TVS

Cornerstone of the evaluation of bleeding in 1st

T.
Most useful
Intrauterine or extrauterine
Viable or nonviable.
Heterotopic pregnancy
Gestational trophoblastic disease
Loss of one fetus from a multiple gestation
Clinical correlates of ultrasound appearances.
 BLIGHTED OVUM (Anembryonic


No fetal parts with sac diameters > 20 mm (TV)
30 mm (TA)
No yolk sac
Irregular sac contour
If unsure repeat in 1
week
MISSED ABORTION
CRL: 6 mm & no cardiac activity or < 6 mm & no
change at the time of repeat scan 7 days later
(embryonic growth rate is 1 mm/d)
Abnormal form of G S

5. COMPLETE ABORTION
The endometrial thickness <15 mm in the
anteroposterior plane
No evidence of retained products of conception
INCOMPLETE ABORTION
The endometrial midline echo: distorted >15 mm
in the anteroposterior plane
Hetrogenous & irregular tissue
INEVITABLE ABORTION GS situated low in

uterus or cervix
Note
IV. THROMBOPHILIAS

Methylene tetrahydrofolate mutation:

Hyperhomocysteinemia, Protein C deficiency,
Antithrombin deficiency: Not associated with RM



Hyperhomocysteinemia
High dose folic acid (5 mg) and vit B12 (0.5 mg)
once daily: reduce levels of homocysteine
. ALLOIMMUNE FACTORS
1.human leucocyte antigen incompatibility
between couples
2.absence of maternal leucocytotoxic antibodies
3. absence of maternal blocking antibodies.
4.altered peripheral blood NK cells
5.raised uNK cell numbers
Intralipid Therapy
Form: 20% IV administered fat emulsion routinely
used as a source of fat and energy for patients in
need of extra intake
Composed of : purified soybean oil, purified egg
phospholipids, glycerol, and water.
Some evidence effective in
1.RPL due to immunologic issues, particularly
elevated natural killer cells or other unidentified
immunologic causes.
2.uRPL
3.uRIF



In vitro studies: Intralipid suppress Natural Killer

cell cytotoxicity: decreases the number of natural
killer cells.
Administration: IV infusion in an office setting.
100 mls of Intralipid are mixed with 500 mls NS.
60-90 minutes. TT start at the start of the IVF
cycle continued monthly should a positive
pregnancy test result until the 24th w of
pregnancy.
Side effects No
Antiphospholipid syndrome
An acquired autoimmune disorder characterized
by -moderate to high levels of antiphospholipid
antibodies (LA or aCl or a-ß2GPI) & -specific
clinical features (arterial or venous thrombosis or
pregnancy morbidity)
Primary: 50%
other features of connective tissue disease are
absent
Secondary: 50%
to connective tissue disease e.g. SLE

1. Recurrent pregnancy loss. 25%.

Majority: in 1st T after the establishment of FHR
activity.
15% of RPL
2. Preeclampsia: 15-50%.
15% of severe PET before 34 w have APL Ab
3. IUGR: 30%
4. Preterm labor
5. Maternal th rombosis
(including strokes)
5. Maternal thrombosis (including strokes)
Postpartum syndrome
Rare
Manifestations
Pleuropulmonary disease
Fever
Cardiac manifestations
Mechanism
Unknown
extensive Img and C3 deposition in myocardium
Mechanisms
1.Inhibition of trophoblastic function&
differentiation
 2. Activation of complement pathways at the
maternal–fetal interface: local inflammatory
response
3. In later pregnancy, thrombosis of the
uteroplacental vasculature neither universal nor
specific
Sydney clinical criteria for APS
(2006)
At least 1 clinical and 1 laboratory criterion.

Not if there is <12 W or > 5 years between

+ve aPLab and the clinical manifestation
I.Clinical 1. Vascular thrombosis One or more
clinical episodes of arterial, venous, or small-
vessel thrombosis in any tissue or organ
confirmed by imaging, Doppler studies, or
histopathology, with the exception of superficial
venous thrombosis. For histopathologic
confirmation, thrombosis should be present
without significant evidence of inflammation of the
vessel wall.
2. Pregnancy morbidity
(a) One or more unexplained deaths of a
morphologically normal fetus at or beyond the 10th
w, with normal fetal morphology documented by
US or by direct examination of the fetus, or
(b) One or more premature births of a
morphologically normal neonate at or before the
34th w because of severe preeclampsia or
eclampsia or severe placental
insufficiency, or
(c) Three or more unexplained consecutive
spontaneous abortions before the 10th w, with
maternal anatomic or hormonal abnormalities and
paternal and maternal chromosomal causes
excluded.
N.B: in practice evaluation after 2 early
miscarriage
•LA: positive or negative more specific. aCL:
international units. more sensitive Titer is related
to risk of fetal loss
•IgG Ab more specific than IgM. better predictors
of fetal outcome
-IgA
-no greater risk

A. Before pregnancy: Pre-conceptional

counseling 1. Clinical: review med and obs
history, asses other risk factors, obesity,
 age 2. Lab: Confirm persistent aPLab
Assess R function CBC: anaemia
thrompocytopenia
3. Treatment Postpone pregnancy if thrombotic
event <6 month Initial low dose aspirin
[increase success]

B. During pregnancy
Objectives:
Improve maternal & fetal-neonatal outcome by
preventing complications
Reduce or eliminate the maternal thrombotic risk
1.TVS: confirm live embryo at 5.5-6.5 W
2.Continue low dose aspirin
3.Initial heparin treatment
Diagnostic tests U/S:/4W beginning at 20 W.
Assess fetal growth & AFV Fetal surveillance:
weekly from 30W. CTG, Uterine a Doppler: at 20
for prediction of PET If early diastolic notch seen:
do 2 weekly growth scans due to high risk of
IUGR Platelet count
Medications:

heparin is the first line treatment (MRCOG, 2011)

Heparin:
Complications:
Hemorrhage
Thrombocytopenia: Rare
Osteopenia:

Un-fractionated heparin Vs LMWH:

•LMWH is widely used in Europe, whereas cost
considerations limit its use in other countries.
•No significant difference in BMD or live birth rate
(Farquharson,2000) LMWH advantages once daily less
thrombocytopenia osteopenia
Dose: A. No history of thrombosis:
 Standard heparin: 1st T: 5000-10000 U /12 h 2nd
and 3rd T: 10000 U/12 hrs LMWH: Enoxaparin
(clexan) 20 mg once daily Dalteprin 5000 U once
daily.
B. History of thrombosis
Standard heparin: /8-12 hrs {maintain the
midinterval heparin levels in the therapeutic
range}. (Heparin level = anti-factorXa levels.)
Women without a LA in whom APTT is normal
can be observed using APTT. LMWH
Enoxaparine: 0.5 mg/kg /12 h or 40 mg once
daily


IV immunoglobulin:
Expensive
No benefit relative to heparin & low dose aspirin.
Reserved for cases refractory to aspirin & heparin
(

abandoned
{do not improve the live birth
significant maternal & fetal morbidity}
(Laski

cerebral thrombosis
C. Postpartum
History of thrombosis: Warfarin
thromboprophylaxis as soon as the patient is
clinically stable after delivery (International
normalized ratio (INR) of 3 is desirable).
No history of thrombosis: UK: Heparin for 5 d
USA: anticoagulant for 6 w.
Breast feeding: Heparin & warfarin: safe
Contraception estrogen-containing are
contraindicated.



Significant increase of RM in patients with high

DNA damage compared with those with low DNA
damage

Significant association between SDF and

pregnancy loss after IVF or ICSI



DFI ≥30: male

infertility 15-30:
RM ≤15: fair