancy.
• Mode of delivery- vaginal delivery

• Macrosomia > 4.5 kg (for predicting macrosomia, shoulder width > 14 cm, EFW > 4.5 kg on ultrasound)
• Demonstrable fetal compromise (Severe IUGR)
• Bad obstetric history
• Other obstetric indications

 

• Blood glucose is maintained between 80–110 mg/dl.Blood sugar monitoring 2 hourly, serum electrolytes 12 hourly, urine sugar, ketones 4 hourly

• Nil per orally
• Blood glucose is maintained between 80–110 mg/dl
• Blood sugar monitoring 2 hourly
  50
• Serum electrolytes 12 hourly
• Urine sugar, ketones 4 hourly 5 unit insulin in 500 ml of 5% dextrose at rate of 100 ml/ hour
• If blood sugar> 140 mg/dl-plain insulin to be given subcutaneously according to sliding scale
• Sliding scale:
  • – 140–180 mg% – 4 units
  • – 181–250 mg% – 8 units
  • – 251–400 mg% – 12 units
  • – > 400 mg% – 16 units
  If blood sugar < 80 mg/dl, infuse 5% dextrose at rate of 100 ml/hour.
  Frequent fetal heart monitoring for high risk pregnancy.

     

• All parameters of iron metabolism decrease during pregnancy except for the two Ts viz total iron binding capacity and trans­ferrin levels, which increase.
• No matter in what form iron is being taken–only 10 % of it is absorbed, which means in order to fulfill the requirement of 4-6 mg/day, approximately 40–60 mg of iron should be taken in diet daily during pregnancy. Which is not possible, this is the reason why Iron supplementation is absolutely necessary in pregnancy.

• Earliest /most sensitive indicator of iron deficiency: Decrease in the levels of serum ferritin.
• M/c anemia in pregnancy: In developing countries it is Dimorphic anemia i.e both due to iron and folic acid deficiency.
• Physiological anemia during pregnancy: The increase in plasma volume (30–40%) is much more than the increase in red cell mass (10–15%) during pregnancy, leading to apparent decrease in hemoglobin level called as physiological anemia of pregnancy.
• Starts at 7th–8th weeks
• Maximum by 32 weeks
• Does not go below 11 gm% in 1st trimester, 10 gm% in 2nd and 3rd trimester. (The rise in RBC volume begins at 20 weeks continues till term Therefore, in 3rd trimester there is slight rise I in hemoglobin concentration).
• This hemodilution during pregnancy serves to reduce maternal blood viscosity, thereby enhancing placental perfusion and facilitating nutrient and oxygen delivery to the fetus.

 

• In the question number 11 patient has Hb 7.4 gm%, Hct 22% and symptoms of early fa tigue, which indicate she is anemic. Her complete blood picture shows MCV and MCH low indicating microcytic anemia. Thus the D/D could be Iron deficiency anemia or Thallassemia.
• But since in this patient Nestrofts test(screening test for thallasemia) is negative thallasemia is ruled out and hence diagnosis is confirmed as Iron deficiency anemia.
• NESTROFT test is ‘naked eye single tube red cell osmotic fragility test’. In this test 2 ml of 0.36 buffered saline solution is taken in one tube and 2 ml of distilled water in another tube. A drop of blood is added to each test tube and both the tubes are left undisturbed for 20 minutes. Both the tubes are then shaken and 53held against a white paper on which a black line is drawn. Normally, the line is clearly visible through the contents of tube containing distilled water. If the line is clearly visible similarly through the contents of tube with buffered saline, the test is negative. If the line is not clearly visible the test is considered positive. The principle is that normocytic normochromic cells when put in hypotonic solution will undergo lysis wheras in thalassemia trait, the cells are microcytic and hypochromic which are resistant to hemolysis due to decreased fragility. It has 91% sensitivity and 95% specificity and the negative predictive value is 99%.7 NESTROFT test is only a screening test for thalassemia. The definite test is the estimation of HbA2 levels by high liquid performance chromatography. In thalassemia HbA2 levels are > 3.5%.

 

• Parenteral iron- It can be given by either intramuscular or intravenous route.

• Body weight in kg × (Desired Hb – patient's Hb) × 2.21 + 1000 mg
• 1000 mg is taken for complete restoration of the stores in patients with continuing blood loss otherwise 500 mg is adequate for patients whose blood loss has been arrested.
  OR
  54
• Give 250 mg elemental iron for each gm of Hb deficit and add another 50% for replenishment of stores.
• Intramuscular iron preparations available are iron dextran, iron sorbitol citrate complex.
• Intravenous iron preparations available are iron dextran, iron sucrose, ferrous gluconate.

1. Intolerance to oral iron
2. Impaired iron absorption
3. Chronic blood loss
4. Gastrointestinal disorders which gets aggravated by oral iron-peptic ulcer disease, ulcerative colitis
5. After 30 weeks period of gestation, parenteral iron is preferred as the compliance is 100%.

• Blood transfusion: 1 unit of blood raises the Hb levels by 0.8-1 gm% within 24hrs.

1. Severe anemia seen beyond 36 weeks of pregnancy
2. Anemia due to active blood loss
3. Refractory anemia

 

• Increased chances of relapse and flare of tuberculosis occurs in puerperium.
• It is not an indication for termination of pregnancy
• ATT can be given at anytime during pregnancy, including first trimester
  55
• INH + Rifampicin are given orally for 9 months (INH resistance-Ethambutol).
• Baby should be given prophylactic INH for 3months, if montoux is negative after 3 months, stop INH and give injection BCG
• In active lesions breast feeding is C/I,ATT is not a C/I for breast feeding.
• Pulmonary TB is not an indication for performing cesarean section

     

• Group B streptococci, Streptococcus agalactiae is a major cause of neonatal mortality and morbidity.
• Neonates present with respiratory distress, apnea, hypotension.
• ACOG recommends universal culture screening for rectovaginal GBS at 35–37 weeks

 

• Most common time of Mother To Child transmission is–at the time of delivery
• ACOG doesnot recommend a routine screening for HSV
• DOC during pregnancy-Acyclovir(safe in lactation also) × 7-10 days
• ACOG recommends daily viral therapy at or beyond 36 weeks for women who have recurrences during pregnancy as it decreases the outbreaks at term and so decreased need for cesarean.
• Cesarean section is indicated for women with active genital lesions or in patients having prodromal symptoms of herpes viz genital pain and tingling (ans 14). Cesarean is not indicated in women with a h/o HSV infection but no active genital tract lesion/prodromal symptoms at the time of delivery.
• If no active breast lesions are present-patient can breast­feed.
• Now with this background about HSV infection, let′s have a look at the options given in Q15.
• Option a: Administer one dose of acyclovir if she has active genital herpes at the time of delivery-incorrect as acyclovir should be given for 7–10 days in case of active herpes infection.
  57
• Option b: Administer prophylaxis with acyclovir from now and uptil delivery whether she has active herpes or not–again incorrect as we have to give acyclovir for 7–10 days, then stop and restart at 36 weeks of gestation.
• Option c: perform elective LSCS even if mother is asymptomatic at the time of delivery. – again Incorrect
• Option d: perform elective LSCS only if mother has active herpes at the time of delivery. – correct

 

• If varicella infection occurs during first half of pregnancy(m/c time of transmission13 to 20 weeks) – it results in congenital varicella syndrome.
• Congenital varicella syndrome is characterized by chorioretinitis, microophthalmia, cerebral cortical atrophy, hydronephrosis and bone or skin defects.
• Congenital varicella syndrome is an indication for doing MTP.
• Congenital defects rarely occurs if varicella infection occurs after 20 weeks.
• Neonatal varicella is characterized by pneumonitis, hepatitis and DIC.
• Perinatal varicella exposure just before or during delivery poses a serious threat to newborns and so Varicella Immunoglobulin (VZIG) should be given to neonates of born to mothers who have clinical evidence of of varicella 5 days before and upto 2 days after delivery.
• The use of VZIG decreases the chances of neonatal varicella and also modify the clinical course but it doesnot always prevent severe or fatal varicella.Expectant treatment with close observation, followed by prompt initiation of antiviral therapy on suspicion of neonatal varicella is recommended.
  58
• DOC for treatment of infected pregnant mothers-i/v acyclovir
• Let me explain Q 17 – here the question says a pregnant woman is exposed to chicken pox rash, she doesnot have chicken pox…so obviously we will not treat her or her baby with acyclovir.Now since the female herself doesnot have chicken pox so why to give VZIG to the infant, rather this female should be given prophylactic VZIG so that she doesnot acquire chickenpox.

 

• M/C after blood transfusion – Hepatitis C
• M/C causing fulminant hepatitis – Hepatitis E
• M/C causing maternal death – Hepatitis E
• M/C leading to vertical transmission – Hepatitis B
• M/C time of transmission – 3rd trimester

   

• Most common-CMV
• Most teratogenic-Rubella
• M/C Time for rubella transmission to fetus-1st trimester (maxmimum-1to 4 weeks),absent transmission-beyond 20 weeks.
• In Rubella –M/C single defect which occurs is –Sensorineural hearing loss
• Heart defects seen in Rubella -PDA and Pulmonary artery stenosis
• After rubella vaccine, pregnancy is contraindicated for 1 month.
• CMV-Transmission can occur in any trimester
• -Most severe infection occurs if transmission occurs in 2nd trimester.
• CMV transmission can occur during vaginal delivery and breast feeding also
• Primary infection – leads to 40% transmission
• Recurrent infection – leads to 0.2%-2% transmission.
• CMV Never Leads to Heart Defects in Fetus
• M/C time for toxoplasma infection-3rd trimester
• Maxmimum/most severely fetus is affected if fetal infection occurs in 1st trimester
• Triad of toxoplasma-intracerebral calcification, chorioretinitis and hydrocephalus
• Treatment-Spiramycin (prevents fetal transmission but it cannot treat fetal infection if it is present.)
• Spiramycin + pyrimethamine and sufonamide combination is given to treat fetal infection and prevent further transmission.

 

• M/C time of vertical transmission:
  1. Peripartum period
  2. During delivery
  60
• Perinatal transmission 15–40%
• Risk depends on following factors- maternal viral load, CD4 count (inversely related), vitamin A deficiency and chorio­amnionitis.
• Screening adopted for HIV is universal.
• Screening-Opt out screening (i.e patient can opt out from the test)
• HIV testing is the first step towards PPTCT (Prevention of parent to child transmission) aimed at reducing the vertical transmission of HIV infection.
• Screening test–ELISA a nd a positive or indeterminate test should be followed by a Western blot for confirmation.
• Antiretroviral therapy is given to pregnant female for 2 reasons:
  1. for benefit of her own health
  2. for preventing Mother To Child Transmission (HAART throughout pregnancy reduces MTCT to <2%)
• Relationship of CD4 count to development of opportunistic infections In a patient of HIV.
• All pregnant women should be given ART for two reasons:
  1. For benefit of her own health– these females should continue with treatment during pregnancy and afterwards
  2. HIV positive pregnant women who do not have indication for antiretro-viral therapy should have ART prophylaxis to prevent mother to child transmission
     (HAART throughout pregnancy reduces MTCT to <2%)
• Salient points of WHO's latest Nov 2009 guidelines which were revised from previous (2006) guidelines:
  1. Although antiretroviral therapy among asymptomatic HIV infected nonpregnant adults and adolesents is generally delayed until the CD4 drops below 350 cells/µL, all pregnant women should be offered treatment regardless of CD4 + Two unit or viral load to reduce MTCT
     For infants of mothers with HIV who are taking therapeutic ART for their own health, the duration of prophylactic ART has been increased irrespective of whether the infant is breastfeeding or not. For breastfeeding infants, it is recommended that daily NVP is instituted from birth until 6 weeks of age. For nonbreastfeeding infants: daily AZT or NVP from birth until 6 weeks of age is recommended.
     61
  2. It is recommended that antepartum ARV prophylaxis should be started in all women from as early as 14 weeks gestation (if she is not already on ARV) or as soon as possible when women present late in pregnancy, in labor or at delivary.

 

• If HAART is given throughout pregnancy it reduces MTCT (Mother to Child transmission) to <2% and in such cases vaginal delivery can be done as cesarean will not decrease further risk of transmission.
• If mother is not properly covered with ARV: Elective cesarean section at 38 weeks should be done or if woman is on ARV and still viral load is > 1000 copies/ml then also elective cesarean section is done.
• After rupture of membranes the advantage of reducing Mother to child transmission by LSCS is lost, hence emphasis is laid on elective cesarean at 38 weeks.
• Drug supplied by NACO: Free of cost-NEVIRAPINE (both for mother and baby)
• If vaginal delivery is being done: Artificial Rupture of Membranes/Forceps/Vaccum//Fetal Scalp Electrodes are contraindicated.
• First born twin has more risk of infection than second of twin.
• After delivery: Breast feeding is not C/I in developing countries. Decision regarding the type of feed, i.e. breastfeed or replacement 62feed, should be made during antenatal period itself depending upon whether replacement feed is Acceptable, Feasible, Affordable, Sustainable and Safe (AFASS): As mixed feed is associated with increased rate of HIV transmission as compared to breastfeed alone, it is suggested the weaning must be complete and abrupt after six months of breastfeed or earlier if replacement feed is AFASS.
• Answer to case study: Women who have been receiving antiretroviral treatment for their HIV-1 infection should continue same treatment during pregnancy, intrapartum and postpartum period except for Efavirenz (EFV). NVP(Nevirapine) should be substituted for EFV, although exposure to EFV during pregnancy is not an indication for abortion for women who become pregnant while receiving an EFV-containing regimen and are in the first trimester of pregnancy.

1. Women who are receiving EFV and are in the second or third trimester of pregnancy can continue the current regimen.
2. NVP should be given in women with CD4 count of 200-350 cells/mm3: There are data to show that women with a CD4 count of > 250 cells/mm3 face a higher risk of severe hepatotoxicity with NVP.

 

• Bullous leisons on the body of the infant and presence of periostitis suggests the diagnosis of congenital syphilis. The only option related to syphilis is VDRL.
  Congenital syphilis:
  • – Transmission of T pallidum across the placenta from a syphilitic woman to her fetus may occur at any gestational age but fetal damage occurs when transmission occurs after 16weeks.
  • – Thus adequate treatment before 16 weeks may prevent fetal damage
  • – Untreated infection leads to fetal loss in 40% cases, IUD, stillbirth and abortions.(stillbirths being more common than abortions)

• If mother has been treated with penicillin in 1st/2nd trimester-
  No treatment for infant
• If mother has not been treated/received treatment with penicillin in third trimester –
  Treat infant with penicillin

 

• Syphilis therapy during pregnancy is given to eradicate maternal infection and to prevent congenital syphilis.
• Parenteral penicillin G remains the preferred treatment for all stages of syphilis during pregnancy.
• There are no proven alternative therapies for syphilis during pregnancy Erythromycin may be curative for mother, but because of limited transplacental passage, it does not prevent all congenital disease.

 

• Beta unit is specific unit
• Secreted by syntiotrophoblast
• Functionally similar to LH and acts via plasma membr LH-Hcg receptors.
• Earliest detected 6-8 days after conception
  65
• Doubling time-48 hrs
• Maxm levels seen at 70 days/10 weeks /1^st trimester
• Most sensitive test to detect hcg- RIA>IRMA
• It disappears from circulation 2 weeks postpartum

 

• Threatened Abortion: It is a clinical entity where the process of abortion has started but has not progressed to a state from which recovery is impossible.
• Inevitable Abortion: It is a clinical entity where process of abortion has progressed to a state from where continuation of pregnancy is impossible.
• Complete Abortion: Here the products of conception are expelled en masse.
• Incomplete Abortion Here the entire products of conception are not expelled but a part is left inside the uterine cavity.
• Missed Abortion: When the fetus is dead and retained inside the uterus for a variable period, it is missed abortion

 

1. Lupus articoagulant
2. Anti cardiolipin Antibody
3. Biologically false positive syphilis test antibody

 

1. Septic abortion
2. IUD
3. Abruptio placentae
4. Amniotic fluid embolism
5. Severe preeclampsia, eclampsia. HELLP syndrome

• Wrong dates
  67
• Twin pregnancy
• Molar pregnancy
• Concealed variety of Abruptio placenta
• Polyhydramnios.

• Multiparity and increased maternal age
• Previous H/O placenta previa 12 times more risk
• H/O any previous uterine surgery 4 time more risk
• Previous uterine currettage
• Increased placental size
• Succenturiate lobe
• Smoking

• Never do P/V examination
• Investigation of choice: TVS(transvaginal scan… surprised don't 68be- because in placenta previa P/V examination is contraindicated since our finger has to inserted inside the internal os inorder to know the exact location of the placenta, which in turn can lead to torrential haemorrhage but in Transvaginal ultrasound, the probe is never taken beyond the internal os, it is kept in the cervical canal and obviously there are no chance of disturbing the placenta).
• Double set up examination (i.e Per vaginal examination in the operation theatre with all arrangements of cesarean section done) can be done in placenta previa.

• Mode of delivery practically in all patients of placenta previa is–Cesarean section
• Low transverse cesarean section should be done but if placenta is anterior give vertical incision…williams 23/ep773
• Whereas according to Dutta 7/e, p249 cesarean section should be done in all cases where placental edge is within 2cms from internal os.
  69
• Now with this background lets have a look at the question.
• G1P0 woman at 29 weeks’ gestation presents to the emergency department complaining of 2 hours of vaginal bleeding, the bleeding recently stopped, her vitals are stable (temperature is 36.8°C (98.2°F), blood pressure is 118/72 mm Hg, pulse is 75/min, and respiratory rate is 13/min), FHS are present and reassuring i.e there is no fetal distress…
• This means we will manage this patient expectantly and there is no need to immediately terminate her preg­nancy..ruling out options c and d
• So now we have to choose between option:
  1. Admit to antenatal unit for bed rest and betamethasone. And option
  2. Admit to antenatal unit for bed rest and blood transfusion.
• The patients Hb is 11.1, there is no need for immediate blood transfusion (ruling out option b), just crossmatch and arrange blood and give betamethasone for hastening lung maturity.

• It occurs due to velamentous insertion of the cord
• Blood loss which occurs is fetal in origin and so there is increased fetal mortality – 75 to 90%, maternal mortality is not increased.
  70
• Can be diagnosed antenatally by Doppler study
• When bleeding occurs: Sinusoidal fetal heart rate pattern seen
• Diagnosis made at the time of bleeding by-Singers alkali denaturation test/apt test
• Management- Emergency Cesarean section.

• Classification of Abruptio placenta is called as sher/page classification
  Management: Once Abruptio is diagnosed you have to manage it actively irrespective of the gestational age.
• In case of abruption: The abruptio delivery interval is important.
• Do not prolong this interval as complications like DIC/Renal failure (acute cortical necrosis) can occur.
• Never give tocolytics in patients of abruptio (no matter how tempted you may feel)
• Pritchard rule for management of abruption is Keep hematocrit atleast 30% and maintain urine output-30ml/hr

   

• Release of thromboplastin in placental abruption leads to DIC. (ans 30 and 31… patient is 34 weeks preganat and involved in a car accident following which she starts bleeding per vaginally and 71has pain in abdomen also… i.e patient has abruption placenta and DIC is its complication which occurs due to release of thromboplastin)
• In managing DIC – use fresh frozen plasma-1unitof FFP raises – 5–10 mg/dl of fibrinogen.
• Cryoprecipitate – also increase fibrinogen but volume is not replenished
• Platelet should be given if count < 50,000/ml. Single unit transfusion raises platelet by 5000-10,000/ml. If Female is Rh negative give 300 mcg of anti d after platelet transfusion
• Side by side in abruptio delivery should be done
• Uncorrected DIC is a contraindication for vaginal delivery/LSCS. (ans 32…in the question patient is having abruption with elevated fibrin degradation products which means she has DIC, which should be corrected prior to delivery by giving fresh frozen plasma.)

 

• Fibrinogen 150 – 600mg/dl
• PT-11-16 sec
• PTT 22–37 sec
• Platelet – 1.5 to 3.5 lac D dimer /mm3
• D dimer – <0.5 mg/l
• Fibrin degradation products <10 mcg /dl
• In case of DIC: All clotting factors are consumed so levels of fibrinogen decrease, PT and PTT, FDP, d dimer all increase.

 

• Eclampsia is seizure or unexplained coma in a patient with preeclampsia
• HELLP syndrome is a variant of preeclampsia defined by following criteria:
  • – Hemolysis identified by Burr cells and schistocytes on an abnormal peripheral smear, an elevated serum bilirubin (>1.2 mg/dl) or LDH level (>600IU/L), or a low serum haptoglobin.
  • – Thrombocytopenia with platelets <100,000/microl is the most consistent finding in HELLP syndrome.
  • – Elevated Liver function tests (i.e transaminases) greater than two times the upper limit of normal.

 

• Always remember Pregnancy induced hypertension (Preeclampsia/Gestational hypertension) are raised BP conditions due to placental pathology(incomplete trophoblastic invasion) and always their definitive treatment would be to Terminate the preganacy and throw out the defective placenta.
• Antihypertensive of choice for Chronic hypertension in pregnancy-Methyldopa
• Antihypertensive of choice for Pregnancy induced hyper­tension(Preeclampsia/Gestational hypertension) Labetalol
• Antihypertensive of choice for Hypertensive crisis is-Labetalol.

   

• Route of delivery: Patients in labor or with a favorable cervix can deliver vaginally, for rest of the cases LSCS is indicated.

• In the question patient has past history of hypertension which was controlled on diuretics and ACE inhibitors prior to pregnancy.Till date her B/P was normal, she was not using any antihypertensive and now all of a sudden her BP is 142/84 mm of hg and proteinuria is 0.35g all this suggests a possibility of superimposed preeclamplsia on chronic hypertension.
• In this situation since BP is not much raised falling in the category of mild preeclampsia and gestational age is 35 weeks, no need to induce labor (labor should be induced at 37 weeks in mild preeclampsia) i.e option b ruled out.
• I/V Furosemide and hydralazine again are not justified in mild preeclampsia patients (Role of antihypertensives is controversial in the setting of mild preeclampsia) i.e options aand c ruled out.
• Her pre pregnancy regime which consisted of a diuretic along with ACE inhibitor cannot be started as ACE inhibitors are contraindicated during pregnancy ruling out optione.
• So we are left with option d-initial inpatient evaluation followed by restricted activity and outpatient manage­ment. Which is the most logical step.
• Also know: Worsening chronic hypertension is difficult to distinguish from superimposed pre eclampsia. If seizures, thrombocytopenia, pulmonary edema, unexplained hemolysis or elevation in liver enzymes develop, superim-posed preeclampsia should be diagnosed. Monitoring trends in BP and urine protein may be helpful. A 24 hr urine calcium measurement may also be helpful in detecting preeclampsia, as levels of urine calcium are lower (< 195 mg total urine calcium in 24 hrs) in preeclampsia patients than in patients with hypertension alone.

• In the question patient is presenting at 28 weeks with rise in BP and proteinuria which confirms her as a case of preeclampsia.
• The only confusion is whether she is a having mild preeclampsia or severe preeclampsia because that has a bearing on the management also.
  76
• Lets say this patient has severe preeclampsia:

  Points in favour of the diagnosis	Points against the diagnosis
  • Severe headache • 24 hour urine collection – 5g protein	• B/P-155/85 mm of hg • Proteinuria + 2

  Read for youself what John Hopkins has to say on this issue.
  “Severe preeclampsia is classified by the following criteria:
  1. BP during bedrest of >160 mm of hg systolic or >110 mm of hg diastolic or
  2. Proteinuria > 300 mg on a 24 hr urine collectioneven if BP is in the mild range”
     Ref. John Hopkins manual of obs and gynae 4/e, p186
• So our confusion about BP is over…now the second confusion is – this patients dipstick result favours mild preeclampsia whereas 24 hr urine result favours severe preeclampsia.
  Again read for yourself what JH manual has to say on this issue:
  “Preeclamptic patients often have a wide variation in urine protein values over time, possibly from renal vasos­pasm. Discrepancies between the random urine dipstick and 24 hr urine collection measurements have been well described. The 24 hr urine coolection, therefore remains the preferred measure for diagnosing preeclampsia ”.
  Ref. John Hopkins manual of obs and gynae 4/e, p186
• Our patient is thus a confirmed case of severe preeclampsia, and should be first managed by giving Mg SO₄ as a prophylaxis against seizures.
• Since she is only 28 weeks pregnant we will not perform cesarean immediately and try to carry the pregnancy uptil 34 weeks.

• Liquor: <200 ml, AFI<5 cms, single pocket<2 cms
• Causes:
• D: Drugs like Prostaglandin synthatase inhibitors, e.g. Indo­methacin
• I: IUGR
• L: Leaking following amniocentesis
• Mein: Maternal conditions like high B.P (PIH)
• P: Post dated pregnancy
• P: PROM
• A: Congenital Abnormalities-triploidy, Amnion nodosum
• R: Renal conditions of fetus like renal agenesis

         

1. Results in i.sinusoidal heart rate pattern.
2. Increased Peak systolic velocity in middle cerebral artery on Doppler study)

• Indirect Coombs test: It is done on maternal blood and if it is positive it indictes, Rh antibodies are formed in mother whereas a negative test indicates that Rh antibodies are not formed i.e isoimmunisation has not occurred.

• Principle behind giving Anti D is, that if anti D is given to a Rh negative mother and suppose due to anyreason fetal blood with Rh antigen enters mothers circulation, this Anti D will lead an antigen antibody reaction and fetal RBC will be destroyed before it could stimulate mothers immune system to produce Rh antibodies.
• Thus the usefulness of administering Anti D is only before maternal Rh antibodies are formed, if maternal antibodies are already formed then there is no point in giving Anti D.
• In other words Anti D should only be give if Indirect coombs test is negative.
• If Indirect Coombs test is positive then donot give Anti D, now it is important to know hoe much these antibodies have affected the fetus.
• Whenever in Rh negative mothers we want know, to how much degree fetus is affected:
  • – Do PUBS (perumbIlical blood sampling) and measure the hematocrit of fetal blood- but that is lil risky, so it should be the last resort.
  • – Since the degradation product RBC is bilirubin therefore when hemolysis occurs fetus has jaundice and this bilirubin is excreted via fetal urine into the amniotic fluid (this is the reason why 80amniotic fluid is golden yellow in colour in Rh negative isoimmunisation) so do amniocentesis and measure the amount- of bilirubin by doing spectrophotometric analysis and measuring the delta optical density 450 and plotting the results on Lileys chart…this is most common method.
  • – In case hemolysis has occured fetus becomes anemic and peak systolic velocity in middle cerebral artery increases on doppler. These days management is being based on it.

 

1. Rh negative nonimmunized women.
2. Rh negative immunized women.

 

1. Infant is Rh positive
2. Direct Coombs test on umbilical cord blood is negative.

     

• Serum antibody titers are done in these women every 4 weeks until the titers are found to be at or above the critical level (1:16).If titres are above critical level, there is no further use of antibody titer and the pregnancy is further monitored by middle cerebral artery peak systolic velocity (MCA-PSV) or amniotic fluid bilirubin concentration.
• If antibody titers remains below critical level up to 36 weeks, the patient should be delivered by elective induction between 38-40 weeks and the birth of unaffected or mildly affected fetus should be anticipated.
• If there is sudden rise of antibody titers above the critical level after 34 weeks but before 37 weeks of gestation, amniocentesis is done to assess the fetal lung maturity. Pregnancy should be terminated if the lungs are mature, but if the lungs are immature and the bilirubin level is low (less than 0.5 mg/dl), the pregnancy should be allowed to continue as long as weekly amniocentesis shows fetal pulmonary immaturity and a low bilirubin concentration. Delivery is contemplated as soon as these fetuses achieve lung maturity.

     

• Primi patient with Rh negative blood group
• She is 37 years old-elderly primi (>30 years) and has risk of Down syndrome (>35 years)
• She is concerned about the risk of having a down syndrome baby at this age and so insists on having amniocentesis done.
  • – Option a: Advise against amniocentesis as it will increase the risk of isoimmunisation –although the risk of isoimmunisation will definitely be increased but still I will not advise her against it seeing her age and her concern.
  • – Option b: Follow Rh titres carefully and give Anti D if evidence of isoimmunisation is present. Come on just now I have explained in that Anti d should be given only if evidence of isoimmunisationt is absent.Thus this statement is absolutely wrong.
    86
  • – Option c: Give Anti D at 28 weeks of pregnancy and after delivery if baby is Rh negative. If baby is Rh negative, no need to give Anti D.
  • – Option d: Give Anti D prior to her amniocentesis: This is the most logical step which should be done in this case.
  • – Option e: Give rubella vaccine as she is Rubella non immune: Now I don't need to explain that Rubella vaccine is contraindicated during pregnancy.

• It 2^nd most common cause of jaundice in pregnancy(m/c being hepatitis in pregnancy)
• It is characterized by accumulation of bile acids in liver.

• Manifestation appears beyond 30 weeks (i:e in 3^rd trimester) and occasionally in late 2^nd trimester.
• 1^st symptom to appear is pruritis-which has a predilection for the palms and soles. (pruritis appears 3 weeks before lab findings)
• Jaundice is sligh-t bilirubin levels rarely exceed 5mg.
• Recurs in subsequent pregnancies and so OCP's are contraindicated in females with H/O cholestasis during pregnancy.
• M/c in twin pregnancy.

 

• Serum bilirubin level increases and increase is always in direct bilirubin but bilirubin levels rarely exceed 5 mg.
• Serum alkaline phosphtase is mildly raised (increase in alkaline phosphatase is seen in liver damage, so it is seen in cholestatsis, 88but because the enzyme is also released by placenta in normal pregnancy so measurements are less useful as a diagnostic tool)
• SGOT/SGPT increased (in nearly 100% cases) rarely more than 250U/L
• Liver biopsy (definitive diagnosis)–no necrosis, no inflammation
• MGT-doc-ursodiol, corticosteroids,antihistaminics,vit k, choles­tyramine can also be used
• Time of delivery 37–38 weeks but if jaundice is present (as in question 42) then patient should be delivered at 36weeks
  Now coming to the Question No. 41
• A pregnant female with idiopathic cholestatic jaundice – is associated with
  Option a: Intense itching – True
  Option b: SGDT, SGPT < 60IU – True
  Option c: S. bilirubin > 5m g/dl – Incorrect
• In Idiopathic cholestasis of pregnancy bilirubin levels are rarely more than 5 mg as supported by:
  “Bilirubin levels rarely exceed 5 mg%” Ref. Williams 22/e, p 1126
  “Hyperbilirubinemia, results from retention of conjugated pigments; but total plasma concentration rarely exceeds 4-5 mg/dl”.
  Ref. Williams 23/e, p1064
  “Hyperbilirubinemia occurs in 20% of women and is almost exclusively direct reacting Bilirubin levels are usually between 2-5 mg/dl.”
  Ref. Mgt of High Risk pregnancy S.S trivedi, Manju puri Jaypee publication – pg 356
  Option d: Markedly increased levels of alkaline phosphatase-Incorrect. In cholestasis of pregnancy alkaline phosphatase may be mildly elevated and is not markedly elevated
• Thus both option c and d are incorrect but if I have to choose one option I would mark option ‘c’ as my answer:
  • – Based on the fact that alkaline phosphatase as such does not carry much significance in the diagnosis of cholestasis (whether it is mildly / Markedly elevated)
  “Alkaline phosphatase increases above the normal elevation but is not much helpful in diagnosis.”

   

• It is associated with disorders of fatty acid transport and oxidation
• Deficiency of LCHAD enzyme i.e. long chair hydroxyl aceyl coenz A dehydrogenase
• Risk are increased in case of:
  • – First pregnancy, male fetuses, preeclampsia, maternal obesity and multiple pregnancy.

• Liver is yellow, soft and greasy
• Swollen hepatocytes with central nuclei and cytoplasm filled with microvesicular fat

• Periportal sparing.
• Acute yellow atrophy.
• Minimal hepatocellular

 

• Patients present in the third trimester (generally at 37 weeks) with nonspecific symptoms like nausea, vomiting, anorexia, vague abdominal discomfort and malaise.
  90
• In many women, persistent vomiting is the main symptom.
• This is followed by jaundice after about one week.
• Acute fatty liver of pregnancy should also be suspected in any woman who presents with new onset nausea and malaise in third trimester.
• Ascities is seen in all patients.
• In 50% cases-features of preclampsia viz-hypertension proteinuria and oedema are present.

• Liver function tests are abnormal:
• Serum bilirubin is increased but less than 10 mg/dl
• Increase in SGOT and SGPT
• Alkaline phosphatase is increased (moderately)
• Prothrombin time may be increased
• Clotting time increased
• Clotting factors viz serum fibrinogen levels are increased
• In severe cases, there may be disseminated coagulation failure.

• increased S. creatinine (present in all patients)
• increased S. uric acid.
• increased S. Ammonia levels

• Decreased level of glucose (hypoglycaemia)
• Decreased platelet count
• Decreased fibrinogen levels.

• T/t of hepatic encephalopathy: Fresh frozen plasma, cryoprecipitate, platelets and blood.
• Rapid delivery is essential (Elective termination at 37 to 38 weeks is preferred).

 

• Hepatic encephalopathy
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• PIH
• DIC
• Renal failure

• Fetal prognosis is poor.
• If the fetuses survive, they may later on develop a Reye like syndrome of hepatic encephalopathy and severe hypoglycemia due to the defect in beta fatty acid oxidation.

 

• It is more likely to deteriorate in women with severe asthma.
• Exacerbations are most frequent between 24 to 36 weeks gestation and are most commonly precipitated by viral respiratory infections and non compliance with inhaled corticosteroid regimens.
• Because asthma exacerbation can be severe, they should be treated aggressively in pregnancy.
• Complications of asthma in pregnancy: Preterm labor, preeclampsia, LBW baby and slight increase in abruptio placenta
• Severity of asthma correlates with FEV1 (the FEV1 ideally is > 80% of the predicted, FEV1 less than 1L or less than 20% of predicted value, correlates with severe disease and PEFR (normally it ranges between 380-550 L/min).

• Mild asthma: inhaled beta agonist (albuterol preferred because of more human data on safety in pregnancy)
• Mild persistent: Low dose inhaled corticosteroids (Budesonide preferred)
• Moderate: Low dose inhaled corticosteroids and long acting b agonist (Salmetrol preferred)
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• Severe: High dose inhaled corticosteroid and long acting beta agonist and oral steroids if needed.
• PGF-2alpha is absolutely C/I in patients of Asthma
• So if in an asthamatic patient PPH occurs drug of choice is PGE1.
• In asthamatic patients DOC for cervical ripening-PGE2 (PGE2 is not contraindicated in asthamatics)

 

• M/C cause-Autoimmune cause-Hashimoto thyroiditis
• Hypothyroidism can lead to Mental retardation in baby, abortion, stillbirth, IUGR, prematurity
• Since maternal Hypothyroidism in pregnancy (whether overt or subclinical) may impair featl neuropsychological development, hypothyroidism should be treated adequately in pregnancy.
• Thyroxine requirement increase during pregnancy and this increased requirement begins as early as 5 weeks.
• DOC for thyrotoxicosis in pregnancy–Propylthiouracil.

• Twin preganancy can be monozygotic (uniovular) or Dizygotic (binovular).
• Uniovular twinning occurs due to fertilisation of a single ovum by a single sperm followed by fission of single fertilized ovum. It is less common than binovular twins (i.e option a is incorrect).
• Uniovular twins are always of the same sex and are identical in appearance, resembling each other both physically and mentally, and even at times showing the same pathological tendencies.
• Uniovular or monozygotic twins can have a single placenta (monochorionic) OR can have separate placenta (dichorionic) depending on the time of division of the fertilized ovum.

 

• Binovular is fertilization of two ova by two sperms. Such twins are more frequent than uniovular (3:1). They may be of the same sex or opposite sexes and show a degree of resemblance no more than that of brothers and sisters from different births, this is the reason they can be called as “fraternal twins”.
• Binovuar or dizygotic twins always have 2 placenta, i.e they are dichorionic.
• Thus dichorionicity can either be due to dizygotic or it could be due to monozygotic twins (i.e option d is incorrect)
• The incidence of monozygotic twins is fixed throughout the world..1 in 250 deliveries, whereas incidence of Dizygotic twins varies from region to region, being maximum in nigeria. (i.e option c is incorrect)
• Although multifetal births account for only 3% of all live births, they are responsible for a disproportionate share of perinatal morbidity and mortality. (i.e option e is incorrect)
• There is a higher risk of low birth weight babies and preterm labor. Multiple pregnancies are commonly associated with moderate to severe anemia, gestational hypertension malpresentation, polyhydramnios, cord prolapse,abruption or placenta previa.
• It's also associa1ted with abnormalities like discordance, twin reversed arterial perfusion (TRAP) or conjoint twins.

• As discussed dizygotic twins always have dichorionic and diamniotic placentas (i.e option a and c are incorrect)
• Monozygotic twins can have monochorionic or monoamniotic placentas depending upon the time of division…but always remember- The amnion develops after the chorion, so dichorionicity implies diamnionicity … it can never be that a twin is dichorionic but monoamniotic (i.e option b is incorrect)

 

• It is always seen in monochorionic placenta.
• There is an AV malformation such that there exists a communication from the umbilical arterial system of the “donor” twin to the umbilical vein of the “recipient” twin.
• The donor twin is growth restricted, hypovolemic, has oligohydramnios and is anemic becoz it gives blood to the recipient twin. The recipient is larger, hypervolemic, has polyhydramnios and is plethoric. It has also been termed as Twin Oligohydramnios/Polyhydramnios Sequence (TOPS).
• The earlier the TOPS appears, worse will be the prognosis.
• TTTS is more common in female fetuses.
• Coming to the question- Twin A is the recipient twin and Twin B is the donor twin since it has oligohydramnios. Thus Twin A can have CHF- due to volume overload, will have hydramnios and can have thrombosis since it has polycythemia which can lead to thrombosis, but never will it have anemia.

 

• Since Arterial supply from the donor twin drains into the venous system of recipient. Doppler can pick up the vessels from one twin's umbilical cord and then finding a continuing vessel with venous flow coursing towards the co-twin's umbilical cord.

 

• Amnioreduction has shown improvement in fetal survival in 65% of cases. When the amniotic fluid exceeds 40 cm, one liter of fluid is removed for every 10 cms rise above normal.95
• This procedure takes care of polyhydramnios and fetuses are born later in gestation and weigh more than untreated cases with TOPS. (Twin oligohydramnios – Polyhydramnios sequence)
• Amniotic septostomy can create artificial opening between the gestational sacs to produce in effect a monoamniotic pregnancy. TTTS is seldom seen in monoamniotic gestations. There is speculation that the donor twin has access to amniotic fluid via the opening so it can correct the oligohydramnios by oral rehydration.
• The vessels on the placental surface can be ablated by neodymium:yttrium-aluminumgarnet laser -Severe twin–twin transfusion syndrome presenting before 26 weeks of gestation should be treated by laser ablation rather than by amnioreduction or septostomy.
• Finally, selective fetoreduction (SFR) can treat TTTS but this method is reserved for refractory cases to other forms of therapy or when in utero death of one of the twins is imminent.

   

• P–Prostaglandin synthatase inhibitor like indomethacin, sulindac
• C–CA channel blocker-Nifedipine
• O–Oxytocin antagonist-Atosiban
• D–Diazoxide
• Mein–Mg SO4
• NO–Nitric oxide inhibitor-Glyceryl triniitrate
• Periodic–progesterone
• Bleeding–b mimetics-salbutamol, ritrodrine, isoxsuprine, terbutaline

   

• Safest tocolytic is atosiban (oxytocin antagonist)
• Beta agonist is contraindicated in cardiac arrthymias, valvular disease and cardiac ischemia because of their sympathomimetic side effects such as tachycardia, palpitation and hypotension.
• Nifedipine is contraindicated in conduction defect, left ventricular failure due to side effects as tachycardia, hypotension, etc.

• Friends there are a number of conditions in which labor can be induced, so for all such Questions remember those conditions in which induction of labor is contraindicated.
• Contraindications for induction of labor-All those condition in which cesarean section necessarily has to be done, are contraindications for induction of labor viz.
• C–Contracted pelvis (Naegles pelvis/Roberts pelvis)/Advanced Cervical cancer
• A–Active genital herpes infection/High viral load HIV
• P–placenta previa/Vasa previa/Cord prolapse
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• U–Uterine scar of classical cesarean section, myomectomy scar, hysterotomy scar
• T–Transverse lie.

   

• Administering a uterotonic agent after the delivery of the shoulder of the baby.
  The uterotonic agent of choice is oxytocin followed by methy­lergometrine.
• Delayed cord clamping, so that the blood in the cord (approx. 40–50 ml) goes to the baby and is not wasted.
• Delivery of the placenta by controlled cord traction/Modified Brandt Andrews technique.
• Massage of the uterus after the delivery of the placenta.

• Preterm or growth restricted fetus due to risk of hypervolemia (even an extra 40-50 ml of blood can cause CHF in premature infants)
• Birth asphyxia (first immediately resuscitate the baby and then think about anything else)
• Rh isoimmunization
• HIV positive female
• Maternal diabetes.

 

• Going with the drill, we should first try 1^st line steps and then others, this rules out option d i.e Push infants head back into the uterus and do cesarean section and e i.e do a symphiosotomy.
• Fundal pressure should never be applied in case of shoulder dystocia ruling out option (b).
• This automatically leaves us with 2 options (a) abduct mothers thigh and apply suprapubic pressure and (c) i.e Flex mothers thigh against her abdomen.
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• Now this is common sense that while doing Mc Roberts manouvre we will first flex the patients legs, and then abduct them and not vice versa…so the immediate next step is flex her thighs, i.e option (c).

• Patient is coming in preterm labor-31 and has contractions every 8 mins lasting for 20–30 secs
• She is not sure whether her water bag has broken or not(i.e unsure whether Preterm premature ruture has occurred or not)
• Cephalic presentation and no fetal distress

• Cervical culture for group B streptococci – incorrect as the usual time for screening for GBS is at 36 weks, since this patient is in preterm labor and GBS status is unknown, we will not do culture and wait for the report…by that time she would have already delivered and infant already infected, so we will give her a shot of penicillin as a prophlaxis against GBS
• Digital cervical examination and assessment of dilation and effacement- incorrect as patient isnot sure whether her bag has broken or not, just in case membranes have ruptured, digital examination is contraindicated.

• Quantification of strength and timing of contraction with external tocometer- not necessary since we have already been given the frequency and duration of uterine contraction.
• Speculum examination to rule out leaking and usually assess cervical dilatation and effacement-this is the logical next step in this patient. In all cases of preterm labor before performing digital examination sterile speculum examination should be done to rule out ruptured membranes and to assess cervical dilatation.

• “Sterile speculum examination- done to inspect visually for bleeding, amniotic fluid pooling,advanced dilatation, bulging membranesand purulent cervical discharge. After ruling out PPROM, perform digital examination for dilatation, effacement, and station.”

• USG examination of the fetus- Iknow most of you must have thought this option is the correct answer but always read the Q very carefully…they are asking the next best step in manangement—which will be Sterile speculum examination… Always remember not only for exams but also for your practice years, whenever a female come to you in labor, before knowing how much she is dilated donot send her for USG, because if she delivers on the way…next day you will be in news…!!!!!

 

• Patient is in labor has been completely dilated and pushing for 3 hrs
• She has taken epidural analgesia.
• She is exhausted and her temp is 37.8^c (i.e maternal distress is present)
• FHS is 170/min with decreased variability. (i.e fetal distress is present.
• P/V shows cervix is fully dilated and fetal head is at +3 station.
• This is a case of prolonged second stage of labor with fetal distress.
• Second stage: Normal duration is 0-30 mins for multiparous and 2 hours for nulliparous.
• Prolonged second stage is defined as:

  Nulliparous	Multiparous
  >2hr	>1hr	Without epidural analgesia
  >3hr	>2hr	With epidural analgesia

• In the question patient is fully dilated i.e she is in second stage of labor and is a primigravida who has taken epidural analgesia, has been pushing for 3 hrsand has still not delivered i.e prolonged second stage.
• Management of prolonged second stage is either instrumental delivery-forceps/ventouse or Cesarean section.

• Forceps are better than vaccum in fetal distress
• In case of fetal distress, with full dilatation of the cervix and station of fetal head at or below +2 station- Forceps are much faster way of delivery than cesarean section.

• Patient is in labor for one hour
• She belives her water bag has broken
• She has H/O previous LSCS for fetal distress.
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• All P/A examination findings are normal
• Fetal heart rate tracing is normal. (baseline FHS 140/min, beat to beat variability is present, occasional heart rate acceleration of 160/min for 15–20 secs. There are also decelarations to 115–120/min with the onset of contractions- note decelerations at the beginning of contraction signify early decelerations are normal becoz when contraction begins, head of the baby is compressed producing decelaration but it recovers soon)

• Augment contractions with oxytocin–personally I would not do it for two reasons
  • – She ia a previous LSCS patient
  • – Oxytocin should be given to augment labor when the patient is in active phase of labor. Avoid using oxytocin in latent phase as chances of fetal distress and cesarean are increased. (and I know she is still in latent phase probably because she is in labor for 1 hour only)
• Monitor and follow labor on partogram- very logical step and should be done in all patients in labor irrespective of whether he is a previous cesarean section patient or not.
• Obtain immediate consent for LSCS: Why will I do it??? There is no indication for doing cesarean in this patient as her previous LSCS was done for fetal distress not for any recurring cause like contracted pelvis.
• Send the patient for BPS: Again no need as there is no fetal distress or any other indication for doing so.
• Perform urgent aminoinfusion–no need, even if her membranes have ruptured, she is already in labour.

• Patient is presenting with C/O decreased fetal movements.
• FHR = 180/min with absent variability (i.e fetal distress is present)
• Uterine contractions are present-every 3 minutes
• O/E-Cervix is long /closed/-2 station.
• Friends always remember–The earliest indication of fetal distress is 103known by the mother–whenever a pregnant female complains of decreased fetal movements, do not ignore it- rule out fetal distress and then send the patient back home.
• In this case patient is complaining of decreased fetal movements and fetal heart rate is 180 i.e fetal distress is present so. Option a–i.e emergency cesarean section should be done. Since cervix is not favourable and fetal distress present we cannot wait for vaginal delivery.

     

• This patient is presenting at 41 weeks with uncomplicated pregnancy and good fetal kick count, i.e there is no fetal distress. I n such a 104situation i.e in uncomplicated pregnancies maximum we can wait uptil 42 weeks for spontaneous labor pains.
• The international definition of prolonged /postterm pregnancy, endorsed by ACOG is 42 completed weeks or 294 days days or more from the Last menstrual period. Pregnancies between 41 weeks and 1 day and 41 weeks and 6 days, although in the 42^nd week, do not complete 42 weeks until the seventh day has elapsed.
• Protocol for management of pregnancy at or beyond 41 weeks.

 

• Nulliparous–cervix dilates by < 1.2 cms/hr or descent of fetal head is < 1cm/hr
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• Multiparous – cervix dilates by < 1.5 cm/hr or descent of fetal head is < 2cm/hr
• Arrest of dilatation–no dilatation for >2hrs
• Arrest of descent–no descent for > 1hr.

 

• Emergency cesarean section
• Forceps delivery only if station of fetal head is below or at +2 station and cervix is fully dilated.

1. Long cord
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2. Polyhydramnios
3. Abnormal lie (transverse, breech, and oblique)
4. Multiple pregnancies
5. Floating (unengaged) head

• Now friends in this question there is a trap, the question which is asked is unrelated to the clinical scenario described before the question.
• The question is simply asking the condition in which we can use forceps:
  • – Option a. Fetal distress during active stage of labor- now friends, active stage of 1^st stage of labor begins when cervix is 3 cms dilated and ends when cervix is fully dilated and one of the prerequisites of forceps is that cervix should be fully dilated thus forceps cannot be applied in the active stage of first stage of labor. In case of fetal distress occurring in107
    active stage of labor the only treatment option is cesarean section.
  • – Option b. Labor complicated by shoulder dystocia- forceps are not used, management is Mc Roberts manouvre.
  • – Option c. Prolonged active stage of labor due to inadequate uterine contraction strength-management is oxytocin to increase uterine contraction strength, again we have already discussed forceps shouldnot be used in active phase of labor.
  • – Option d. Prolonged latent stage of labor due to inadequate uterine contraction strength-again latent phase of labor is when cervix begins dilating and lasts uptil it is 3 cms and so forceps cannot be applied.Prolonged latent phase is managed by therapeutic rest.
  • – Option e. Prolonged second stage of labor due to adequate uterine contraction strength. Second stage of labor begins when cervix is fully dilated and ends with the delivery of the baby, so logically in this stage forceps can be applied if uterus is contracting (which is so in this patient also)

• Fetal distress in the second stage of labor
• Maternal distress in the second stage of labor
• Prolonged second stage of labor
• Prophylactic use of forceps is done when mother has heart disease or PIH, to cut short the second stage of labor.

 

• The most important point of reference in the use of forceps is the station of Biparietal diameter.
• Usually forceps should not be applied if head is above + 2 station and if head is unengaged.

   

• Option a: Fetus should be in vertex or mentoanterior position is correct
• Option b: Sagittal suture should be less than 15° from antero posterior plane is incorrect
• Forceps can be applied till maximum 45° rotation
• Option c: There should be no caput succedaneum- Again incorrect as presence of caput succedaneum is not a contraindication for forceps application
• Option d: Head should be at zero station also incorrect as outlet forceps is applied when head reaches the perineum

• Normally all the parts of fetal body are flexed, i.e the fetus lies in an attitude of flexion, now this is common sense that when there is face presentation the head has to be extended, i.e a deviation from the the normal attitude.
• Important Terms Frequently Asked
• Fetal lie: Refers to relation of long Axis of fetus to long axis of mother

• Fetal presenting part-It is that part of the presentation which overlies the internal os.
• In cephalic presentation the most common presenting part is Vertex, since head of the fetus is flexed mostly.
• Others could be Brow or face presentation, depending on the degree of extention.

• Fetal position is the relationship of point of direction of presenting part to one of the four quadrants of maternal pelvis. Most common being Left Occipito transverse followed by Left occipito anterior.
• M/C fetal malposition is occipito posterior position (management is wait and watch).

• Gestational age is 37 weeks.
• On vaginal examination the cervix is 50% effaced and 1- 2 cm dilated.
• The presenting breech is high out of pelvis, i.e it is not engaged and version can be attempted.
• The estimated fetal wt. is about 7 lb (i.e it is not much that vaginal breech delivery cannot be attempted)
• Usg confirms fetus is in frank breech position, there is a normal amount of amniotic fluid present, and the head is well flexed.(all factors favoring version and vaginal breech delivery).
• Since patient is 37 weeks pregnant and presenting part is high out of the pelvis, amount of amniotic fluid is adequate so we can attempt external cephalic version and yes since version carries a risk of fetal distress and cesarean section. I will give the patient a chance to discuss with her family members and come back to me in a few days if she wishes for external cephalic version. ( i.e option d is correct).

• Pregnancy-1st trimester
• After vaginal delivery-after 24 hrs
• After cesarean section-after 24 hrs.

• Kiegels exercise has a limited effect as it affects mainly voluntary muscles viz bulbocavernous, levator ani, superficial and deep transverse perineal muscles and not the main fascial supporting tissues.

   

• Warfarin is contraindicated in the first trimester of pregnancy as it can lead to contradi syndrome comprising of microcephaly, optic atrophy, nasal hypolplasia and chondrodysplasia punctate. It can also lead to IUGR, abortions and IUD.
• But warfarin is absolutely safe during lactation as an extremely minute quantity of it is excreted in breast milk.

• If patient would have been an asthamatic then our answer would have been misoprostol since PGF2a is contraindicated in them.
• If patient would have presented 24 hours after delivery then the answer would have been Dilatation and curettage as the most common cause of secondary PPH is retained placental bits.

 

• Globulin
• Fibrinogen
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• Transferrin and Total iron binding capapcity
• Leukotrienes.

 

• It is the other name for pregnancy specific B1 glycoprotein.
• Produced by trophoblast.
• Can be detected 18 days after ovulation.
• Its concentration rises steadily and reaches 200mg/ml at term.
• Role-measure of placental function for fertility control.

   

• Size of kidney ↑ ‘s (1 cm longer)
• Dilatation of kidney resembling hydronephrosis
• Ureter – Dilatation (Right > Left) → occurs in midpregnancy
• Ureteral elongation which resembles angulations on X-ray.
• Bladder – due to ureter dilatation = hyperemia occurs.

 

1. Bimastoid
2. Bitemporal
3. Occito frontal
4. Submento vertical

 

• Measured between 11–13 weeks
• NT-upto 3mm is normal and > 3 mm is marker for Downs syndrome(60% cases)
• Nuchal fold thickness > 5mm is the most imp sonographic marker of aneuploidy in second trimester

     

• HCG
• Estriol
• Alpha feto protein (Maternal).

     

1. Alpha fetoprotein
2. HCG
3. Estriol
4. Inhibin: Note levels of inhibin are increased in Downs. Syndrome. (Remember I = for Inhibin and I for increased)

 

• Done at 10–12 weeks preferebly
• Done transcervically: 10–12 weeks
• Done transabdominally: 10 weeks to term.
• M/C complication is-Fetal loss
• If done before 9 weeks it results in oromandibular limb defects
• Chorionic villi sampling can detect
  1. Chromosomal anomaly of the fetus like downs syndrome
  2. Metabolic diseases like- Gauchers disease, Tay sachs disease, Niemann pick disease, Phenylketonuria
  3. Hemoglobinopathies –sickle cell anemia, Hemophilia

 

• An intrauterine Gestational Sac should be seen by TVS when maternal serum Bhcg level is 1000-1200 micro IU/ml and by TAS with levels of 3000-6000 micro IU/ml.
• Gestational sac is eccentric and can be seen at 4weeks and 5 days on TVS
• Double decidua sign of gestational sac is due to interface between the decidua and the chorion, which appears as 2 distinct layers of wall of the gestational sac and differentiates gestational sac from pseudogestational sac of ectopic pregnancy.

 

1. To confirm pregnancy
2. To confirm the no of fetuses
3. To detect congenital anomaly-
   • – Earliest congenital anomaly detected by USG is anencephaly
   • – Earliest time to diagnose anencephaly-10 weeks
   • – Anencephaly is best diagnosed at 14 weeks
   • – To detect all congenital anomalies single scan should be performed at 16-20 weeks
   • – Marker for Downs in 1^st trimester on USG are –Absent nasal bone and increased nuchal translucency
   • – Banana and Lemon sign are seen on USG in case of -Spina Bifida122
4. To confirm gestational age:

   Trimester	USG parameter used
   1st Trimester	CRL-crown rump length
   2nd Trimester	HC (head circumference)>BPD (biparietal diameter)
   3rd Trimester	FL (femur length)>HC, BPD
   Overall best parameter and best time to confirm gestational age is	CRL and first trimester.

5. To assess fetal growth–Best parameter-AC (abdominal circumference).

• It is a glycoprotein^a synthesied by the fetal yolk sac^a in the early weeks of gestation and by the gastrointestinal tract and liver later.
• Concentration AFP is maximum in fetal serum at 13 weeks. Maximum concentration of AFP is seen in fetal serum.
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• AFP passes from the fetus to the amniotic fluid by the way of urine and can be detected in amniotic fluid by amniocentesis (diagnostic test)
• It passes into the maternal serum by diffusion and can be detected in maternal serum after 12 weeks
• Maternal screening is done between 15-20 weeks. In maternal serum levels peak at 32 weeks.

 

• Fetal serum contains AFP in a concentration 150 times that of maternal serum.
• Acetyl cholinesterase levels in amniotic fluid is more specific than AFP in predicting Neural tube defects

 

• Induction of abortion (Instillation of chemicals e.g; hypertonic saline, urea, prostaglandin)
• Repeated decompression of the uterus in acute hydramnios.

• Decompression of uterus in unresponsive cases of chronic hydramnios
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• To give intrauterine foetal transfusion in severe hemolysis following Rh-isoimmunisation.
  • – Time for performing amniocentesis- 16-20 weeks
  • – A 20–22 gauze spinal needle is used.
  • – Length of needle is 4² (014inches or 10 cm)
  • – Amount of amniotic fluid to be collected for diagnostic purposes is 10 ml.

• Prior USG localization of placenta to prevent feto-maternal bleeding.
• Prophylactic administration of 100 microgram of anti-D Ig in Rh-negative non- immunised mother.

 

• Trans-isthmic suprapubic approach after lifting the presenting part OR
• Through the flanks in between the foetal limbs OR
• Below the umbilicus behind the neck of the fetus.

 

• Seen in 0.7-0.8% single pregnancy and 5% twin pregnancy
• Increased incidence is seen in Diabetic pts, black pts, with eclampsia, APH, hydramnios and oligohydramnios
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• Finding of a single umblical is not insignificant as it means increased incidence of congenital malformations(renal/genital), Trisomy 18 and abortion, IUGR, preterm labor in the fetus.

• Möbius syndrome is an extremely rare congenital neurological disorder which is characterized by facial paralysis and the inability to move the eyes from side to side.
• Most people with Möbius syndrome are born with complete facial paralysis and cannot close their eyes or form facial expression.
• They have normal intelligence
• Möbius syndrome results from the underdevelopment of the VI and VII cranial nerves
• Causes: The causes of Möbius syndrome are poorly understood. Möbius syndrome is thought to result from a vascular disruption (temporary loss of bloodflow) in the brain during prenatal development. There could be many reasons for the vascular disruption leading to Möbius syndrome. The use of the drugs misoprostol or thalidomide by women during pregnancy can lead to mobius syndrome.

• There are increased chances of preterm delivery, placenta previa, abruptio and Abortion.
• It leads to Congenital heart defects, gastrochisis and small intestine atresia, cleft lip and palate in the fetus.

1. Dysmorphic facial features-
   1. Small palpebral fissures
   2. Thin vermilion border
   3. Smooth philtrum
2. Prenatal/and or postnatal growth impairment
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3. CNS abno rmalities:
   1. Structural: Head size < 10 percentile, significant brain abnormalit y on imaging
   2. Neurological
   3. Functional Global cognitive or intellectual deficits, functional deficits in atleast three domains.

1. Cardiac-atrial or ventricular septal defect, aberrant great vessels, conotruncal heart defects.
2. Skeletal-radioulnar synostosis, vertebral segmentation defects, joint contractures, scoliosis.
3. Renal-aplastic or hypoplastic kidneys, dysplastic kidneys, horse shoe shaped kidney, ureteral dilatation.
4. Eyes-Striabismus, ptosis, retinal vascular abnormalities, optic nerve hypoplasia.
   Ears-Conductive or neuriosensory hearing loss
   Minor-Hypoplastic nails, clinodactyly, pectus carinatum or excavatum, camptodactyly, hockey stick palmar crease, railroad track ears.

• Symptoms lastfor < 10 days
• Abnormal respiratory function during sleep can lead to sudden death.

   

• NST testing should be started 32-34 weeks
• Interval between NST testing
  • – Ideally – repeated weekly (a reactive NST means that fetus is not in danger for atleast 7 days
  • – In high risk pregnancies like diabetes mellitus, IUGR and Gestational hypertension! twice weekly
  • – In severe preeclampsia remote from term – done daily
• The positive and negative predictive value of a NST is typically less than 50% and more than 90% which means a reactive NST is more reliable in excluding fetal hypoxia than a non reactive test in predicting fetal compromise
• A non reactive NST earlier was being followed by a CST (contraction stress test) to confirm the diagnosis of hypoxia but CST is associated with risk of initiating labour and hence these days a non reactive NST is being followed by a biophysical score (Manning score)

• Early-(Type1)-Head compression/vagal nerve stimulation
• Late (Type 11)-uteroplacental insufficiency and fetal hypoxia
• Variable deceleration (M/C type) -cord compression
• Sinusoidal heart rate pattern - Stable, fixed heart rate with fixed variabilty and without any accelerations. Seen in fetal anemia and fetomaternal haemorrhage.

   

• Small BPD
• Venticulomegaly (> 10 mm)
• Frontal bone scalloping- Lemon sign – as shown in the usg given in the question.
• Elongation and downward displacement of cerebellum-called as Banana sign(banana sign disappears after 24 weeks)
• Obliteration of cisterna magna
  NOTE: Ninety nine percent of fetuses with NTD have one of the above-mentioned 5 specific cranial abnormalities.
  Lateral ventricle is measured at the atrium-normal =7mm from15 wks onward
• Mild-ventriculomegaly-10-15 mm
• Overt->15 mm
• A dangling choroid plexus is seen in severe cases
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• OOCPs and IUCD
• Mycophenolate
• Mehotrexate

 

• Second twin transverse lie
• Always do under GA
• M/C complication-Rupture uterus

• ≥ 35 yrs   In singleton pregnancy
• ≥ 31 yrs   In twin pregnancy
• ≥ 31 yrs   In h/o previous down syndrome

   

• IUGR (most important investigation for management)
• Rh iso immunization
• Prediction of PIH
• Diagnosis of placenta accreta/ percreta, vasa previa.

   

• – A normal systolic/ diastolic (S/D) ratio indicates that the fetus is receiving adequate blood supply.
• – Rising S/D is the earliest change in IUGR.
• – Absence of diastolic flow in umbilical artery is an ominous sign and Intrauterine fetal death can be expected within 7 days.
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• – In extreme cases diastolic flow may become reversed and IUFD will occur with in 48 hours.

     

1. Associated midpelvic or outlet contraction
2. Presence of complicating factors like-
   • – Elderly primi
   • – Malpresentation
   • – Post maturity
   • – Post cesarean section
   • – Preeclampsia
   • – Medical disporders like DM, heart dis.

 

• In Contracted pelvis-obstetric conjugate <10 cms
• If Obstetric Conjugate is 9.6 cms to 10 cms –mild contraction
• If it is 8.6 to 9.5 cms –moderate contraction
• If <8.5 –Severe contraction

 

• DOC to prevent and treat convulsions in eclampsia
• Mech-decr acetylcholine release and blocks ca channel(so use carefully with Ca channel blockers)
• Therapeutic range-4 to 7 meq/l
• First sign of toxicity- loss of knee jerks->10 meq/l
• Respiratory depr occurs if mg conc >12meq/l
• Regime followed-Pritchard regime

• Bacterial Count >105 /ml in midstream clean catch sample on 2 occasions in an asymptomatic patient is referred to as Asymptomatic bacteriuria.
• M/C organism -Ecoli
• Incidence in pregnancy and non pregnant -1 to10%
• m/c in multiparity, diabetic patients and sickle cell trait patients.