Zareh.F.MD. All bleeding during pregnancy should be investigated by examination and imaging studies.

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Zareh.F.MD

Transcript of Zareh.F.MD. All bleeding during pregnancy should be investigated by examination and imaging studies.

Page 1: Zareh.F.MD. All bleeding during pregnancy should be investigated by examination and imaging studies.

Zareh.F.MD

Page 2: Zareh.F.MD. All bleeding during pregnancy should be investigated by examination and imaging studies.

All bleeding during

pregnancy should be

investigated by examination

and imaging studies

Page 3: Zareh.F.MD. All bleeding during pregnancy should be investigated by examination and imaging studies.

• 1/4 of women who bleed at 14-26 w had pp or ap.

• 1/3 of pregnancy with vag bleeding after 26 w had

poor outcome. Unexplained vag.bleeding

at term must be considered for

delivery.

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etiologies

• Placenta previa• Placenta abruption• Vasa previa• Cervical lesions (carcinoma,polyps)• Vaginal laceration

(trauma,carcinoma)• Uterine rupture or dehiscence

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Placenta previaincidece

• 0.5-1% of all pregnancies

• Fatal 0.03% of cases

• Incidence in multipar :1/20

• Incidence in nulipar : 1/1500

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difinition• Dillated cervix:

complete previa partial previa

marginal previa low lying

• Closed cervix:complete

partial / marginal<1 cm from int.os1-2 cm from int.os>2 cm from int.os

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pathophysiology

• Abnormal endometrial tissue less favorable location for implantation: poor vascularization thinner myometrium

• Uterine trauma from c/s (6 fold)

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Risk factors• Perior c/s

• Black , minority

• Older women >35 y

• High gravidity & parity

• Cigarette smoking 2.6-4.4 fold

• Previous abortion

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diagnosis

• Abdominal sonographymisdiagnosis :

full distended bladderlower ut segment contraction

pp in 2nd trimester 90-95% resolved by the 3rd trimester (but no central)

• 3 dimensional scanning• transvaginal scan• Transperineal scan• Double set up examination • MSAFP>2 MoM

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Clinical features

• Asymptomatic

• Vaginal bleedingvariableintermittentred to brownish

maternal origin

• the fetus usually not in jeopardy

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complication

• Hospital stay• c/s• Abruptio placenta• Malpresentation• Post partum hemorrhage• Growth restriction• Placenta accreta

pp+previous c/s10-35% +multiple c/s 60-65%

• Coagulation defect

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Other complications

• A.T.N• Sheehan syndrome• Maternal mortality<1% • Perinatal mortality <5%

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outcome• IUGR ?

• Preterm birth

• Congenital anomaly

• Respiratory distress syndrome

• Anemia

• Recurrence rate 2-3%(6-8 fold)

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management

no bleeding• 2nd trimester

intercourse avoidusual activityrepeat sonography

• 3rd trimester decrease physical activity travel away from home

prolonged bed rest

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management with Bleeding• Evaluation of the patient• Fetal status• IV fluid• Blood cross match• RHoGam if necessary• Steroid if 24-34 W• Delivery after 34-36W

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management

Severe hemorrhage• Medical team for immediate

delivery• 2 large bore IV line• Blood cross match• Foley catheter• Coagulation panel• Continuous Fetal monitoring• delivery

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Premature separation of placenta.

• 0.5-1% of deliveries

• Perinatal mortality is 20-25%

• Preterm birth is 40%

• Cause of 15% of stillbirth

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Definition

Preplacental or subamniotic

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retroplacental

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Risk factors

Socioeconomic:• High parity

• low education

• infertility

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Risk factors

Uterine:• ut.malformation

• ut.septum

• Myoma

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Risk factors

Medical:• Diabete pregestational

• Hypertension _chronic&gestational

• PROM with chorioamnionitis

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Risk factorsThrombophilias

• Antiphospholipid syndrome

• Prothrombin 20210A mutation

• Hyperhomocysteinemia

• Factor V leiden mutation

• Activated protein C resistance

• Protein C and S deficiency

• dysfibrinogenemia

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Risk factor iatrogenic• Sudden decompression(amniocentesis)

• External cephalic version

• Cigarette smoking

• Cocaine abuse

• Blant trauma

• Heavy physical activity

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pathophysiology• Blunt trauma : forceful shearing effort • Majority of other case : cell death

(apoptosis) induced through ischemia ,hypoxia.

• Thrombophilia : thrombose in decidua basalis

• Chorioamnionitis: infectious agents (lipopolysacharids & endotoxins) cytokines,superoxide ischemia and hypoixia

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Pathophysiologycont.

• Nicotine(cigarete) and cocaine vasoconstriction ischemia placental lesions(infarction,oxidative stress,appoptosis and necrosis)

• Circumvalate placenta(chorion leave don’t insert at the edge of placenta) A.P,IUGR,PROM,preterm labor

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diagnosis Clinically• vaginal bleeding

• Uterine pain• tetanic contraction

• fetal heart abnormality

sinusoidal pattern

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diagnosis Paraclinic• Ultrasound • MRI• Doppler • Biochemical testUnexplained elevated of MSAFP AP>10

foldPreterm labor+AFP>2MoM = AP (67%)Preterm labor+AFP>2MoM+bleeding= AP

(100%) HCG Inhibin A Fetal Hb

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management• Marginal Abruptio

hospitalize a patient with any bleeding after fetal viability

• Large retroplacentalusually require acute &

aggressive management

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Large bleeding

• Continues fetal monitoring

• Foley catheter

• Frequent maternal v/s

• Steroid therapy (24-34w , membrane intact)

• Folic acid 1mg ,vit B12 ,vit B6

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discharge• Mild bleeding : 2-5 days without any further bleeding

• Large bleeding :decision is difficult

with any bleeding , pain , contraction no discharge

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Tocolytic use• Now become acceptable to consider a

short course of tocolytic therapy for: stable patient , limited abruptio ,

established fetal well being, preterm G.age

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Which tocolytic

• B mimetics (terbut,ritod): mask cardiovascular response to volume depletion

• Ca channel blockers (nifidipine): reduce BP

• Mgso4 : most acceptable agents

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delivery

Vaginal or c/s Depending on the: Degree of bleeding Presence or absence of: Active labor Fetal distress

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complications

• c/s 50% of case

• Shock

• DIC

• Renal failure

• Couvelaire uterus

• Recurrence : 10 fold

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Fetal outcome

• Mortality: term babies 25 fold

• Prematurity: 40%

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Thrombophilia defects• Anticardiolipin antibodies

• Lupus anticoagulant

• Pr c, Pr s and antithrombin 3 deficiencies

• Factor v leiden “activated pr c resistance”

• Metilentetrahydrofulate reductase gene mutation • Prothrombin 20210A gene mutation

• Congenital dysfibrinogenemia

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Factor V leiden• Activated protein C resistance

• Most common genetic factor predisposing to thrombosis

• Most common identifiable causes

• Substitution of adenine for guanine

• “ Amino acid arginine for glutamine

• Increased tendency to form clots

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hyperhomocysteinemia

Methionine metabolise

homocysteine damage

vascular Remethylate MTHFR endothelium

folate vit.B12 , vit. B6

Methionine

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Hadi
Hadi
Page 50: Zareh.F.MD. All bleeding during pregnancy should be investigated by examination and imaging studies.