Presentation on the description of normal and abnormal uterine bleeding, menstrual cycle, FIGO classification with PALM-COEIN, common differentials of AUB, assessment, diagnosis, and management.
Presentation on the description of normal and abnormal uterine bleeding, menstrual cycle, FIGO classification with PALM-COEIN, common differentials of AUB, assessment, diagnosis, and management.
Interesting Update on Recurrent Miscarriage for Indian Gynaecologoists D...Lifecare Centre
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The effect of Metformin on endometrial tumor-regulatory genes and systemic metabolic parameters in polycystic ovarian syndrome – a proof-of-concept study
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Surgical Site Infections, pathophysiology, and prevention.pptx
Bad obstetric history
1.
2.
3. Bad Obstetric History (BOH)
What to do about it?
By Dr Yong Soon Leong
Supervisor: Dr Haris N Suharjono
4. Definition
• The term “bad obstetric history” is often
loosely used to signify that a woman has
had previous disappointments in
childbearing.
Donald, I. (1969): Practical Obstetric Problems, 4th ed., p. 99.
London: Lloyd-Luke Medical Books.
5. Bad Obstetric History
• What can be construed as BOH?
1st or 2nd trimester miscarriages
Still births or neonatal deaths
Pre-term labour
Fetal anomalies?
How about h/o HIE leading to cerebral palsy?
Shoulder dystocia? Massive PPH? Classical
caesarean section?
6. What to do about it?
• A detailed obstetric history is important.
• Review the previous medical records and any investigation
results.
• Identify any recurrent or non-recurrent causes of
pregnancy loss and put in place a management plan to
reduce or modify the risks in the current or future
pregnancies.
THE AIM IS TO LEARN FROM THE PAST PREGNANCIES
AND ENSURE A MORE FAVOURABLE OUTCOME IN THE
CURRENT OR FUTURE PREGNANCY...
7. Detailed History
• Consanguinity
• Previous pregnancy performance
• Drug and environmental exposure
• Family history of thrombotic events, pregnancy losses or
complications
• History of infertility
• Symptoms of metabolic disorders, autoimmune disorders
8. What causes it?
• There are a multitude of possible causes of
BOH…identify the cause and we are
halfway there!
• One of the biggest obstacle however is the lack of details in previous
pregnancies…APPROPRIATE DOCUMENTATION HELPS!
12. Acquired / Inherited
Thrombophilia
Acquired
• Antiphospholipid
syndrome
Inherited
• Protein C deficiency
• Protein S deficiency
• AT deficiency
• Activated protein C
resistance
• PT gene mutation
13. Antiphospholipid
Syndrome
• Refers to association between antiphospholipid
antibodies and adverse pregnancy outcome or vascular
thrombosis.
• Adverse pregnancy outcome includes
• ≥ 3 consecutive miscarriage < 10 weeks gestation
• ≥ 1 morphological normal fetus losses after 10th week of
gestation
• ≥ 1 preterm birth before 34th week owing to placental
disease
14. Antiphospholipid
Syndrome
• Mechanism of disease
• Inhibition of TROPHOBLASTIC function and differentiation
• Activation of complement pathways at the maternal-fetal interface
resulting in a local INFLAMMATORY response
• Thrombosis of utero-PLACENTAL vasculature in later
pregnancy
• Present in 15% of women with recurrent miscarriage.
• Without treatment, live birth rate is as low as 10%.
16. Antiphospholipid
Syndrome
• Fetal death can follow IUGR, oligohydramnios, pre-eclampsia.
• Risk of IUGR: > 30%
• Increase risk of non-reassuring fetal heart rate pattern in labour
• Pre-eclampsia is often severe.
• Previous recurrent loss: 10%
• Previous thrombosis / late fetal death: 30% – 50%, PET may develop as
early as 15 weeks.
• Preterm birth risk.
• Previous recurrent loss: 10%
• SLE / previous thrombosis / late fetal death: 30% – 40%,
17. Inherited thrombophilia
defects
• Protein C & S deficiency
• Anti-thrombin III deficiency
• Activated protein C resistance (due to Factor V Leiden mutation)
• Prothrombin gene mutation
• Hyperhomocysteinaemia
• Mechanism:
• thrombosis of uteroplacental circulation
18. Inherited thrombophilia
defects – recurrent risk of thrombosis
Protein S
deficiency
Protein C
deficiency
Anti-thrombin III
deficiency
19. Inherited thrombophilia
defects – recurrent risk of thrombosis
Protein S
deficiency
Protein C
deficiency
Anti-thrombin III
deficiency
15% (12-17%)
25% (22-26%)
35% (32-51%)
20. Inherited thrombophilia
defects – recurrent risk of thrombosis
Protein S deficiency
Protein C deficiency
Anti-thrombin III deficiency
Activated protein C resistance (due to
Factor V Leiden mutation)
Prothrombin gene mutation
Low
prevalence
in Asians
& Africans
21. Inherited thrombophilia
defects
• Adverse pregnancy outcome:
• Pre-eclampsia
• IUGR
• Placental abruption
• Recurrent early miscarriage
• Late fetal demise
• Intrauterine death and stillbirth
22. Parental genetic
disorders
• One of the parents carries a balanced structural
chromosomal anomaly
• Most commonly a balanced reciprocal or Robertsonian
translocation
• Possible outcome:
• Miscarriage
• Live birth with multiple congenital malformation and/or
mental disability due to unbalanced chromosomal
rearrangement
24. Anatomical factors
• Uterus
• Congenital uterine malformation
• Arcuate uteri tend to miscarry in second trimester
• Septate uteri more likely to miscarry in first trimester
• Term delivery rate of only 50%
• Acquired: submucosal fibroid, uterine synechiae
• Cervical incompetence
• History of second trimester miscarriage preceded by SROM
or painless cervical dilatation
26. Infections
• Bacterial vaginosis
• BV in the first trimester is a risk factor for second trimester
miscarriage and preterm delivery.
• Treatment with oral clindamycin reduces complication rate.
• ? TORCHES
• Not recommended as these diseases do not persist in genital
tract and, patients often symptomatic and were treated
earlier.
• Thus, less likely to cause repeated pregnancy loss
30. Pre-eclampsia - prediction
Is uterine artery Doppler velocimetry of
value in the clinical management of women
at high risk of pre-eclampsia / IUGR?
- Still a controversial issue whether to screen in
the first trimester, 20 weeks, 24 weeks?
31. Investigations
Acquired / Inherited thrombophilia
• APS screening (2 positive tests ≥ 6 weeks apart either lupus
anticoagulant / anticardiolipin antibody in a median / high titre over
40 g/l / ml/l or above 99th percentile)
• Lupus anticoagulant:
• Activated partial thrombin time (APTT) vs Dilute Russell
viper venom time (dRVVT)….the latter is more sensitive and
specific
• Thrombophilia screening (Factor V Leiden, Factor II (prothrombin)
gene mutation , Protein S)
33. Thrombophilia screening
• A history of recurrent, atypical, or unprovoked (not
associated with COC, pregnancy, trauma, or surgery)
thromboembolism
• A family history of thromboembolism
• Universal screening of women with BOH for inherited
thrombophilia? Not recommended, only screen those with
risk factors
34. Investigations
Parental genetic disorders
• Cytogenetic analysis on POC of 3rd & subsequent consecutive
miscarriage
• Parental peripheral blood karyotyping if POC reports unbalanced
strucutural chromosomal anomaly
Anatomical factors (uterine)
• Initial 2D pelvic US ± HSG as screening, combined hysteroscopy +
laparascopy ± 3D US for definitive diagnosis
Anatominal factors (cervix)
• The following investigations are not recommended
• Hysterography
• Cervical resistance index
• Insertion of cervical dilators
35. Investigations
Endocrine factors)
• Diabetes (HbA1c, Random blood glucose)
• Thyrotoxicosis (thyroid function test, antithyroid antibodies
especially thyroid peroxidase antibodies)
Infection
• Screen for BV: Amsel criteria, take smear at the posterior fornix to
detect BV (please do not take HVS)
Rh Isoimmunisation
• Maternal and paternal blood group and rhesus
• Kleihauer test
36. POSTCONCEPTION
EVALUATION
• Confirm intrauterine pregnancy, viability
• CVS / Amniocentesis if indicated
• Serial TVS to monitor cervix if incompetence suspected
• Detailed anomaly scan at 20 weeks
• MOGTT at 24-28 weeks and repeated at 32 weeks if negative
• Smear to detect bacterial vaginosis before 20 weeks of
gestation
• Serial scan for fetal growth
• Karyotyping analysis of POC if she aborts / post-mortem
• Monitor cases of Rh isoimmunisation
37. Management
• 15% reduction in the risk of
PET
• 8% reduction in the risk of
delivery < 37 weeks
• 14% reduction in the risk of
death (stillbirth,
neonatal/infant death)
• No overall difference in the
risk of PIH, placental
abruption and SGA
Pre-eclampsia
(aspirin)
40. Management
• Halve the risk of pre-
eclampsia and reduce
serious morbidity and
death in women at high
risk and with low dietary
intake
Pre-eclampsia
(calcium)
41. Management
• magnesium
• folic acid
• antioxidants (vitamins C
and E)
• fish or algal oils
• garlic
• restricting salt intake
Pre-eclampsia
(no role)
43. Management
• Low dose aspirin + heparin
• Reduce pregnancy loss by 54%
• No difference of efficacy and safety
between unfractionated heparin & LMWH
• LMWH: less risk of thrombocytopenia /
oestopenia
Antiphospholipid
Syndrome
(previous late fetal loss,
neonatal death, adverse
outcome due to pre-
eclampsia, FGR, or
abruption)
44. Management
• Start low dose aspirin
• Warfarin?
• LMWH?
Antiphospholipid
Syndrome
(prior thrombosis)
LMWH is preferred. But, if risk of thrombosis is not
reduced by LMWH itself, warfarin can be continued but
avoid during 6-12 weeks of gestation by replacing with
LMWH temporarily. This is to avoid risk of fetal warfarin
embryopathy.
47. Management
• Prompt referral to a clinical
geneticist
• Genetic counseling
• Continue to conceive with /
without prenatal diagnosis test,
gamete donation, adoption
• PIGD with IVF
• 50 – 70% chance of a healthy live
birth in future untreated pregnancy
via natural conception, compared
with PIGD + IVF (30%)
Parental genetic
factors
48. Management
• Congenital uterine malformations
• Insufficient evidence to assess
the effect of uterine septum
resection to prevent further
miscariage
• Open uterine surgery: infertility,
scar rupture during pregnancy
• Uterine fibroid
• Hysteroscopic resection of
submucous fibroids, intrauterine
adhesion
Anatominal
Factors
(Uterine)
49. Management
• Cervical incompetence
• Cervical survelliance if
history of one second
trimester miscarriage with
suspected cervical weakness
• US-indicated cerclage if
cervical length ≤ 25 mm by
TVS before 24 weeks of
gestation.
• Progestrone therapy
Anatominal
Factors
(Cervix)
50. Management
• Insufficient evidence to prevent
miscarriage
• Pregestrone supplementation
• hCG supplementation
• Suppression of high LH in
PCOS
• Metformin supplementation
• Diabetes mellitus
• Ensure glycaemic control
Endocrine
factors
51. Management
• Insufficient evidence to evaluate the effect
of heparin to prevent a miscarriage in
recurrent 1st trimester miscarriage.
• Heparin therapy may improve the live birth
rate in women with previous 2nd-trimester
miscarriage
Inherited
Thrombophilia
• Appropriate antibiotics for specific
organism identified.
• No role for empirical antibiotics.
Infection
52. Preterm Birth (PTB)
• Incidence of 5-10% of pregnancies
• 1/3: Preterm labour with intact membrane
• 1/3: PPROM
• 1/3: Iatrogenic
54. Progestrone & PTB
• Suppress immunity to
prevent rejection of
fetal cells
• Promotes uterine
quiscence
55. Progestrone & PTB
• singleton gestations with no prior PTB, with unknown CL?
• singleton gestations, with no prior PTB, but short CL?
• singleton gestations with prior PTB, and unknown or
normal CL?
• singleton gestations with prior PTB, and short CL?
• multiple gestations, and unknown or normal CL?
• multiple gestations, and short CL?
• prevention of PTB in preterm labor?
• prevention of PTB in preterm premature rupture of
membranes?
56. Progestrone & PTB
• Singleton gestations with no prior PTB, with unknown CL?
No evidence of effectiveness
57. Progestrone & PTB
• singleton gestations with no prior PTB, with unknown CL?
• singleton gestations, with no prior PTB, but short CL?
17-alpha-hydroxyprogestrone Vaginal progestrone
- No difference compared to
placebo
- Less effective than cerclage in
reducing PTB
- Reduction in PTB and
composite perinatal morbidity &
mortality.
- Can be offerred if CL ≤ 20mm
at ≤ 24 weeks
58. Progestrone & PTB
• singleton gestations with no prior PTB, with unknown CL?
• singleton gestations, with no prior PTB, but short CL?
• singleton gestations with prior PTB, and unknown or
normal CL?
17-alpha-
hydroxyprogestrone
Vaginal progestrone Oral progestrone
Which is the winner?
Progestrone administration is beneficial. Limitted data comparing the
different preparations of progestrone. There is present strongest evidence
of effectiveness for 17P. Recommendation: IM 17P 250mg weekly at 16-
20 weeks till 36 weeks.
59. Progestrone & PTB
• singleton gestations with no prior PTB, with unknown CL?
• singleton gestations, with no prior PTB, but short CL?
• singleton gestations with prior PTB, and unknown or
normal CL?
• singleton gestations with prior PTB, and short CL?
17-alpha-hydroxyprogestrone Vaginal progestrone
Insufficient evidence to assess efficacy of different preparation of
progestrone therapy if CL < 25mm at < 24 weeks.
Recommendation: IM 17P weekly till 36 weeks + cerclage
60. Progestrone & PTB
• singleton gestations with no prior PTB, with unknown CL?
• singleton gestations, with no prior PTB, but short CL?
• singleton gestations with prior PTB, and unknown or
normal CL?
• singleton gestations with prior PTB, and short CL?
• multiple gestations, and unknown or normal CL?
No evidence of effectiveness
61. Progestrone & PTB
• singleton gestations with no prior PTB, with unknown CL?
• singleton gestations, with no prior PTB, but short CL?
• singleton gestations with prior PTB, and unknown or
normal CL?
• singleton gestations with prior PTB, and short CL?
• multiple gestations, and unknown or normal CL?
• multiple gestations, and short CL?
No evidence of effectiveness
62. Progestrone & PTB
• singleton gestations with no prior PTB, with unknown CL?
• singleton gestations, with no prior PTB, but short CL?
• singleton gestations with prior PTB, and unknown or
normal CL?
• singleton gestations with prior PTB, and short CL?
• multiple gestations, and unknown or normal CL?
• multiple gestations, and short CL?
• prevention of PTB in preterm labor?
• prevention of PTB in preterm premature rupture of
membranes?
No role
64. General management
• Stop smoking/drugs, avoid alcohol
• Preconception: folic acid supplementation, good glycaemic
control in overt diabetes
• Psychological support
• ? Role of induction of labour at 38-39 weeks
• Can be offered after counseling with the couple in term of
weighing the small risk of stillbirth at term and the risk of IOL.
65. Unexplained cause
• GOOD prognosis for future pregnancy (75%) outcome without
pharmacological intervention but with supportive care alone.
• REASSURANCE plays an important role
• Appropriate f/up in antenatal specialist clinic needed as part of
providing reassurance and adequate monitoring
• Prognosis worsens with increasing maternal age and number of
previous miscarriages.
• Role of Aspirin ± Heparin???
• Not recommended
66. Conclusion
• Managing BOH should be individualised.
• Detailed history taking is required to identify targeted risk
factors.
• Proper documentation of the workout investigation result
will ease the subsequent antenatal care.
• Use the correct weapon to shoot the correct target.
• Hopefully, we can yield a fruitful pregnancy outcome.
- Will uterine artery dopplers change the clinical management in patients who are already high risk of pre-eclampsia?Uterine artery Doppler velocimetry is a poor predictor of pre-eclampsia as it has limited test accuracy.Those studies involved only small numbers of sample size and the sample are often mixed groups of patients.
There were studies comparing 60mg, 75mg, 100mg, 150mg. 60mg showed marginal statistical significant, 75mg showed statistical significant. 100mg or more was inconclusive (some studies proved higher dose is more effective but some studies did not yield statistical significant result due to underpowered study). Furthermore, current reassurance about safety of aspirin in pregnancy only applies to lower doses.
