2009-32009-3 11

Early Pregnancy ComplicationsEarly Pregnancy Complications

• Spontaneous abortion

• Ectopic pregnancy

22

Spontaneous AbortionSpontaneous Abortion

Definition of abortionDefinition of abortion

Before 20 weeks gestationBased on LMP

Or delivery of fetusWeight less than 500 grams

2009-32009-3 44

Etiology of spontaneous abortionEtiology of spontaneous abortion

• 50% of SA during the first 12 weeks with abnormal karyotype (Aneuploidy)

• Abnormal development noted in majority of cases

• Incomplete cervix cause of second trimester loss

2009-32009-3 55

Etiology of spontaneous abortionEtiology of spontaneous abortion

• Maternal factors– Systemic disease– Uterine defects– Immunologic disorders– Malnutrition

• Toxic factors

• Trauma

Abortion classificationAbortion classification

Threatened abortionInevitable abortionIncomplete abortionComplete abortionMissed abortionSeptic abortionRecurrent abortion

2009-32009-3 77

Threatened abortionThreatened abortion

• Bleeding during early pregnancy

• Prognosis worse with pain or cramping

• Rule out other course of bleeding– Cervical lesions– Polyps– Implantation bleeding

2009-32009-3 88

Management of threatened Management of threatened abortionabortion

• Serial hCG

• Serial progesterone

• Vaginal sonograms

• Pelvic rest

• Bed rest

2009-32009-3 99

Inevitable abortionInevitable abortion

• Certain to occur

• Rupture of membranes

• Cervical dilation

2009-32009-3 1010

Management of inevitable or Management of inevitable or incomplete abortionincomplete abortion

• Evacuation of the uterus by suction D and C

• Prognosis is excellent if the retained tissue is promptly and completely evacuated.

1111

ECTOPIC PREGNANCYECTOPIC PREGNANCY

1212

Yanwen XuYanwen Xu, M.D., PhD, M.D., PhD

The First Affiliated Hospital of SThe First Affiliated Hospital of Sun Yat-sen Universityun Yat-sen University

ECTOPIC PREGNANCYECTOPIC PREGNANCY

2009-32009-3 1313

2009-32009-3 1414

Definition:

A fertilized ovum implants in an area other than the endometrial lining of the uterus.

Definition:

A fertilized ovum implants in an area other than the endometrial lining of the uterus.

2009-32009-3 1515

Sites of ectopic pregnanciesSites of ectopic pregnancies

2009-32009-3 1616

2009-32009-3 1717

2009-32009-3 1818

2009-32009-3 1919

2009-32009-3 2020

2009-32009-3 2121Residual uterus Residual uterus pregnancypregnancy

Uterus

2009-32009-3 2222

Fimbrialand

interstitial19%

Isthmic25%

Ampullary56%

Fimbrialand

interstitial19%

Isthmic25%

Ampullary56%

Tubal ectopic pregnancyTubal ectopic pregnancy

2009-32009-3 2323

EtiologyEtiology

Tubal factorOvarian factors

Other factors

IUD

2009-32009-3 2424

Time of RuptureTime of Rupture

Rupture is usually spontaneousRupture is usually spontaneousIsthmic pregnancies 6-8 week’s gestationIsthmic pregnancies 6-8 week’s gestation

Ampullary pregnancies 8-12 week’s gestatAmpullary pregnancies 8-12 week’s gestationion

Interstitial pregnancies 12-16 weeks’s gesInterstitial pregnancies 12-16 weeks’s gestationtation

2009-32009-3 2525

PathologyPathology

• Little or no decidual reaction and minimal defense against the permeating trophoblast in the ectopic implantation sites.

• A hematoma in the subserosal space enlarges as pregnancy progress.

• Bleeding is of uterine origin and is caused by endometrial involution and decidual sloughing.

• The Arias-Stella reaction in endometrium is non specific.

2009-32009-3 2626

    Clinical findingsClinical findings

  Three major symptoms ：

Amenorrhea

Pain

Vaginal bleeding

  Three major symptoms ：

Amenorrhea

Pain

Vaginal bleeding

2009-32009-3 2727

Clinical findingsClinical findings

Dizziness, lightheadedness, and/Dizziness, lightheadedness, and/or syncope is present in one-thiror syncope is present in one-third to one-half cases.d to one-half cases.

2009-32009-3 2828

SignsSigns

• General condition• Abdominal examination

– Diffuse or localized abdominal tenderness

• PV ：– A unilateral adnexal mass– Adnexal and/or cervical motion tenderness– Uterus may undergo typical changes of pregnancy

2009-32009-3 2929

Laboratory findingsLaboratory findings

• Hematocrit– Depending on the degree of intraabdominal bleeding

• White blood count• Pregnancy tests

– Theβ-HCG is positive.– Two-thirds of ectopic pregnancy have abnormal serial

titers.

• Ultrasound• Culdocentesis

2009-32009-3 3030

Normal Pregnancy

Ectopic Pregnancy

2009-32009-3 3131

CuldocentesisCuldocentesis

2009-32009-3 3232

CuldocentesisCuldocentesis

Nonclotting blood shows intra-abdominal bleeding.

If the blood clots, it is likely from a punctured vessel in the vaginal wall.

If culdocentesis is positive, laparoscopy or laparotomy should be performed immediately.

A negatively result may rule out a ruptured or leaking ectopic but not an intact one.

2009-32009-3 3333

Differential DiagnosisDifferential Diagnosis

• Abortion

• Acute salpingitis

• Hemorrhagic corpus luteum

• Acute appendicitis

• Ovarian cyst torsion

2009-32009-3 3434

TreatmentTreatment

• Expectant management– The β-HCG titers are low (<200 mIU/mL) or d

ecreasing.– The risk of rupture is low.

• Surgical treatment– Conservative surgery in the hemodynamically

stable patient with an ampullary pregnancy.– Laparoscopy is preferred over laparotomy in s

table pregnancy.

2009-32009-3 3535

Treatment in hemodynamically unstable Treatment in hemodynamically unstable patients----Salpingectomypatients----Salpingectomy

2009-32009-3 3636

TreatmentTreatment

• Interstitial pregnancies require a corneal wedge resection, with uterine reconstruction and sometimes salpingectomy on the affected side.

• Cervical ectopics with methotrexate or hysterectomy.

• Ovarian pregnancy requires oophorectomy and sometimes salpingectomy on the affected side.

• Abdominal pregnancy involves delivery of the fetus with ligation of the umbilical cord. The placenta is left.

2009-32009-3 3737

Medical managementMedical management

① Small (<3cm)

② Intact

③ Extr-auterine gestation with no

fetal heart motion

MTX or 5-FU

3838

Pre-eclampsia & Pre-eclampsia & eclampsiaeclampsia

Yanwen XuYanwen Xu, M.D., PhD, M.D., PhDThe First Affiliated Hospital of Sun Yat-sen UniversiThe First Affiliated Hospital of Sun Yat-sen Universi

tyty

2009-32009-3 3939

Patient historyPatient history

• 謝 x芳， 30 y/o F• Chief complain: Twin pregnancy at 32+

gestational weeks with elevated BP and vaginal watery discharge since 8/8 12:00am

• Past history:denied any systemic disease, such as HTN, DM, CAD, pulmonary dx

• Allergy history:denied• Drug use history:denied• OP and anesthesiology history:denied

2009-32009-3 4040

Present pregnancy history and Present pregnancy history and menstrual historymenstrual history

• G1P0, got this pregnancy by ET

• LMP:94-12-26, EDC:95-10-12

• Routine pregnancy exam. no abnormality was told such as GDM, PIH before 8/2

2009-32009-3 4141

Symptom and signSymptom and sign

8/2 8/3 8/4 8/5 8/6 8/7 8/8

Epiphora

Proteinuria

Abdominal edema at lower abdomen

Fetal movement decrease in right side

Dyspnea, orthopnea

Insomnia, urinary frequency

BP:136/80 BP:210/100

2009-32009-3 4242

Events at 8/8Events at 8/812am 4pm 5pm

18am watery discharge

BP:210/100mmHgBT:1’30”, CT:1’40”WBC:8.4x103/ulRBC:3.19x106/ulHb:10g/dl, Hct:29%Plt:9.7K/μL

O2, adalate, trandate(5mg)

refer to ER

BT:37.6HR:129BP:198/118SpO2:100%RR:27/min

Admission to 5FD

BT:37.6HR:120

BP:181/102RR:22/min

5:40pmBP:161/104

HR:110SaO2:100%

MgSO4:10ml/hr

2009-32009-3 4343

6pm 6:30 6:40 接獲通知，前往探視

送入 DR

O2 mask 3L, SaO2:93% room air, SaO2:97% 70% 97% BP:232/148 ， HR:105

dyspnea could not lie down，edema ， difficult in breathing， cough with frothy sputum

Induction Etomidate:20mg laryngoscopy Trandate:15mg LMACisatracurium:10mg laryngoscopy

ENT standby備 fiber

ASA VE

2009-32009-3 4444

6:40 7:00 8:00Maintenance

Sevoflurane:0.2-0.3MAC add N2O Lasix:40mg Morphine:10mg midazolam:5mg bicarbonate:5amp ventilation: volume control ,PEEP:8 cmH2O suction

6:42 Operation6:47 twin A F 1510g ， 17 twin B F 1698g ， 48

7:45 finish, IV:150mlblood loss:200ml

On A-line ABG:7.05/77.3/162/21.5/-9.4/12.3/37/98.4/193/5.2/144/4.4/112.8/1.03

Endo:6.5mm fix 21cm

2009-32009-3 4545

0

50

100

150

200

250

SAP(mmHG)

DAP(mmHg)

HR/min

ETCO2( mmHg)

SaO2(%)

2009-32009-3 4646

Lab data 8/8 pre OPLab data 8/8 pre OP

• WBC:11.55 K/uL• RBC:3.75M/uL• Hb:11.1 g/dL• HCT:34.4%• PLT:107K/uL

• PT:11sec• PTT:29.5sec• INR:0.93

2009-32009-3 4747

Lab data Lab data

• AST:36U/l• ALT:18U/l• CRP:0.52mg/dl• Alb:2.67g/dL• D-Bil:0.1mg/dl• Na:140mmole/l• K:3.5mmole/l• Cl:110mmole/l• Mg:0.74mmole/l• BUN:6.4mg/dl• Cre:0.8mg/dl

• FDP:53.2ug/mL• D-Dimer:2978• Random urine:

Sp.Gr.:1.01

pH:5.5

protein:1+ (70mg/dL)

Glu.:-

2009-32009-3 4848

Definitions - pre-eclampsiaDefinitions - pre-eclampsia

• Persistent hypertension from gestation 20Persistent hypertension from gestation 20thth week week onwards defined by eitheronwards defined by either::

– Diastolic bp >90 Diastolic bp >90 TorrTorr– Systolic bp >140 Systolic bp >140 TorrTorr– Or relative increase diastolic bp >15 Or relative increase diastolic bp >15 TorrTorr or systolic or systolic

bp>25 bp>25 TorrTorr• ProteinuriaProteinuria > 0.3g in 24 hours > 0.3g in 24 hours• Generalised Generalised oedemaoedema (mainly lower extremities, hands) (mainly lower extremities, hands)

2009-32009-3 4949

Definition of EclampsiaDefinition of Eclampsia

• One or more One or more convulsionconvulsion, not caused by other , not caused by other cerebral condition, in a patient with pre-cerebral condition, in a patient with pre-eclampsiaeclampsia

2009-32009-3 5050

Definition of severe Definition of severe pre-eclampsiapre-eclampsia

• Features of pre-eclampsia plus one the followingFeatures of pre-eclampsia plus one the following::

– Systolic bp >Systolic bp >160 160 TorrTorr– Diastolic bp >110 Diastolic bp >110 TorrTorr – Proteinuria > Proteinuria > 22 gg per 24 hours per 24 hours– Cerebral or visual disturbancesCerebral or visual disturbances– Oliguria Oliguria ≤≤ 500ml 500ml per 24 hours per 24 hours– EpigastricEpigastric painpain– Pulmonary oedemaPulmonary oedema– Haemolysis, elevated liver enzymes and low platalet Haemolysis, elevated liver enzymes and low platalet

syndromesyndrome = = HELP syndromeHELP syndrome

2009-32009-3 5151

Mild and severe preeclampsiaMild and severe preeclampsiamild severe

SAP <160mmHg >=160

DAP <110mmHg >=110

Urinary protein <5g/24hr 1+or2+ >=5 3+or4+

Urine output >500ml/24hr <500

headache No Yes

Visual disturbances No Yes

Epigastric pain No Yes

RUQ pain No Yes

Pulmonary edema No Yes

cynosis No Yes

HELLP No Yes

Platelet count >100000/mm3 <100000

2009-32009-3 5252

EpidemiologyEpidemiology

• Incidence Incidence pre-eclampsiapre-eclampsia 66 %% all pregnancies all pregnancies

• Incidence Incidence eclampsiaeclampsia 2- 2-55 in 1000 deliveries in 1000 deliveries

• PEE is associated PEE is associated with 1.8with 1.8 % maternal mortality and 7% maternal mortality and 7 % % fetal/ neonatal mortalityfetal/ neonatal mortality

2009-32009-3 5353

PathogenesisPathogenesis

• Factors predisposingFactors predisposing– Increase Oxygen demand statesIncrease Oxygen demand states e.g. e.g.

• Multiple preganciesMultiple pregancies• Fetal macrosomiaFetal macrosomia

– Decrease Oxygen transferDecrease Oxygen transfer• Maternal anemia, High altitude (Tibet,Nepal,Peru)Maternal anemia, High altitude (Tibet,Nepal,Peru)• Microvascular diMicrovascular dissease e.g. Hypertension, Diabetes, collagen ease e.g. Hypertension, Diabetes, collagen

diseasedisease, smoking, smoking• Abnormal placentationAbnormal placentation

– GeneticGenetic e.g. Angiotensin gene e.g. Angiotensin gene– Immune mechanismImmune mechanism e.g. antiphospholipid syndrome e.g. antiphospholipid syndrome

2009-32009-3 5454

PathogenesisPathogenesis

• Primary defect involves abnormal migration of Primary defect involves abnormal migration of extravillous trophoblast in placentaextravillous trophoblast in placenta

• Myometrial vessels retain musculoelastic architecture Myometrial vessels retain musculoelastic architecture instead of being converted into sinusoidal vessels( as instead of being converted into sinusoidal vessels( as occurs in normal pregnancy)occurs in normal pregnancy)

• Defect occurs with the inhibition of second wave of migration Defect occurs with the inhibition of second wave of migration i.e. in second trimesteri.e. in second trimester

• ConsequenceConsequence of this defect includes of this defect includes– HypoperfusionHypoperfusion and and hypoxiahypoxia of placenta endothelial cells of placenta endothelial cells– Change in ratio of vasopressor substances Change in ratio of vasopressor substances tromboxane tromboxane

prostacyclin ratioprostacyclin ratio by endothelium causing vasospasm by endothelium causing vasospasm

2009-32009-3 5555

Faulty placentationGenetic, immunologic, inflammatory factors

Maternal vascular disease

Excessive trophoblast

Reduced uteroplacental perfusion

Endothelial activation

Capillary leak

hemoconcentration

edema proteinuria

VasospasmActivation of coagulation

thrombocytopenia

Vasoactive agents:

Prostaglandins

nitric oxide

endothelins

Noxious agents:CytokinesLipid peroxidases

oliguria

HTN

seizures abruption

liver ischemia

2009-32009-3 5656

Pathophysiology - cerebralPathophysiology - cerebral

• Cerebral involvement includeCerebral involvement include– Eclamptic convulsionsEclamptic convulsions – principal sequlae – principal sequlae

pathogenesis may be due to:pathogenesis may be due to:• Focal cerebral vasospasm and hypoperfusion causing Focal cerebral vasospasm and hypoperfusion causing

abnormal electrical activity with hypertension occurabnormal electrical activity with hypertension occurrring as ing as secondary response – most likely explanationsecondary response – most likely explanation

• Hypertension causes breakdown in cerebral autoregulation, Hypertension causes breakdown in cerebral autoregulation, leading to overdistension of vessels and extravasation of leading to overdistension of vessels and extravasation of fluidfluid

– Visual disturbances i.e. Visual disturbances i.e. cortical cortical blindness (rare)blindness (rare)– Cerebral haemorrhageCerebral haemorrhage

2009-32009-3 5757

Pathophysiology - circulationPathophysiology - circulation

• CirculationCirculation– Uteroplacental vascular resistance increases with Uteroplacental vascular resistance increases with

decrease in blood flowdecrease in blood flow, leading to placental ischaemia , leading to placental ischaemia and fetal growth retardationand fetal growth retardation

– Systemic circulation – 2 modelsSystemic circulation – 2 models• Traditional model – occurs in 80% pre-eclampsia with picture Traditional model – occurs in 80% pre-eclampsia with picture

ofof– Decreased plasma volumeDecreased plasma volume– VasoconstrictionVasoconstriction

and therefore hypoperfusion of placenta and kidneyand therefore hypoperfusion of placenta and kidney• Hyperdynamic model – high CO with compensatory Hyperdynamic model – high CO with compensatory

vasodilationvasodilation

2009-32009-3 5858

Pathophysiology - renalPathophysiology - renal

• Renal involvement occurs in 2 stages:– Impairment of tubular function occurs early – reflected

by development of hyperuricaemia.• Serum uric acid levels are a sensitive marker of progression

and risk

– Glomerular filtration impaired later in disease – reflected by proteinuria > 0.5g in 24 hours or in severe pre-eclampsia > 2 g in 24 hours

– Acute renal failure (rare) due to:• Acute tubular necrosis (more common and reversible)• Acute cortical necrosis (permanent)

2009-32009-3 5959

Pathophysiology – Pathophysiology – BloodBlood

• Platelets – usually associated with thrombocytopaenia ( < 100,00

0/mm3 ) and increase in mean platelet volume• Immune mediated

– Increase platelet activation• Possibly due to endothelial activation or intrinsic

changes in platelets

2009-32009-3 6060

Pathophysiology – Pathophysiology – bloodblood

• Coagulation cascade activated to greater extent Coagulation cascade activated to greater extent than normal pregnancythan normal pregnancy

– Increase factor VIII consumptionIncrease factor VIII consumption– Increase thrombin activityIncrease thrombin activityAll leads to heightened All leads to heightened risk of thrombosisrisk of thrombosis

• Anticoagulant protein levels decreasedAnticoagulant protein levels decreased– Decreased antithrombin IIIDecreased antithrombin III– Decreased protein C and SDecreased protein C and S

• Fibrinolytic systemFibrinolytic system – conflicting results – conflicting results

2009-32009-3 6161

Pathophysiology – liverPathophysiology – liver

• Liver complications consists of:Liver complications consists of:

– ImpairedImpaired liver function liver function tests due to vasoconstriction tests due to vasoconstriction of hepatic bed causing of hepatic bed causing

• Periportal fibrin depositionPeriportal fibrin deposition• Hepatocellular necrosisHepatocellular necrosis

– Hepatic infarction and rupture – worst but rare Hepatic infarction and rupture – worst but rare conditioncondition

– HELLP syndromeHELLP syndrome-hemolytic anemia, elevated liver e-hemolytic anemia, elevated liver enzymes, and low platelet countnzymes, and low platelet count

2009-32009-3 6262

Pathophysiology – HELLP Pathophysiology – HELLP syndromesyndrome

• Constellation of laboratory findings in pre-eclampsia

– Haemolysis- seen on peripheral blood smear and bilirubin levels > 1.2mg/dL

– Elevated Liver enzymes – serum aspartate aminotransferase (AST) levels > 70 U/L

– Low Platelets < 100,000/mm3

• Pathogenesis uncertain but may be due to vasospasm

2009-32009-3 6363

Pathophysiology –Pathophysiology –pulmonary sypulmonary systemstem

• Pulmonary edema occur with severe pre-eclampsia or eclampsia.

– Excessive fluid administration– Delayed mobilization of extravascular fluid– Decreased plasma colloid oncotic pressure fr

om proteinuria– Decreased hepatic synthesis of albumin

2009-32009-3 6464

• Hypertension• Proteinuria

– An indicator of fetal jeopardy

• Edema– Weight gain >2 lb/wk or a sudden weight gain

over 1 to 2 days

Clinical FindingsClinical Findings

2009-32009-3 6565

SymptomsSymptoms

• Headache

• Oedema

• Visual disturbance

• Focal neurology, fits, anxiety, amnesia

• Abdo pain

• Decreased urine output

• None

Multisystem disease with varying clinical presentations.

2009-32009-3 6666

SignsSigns

• Hypertension• Tachycardia and tachypnoea• Creps or wheeze on auscultation• Neurological deficit• Hyperreflexia• Petechiae, intracranial haemorrhage• Generalised oedema• Small uterus for dates

2009-32009-3 6767

ComplicationsComplications

• Early delivery and fetal complications due to prematurity.

• Chronic uteroplacental insufficiency increases the risk of IUGR and oligohydraminos.

• Abruptio placentae

2009-32009-3 6868

Treatment-mild preeclampsiaTreatment-mild preeclampsia• Maternal Maternal treatmenttreatment should include: should include:

– Bed restBed rest– Serial or continuous Serial or continuous blood pressure monitoringblood pressure monitoring– Urinanalysis for proteinuriaUrinanalysis for proteinuria – quantification for degree of severity – quantification for degree of severity– Blood testBlood test include include

• BBP +P + platelet count and morphology platelet count and morphology• Haemocoagulation systemHaemocoagulation system• Uric acid, creatininUric acid, creatinin for renal function for renal function• Serum uric acid – useful early and for progressionSerum uric acid – useful early and for progression• Hepatic enzymes (AST,ALT, GMT)Hepatic enzymes (AST,ALT, GMT)

– Fluid balance – urine output, CVP, Sa02 etcFluid balance – urine output, CVP, Sa02 etc– ECGECG, medical , medical Management Consulting ((neurologists,neurologists, internists)internists)

2009-32009-3 6969

Assessment of fetAssessment of fetal statusal status

• Fetal monitoring:Fetal monitoring:

– Regular fetal HR monitoringRegular fetal HR monitoring NST NST – – for acceleration, loss for acceleration, loss of variability or decelerationsof variability or decelerations

– Fetal ultrasoundFetal ultrasound may be useful for fetalmay be useful for fetal sizesize and and morphology, amnioticmorphology, amniotic fluidfluid volume estimationvolume estimation,, placentaplacenta maturationmaturation

– Amniocentesis to determine the L:S ratioAmniocentesis to determine the L:S ratio– Corticosteriods to accelerate fetal lung maturityCorticosteriods to accelerate fetal lung maturity

• If delivery may occur in the next 2-7 daysIf delivery may occur in the next 2-7 days

2009-32009-3 7070

Treatment-severe preeclampsiaTreatment-severe preeclampsia

• GoalGoals of management:s of management:

– Prevention of Prevention of convulsionconvulsionss

– Control of blood pressureControl of blood pressure

– Maintain placental perfusion with delivery Maintain placental perfusion with delivery timed appropriatelytimed appropriately

2009-32009-3 7171

Management – Management – Anticonvulsant therapyAnticonvulsant therapy

• Magnesium sulphateMagnesium sulphate : anticonvulsant of choice : anticonvulsant of choice

– Action byAction by::• antagonism of calcium and hence decreased systemic and antagonism of calcium and hence decreased systemic and

cerebral vasospasm cerebral vasospasm • Increase release of PGIIncrease release of PGI 2 by vascular endothelium2 by vascular endothelium

– Other effectsOther effects in parturient include: in parturient include:• TocolysisTocolysis• Decreased cathecholamine releaseDecreased cathecholamine release• Mild antihypertensiveMild antihypertensive• Increases renal and uterine blood flowIncreases renal and uterine blood flow

2009-32009-3 7272

Management – anticonvulsant Management – anticonvulsant therapytherapy

• Magnesium continuedMagnesium continued– Renally excretedRenally excreted – so reduce dose in renal failure – so reduce dose in renal failure– Therapeutic level Therapeutic level 4.8-8.4mg4.8-8.4mg//dLdL ; must monitor for toxicity ; must monitor for toxicity– Repeated seizures despite therapeutic levels need to Repeated seizures despite therapeutic levels need to

consider othersconsider others

• Monitoring during MgSOMonitoring during MgSO44 treatment treatment– Deep tendon reflexDeep tendon reflex– Urine output at least 100mL during the preceding 4 hoursUrine output at least 100mL during the preceding 4 hours– Respirations 12/minRespirations 12/min– 10mL of 10% calcium chloride or calcium gluconate10mL of 10% calcium chloride or calcium gluconate

2009-32009-3 7373

Management – Management – Anticonvulsant therapyAnticonvulsant therapy

• DiazepamDiazepam : effective especially if needed acutely but : effective especially if needed acutely but causes fetal/ neonatal complicationscauses fetal/ neonatal complications

– Adverse effectAdverse effect• depression of muscle tone and breath centredepression of muscle tone and breath centre• Competing with bilirubin for albumin bingding, preCompeting with bilirubin for albumin bingding, pre

disposing the infant to kernicterusdisposing the infant to kernicterus

2009-32009-3 7474

Management of eclamptic Management of eclamptic seizuresseizures

• Airway protectionAirway protection

• Maintain oxygenationMaintain oxygenation (O2 inhalation via mask) (O2 inhalation via mask)

• Control of seizuresControl of seizures

– Continued convulsions may indicate other cerebral pathologyContinued convulsions may indicate other cerebral pathology– Management may involve treatment cerebral oedemaManagement may involve treatment cerebral oedema (CS) (CS)

• Delivery of fetus when mother Delivery of fetus when mother is in stable condition, even is in stable condition, even in some situation SC is needed acutelyin some situation SC is needed acutely

2009-32009-3 7575

Management – Management – Antihypertensive therapyAntihypertensive therapy

• Treatment required whenTreatment required when::•

– Diastolic bp > 110 Diastolic bp > 110 mmHgmmHg– The goal is to bring Bp into 90-100 mmHgThe goal is to bring Bp into 90-100 mmHg

• HydralazineHydralazine : agent of choice : agent of choice

– Causes direct arteriolar vasodilationCauses direct arteriolar vasodilation– Improves renal and uteroplacental blood flowImproves renal and uteroplacental blood flow

• LabetalolLabetalol : : nonselective beta blockernonselective beta blocker– causes rapid decrease in arterial bp without compromising causes rapid decrease in arterial bp without compromising

uteroplacental flowuteroplacental flow– May cross placenta but fetal complications rareMay cross placenta but fetal complications rare

2009-32009-3 7676

Management – Management – Antihypertensive therapyAntihypertensive therapy

• Nifedipine Nifedipine : causes direct relaxation of arteriolar smooth : causes direct relaxation of arteriolar smooth musclemuscle

– Maintains uterine perfusionMaintains uterine perfusion– Can cause uterine muscle relaxation – Can cause uterine muscle relaxation – increase risk increase risk

of post partum haemorrhageof post partum haemorrhage– Contra-indicated with use of MgContra-indicated with use of Mg

• Sodium nitroprussideSodium nitroprusside : hypertensive emergencies : hypertensive emergencies

• Nitroglycerin Nitroglycerin : useful especially when pulmonary oedema : useful especially when pulmonary oedema complicates situationcomplicates situation

2009-32009-3 7777

Management – Management – Antihypertensive therapyAntihypertensive therapy

• Unsuitable therapies :Unsuitable therapies :

– αα--MethyldopaMethyldopa – slow onset – slow onset– ClonidineClonidine – rebound hypertension on cessation – rebound hypertension on cessation– B-blockersB-blockers – risk of hepatotoxicity, decrease – risk of hepatotoxicity, decrease

uteroplacental perfusion, fetal complicationsuteroplacental perfusion, fetal complications– ACE-InhibitorsACE-Inhibitors – contraindicated in pre-delivery – contraindicated in pre-delivery

because of intrauterine death, oliguria, renal failure in because of intrauterine death, oliguria, renal failure in mum and neonatemum and neonate

– DiureticsDiuretics –avoid –avoid - - because deplete intravascular because deplete intravascular volumevolume

2009-32009-3 7878

ConclusionConclusion

• Pre-eclampsia due to a primary disturbance of placental Pre-eclampsia due to a primary disturbance of placental vasculaturevasculature is is leading to increase systemic vascular leading to increase systemic vascular resistance and resistance and bears a bears a potential for multiorgan potential for multiorgan disturbances / failure secondary to vasospasm.disturbances / failure secondary to vasospasm.

• Mainstay of management is early diagnosis, prevention of Mainstay of management is early diagnosis, prevention of hypertension and seizures.hypertension and seizures.

• Severe pre-eclampsia requires intensive management and Severe pre-eclampsia requires intensive management and the ultimate cure being delivery of fetus.the ultimate cure being delivery of fetus.

• EEclamptic seizures and pulmonary oedema often occur in clamptic seizures and pulmonary oedema often occur in the post-partum periodthe post-partum period (strict patient control after delivery) (strict patient control after delivery)..

2009-32009-3 7979

Maternal MortalityMaternal Mortality- Obstetrical Hemorrhage -- Obstetrical Hemorrhage -

4(4%)D.I.C.

9(10%)Couvelaire uterus

17(16%)Abruptio placenta

7(7%)Placenta previa

66(63%)Uterine atony

Patients (n=103)

Indication

2009-32009-3 8080

Placenta PreviaPlacenta Previa

2009-32009-3 8181

The placenta provides the fetus with oxygen and nutrients and takes away waste such as carbon dioxide via the umbilical cord.

2009-32009-3 8282

• Definition    – Placenta previa is a condition that may occur during

pregnancy when the placenta implants in the lower part of the uterus and obstructs the cervical opening to the vagina (birth canal).

2009-32009-3 8383

IncidenceIncidence

• The incidence of placenta previa is approximately 1 out of 200 births.

• Increases with each pregnancy, and it is estimated that the incidence in women who have had 6 or more previous deliveries may be as high as 1 in 20 births.

• Doubled in multiple pregnancy (such as twins and triplets).

2009-32009-3 8484

• Risk factors

– Multiparity (previous deliveries)

– Multiple pregnancy

– Previous myomectomy (removal of uterine fibroids through an incision in the uterus)

– A previous C-section (if the scar is low and close to the vaginal cervix region).

2009-32009-3 8585

EtiologyEtiology

• Endometrium factors:– a scarred endometrium (lining of the uterus)– Curretage for several times – an abnormal uterus

• Placental factors– Large– Abnormal formation of the placenta (succentu

riate lobe or placenta diffusa).

• Development retardation of fertilized egg

2009-32009-3 8686

Mechanisms of bleedingMechanisms of bleeding

• Mechanical separation of the placenta from its implantation site

• Placentitis

• Rupture of poorly supported venous lakes in the deciduas basalis

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ClassificationClassification

• Total placenta previa

The internal cervical os is covered completely by placenta

• Partial placenta previa

The internal os is partially covered by placenta• Marginal placenta previa

The edge of the placenta is at the margin of the intenal os.

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classificationclassification

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Clinical findingsClinical findings

• Symptoms    – Spotting during the first and second trimesters – Sudden, painless, and profuse vaginal

bleeding in pregnancy during the third trimester (usually after 28 weeks)

--Bleeding may not occur until after labor starts in some cases

--Anemia, shock

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• Signs – The uterus is usually soft, relaxed and nonten

der.– The infant position is oblique ( // ) or transver

se ( == ) in about 15% of cases.– Fetal distress is not usually present unless va

ginal blood loss has been heavy enough to induce maternal shock, placenta abruptio, or a cord accident occurs.

– No vaginal and rectal examination

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Accessory examinationsAccessory examinations

• Ultrasonography:– Accuracy 95%– 34th week

• Postpartum examination of placenta and membrane– 7cm

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• Differential diagnosis– Placental abruption

vagina bleeding with pain, tenderness of uterus. – Vascular previa– Abnormality of cervix

cervical erosion or polyp or cancer

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ComplicationsComplications      

• Maternal complications– major hemorrhage, shock, and death. – Implanted placenta– Anemia and infection

• Fetal complications– Prematurity (infant is less than 36 weeks gestation) is

responsible for about 60% of infant deaths secondary to placenta previa.

– Fetal blood loss or hemorrhage may occur because of the placenta tearing away from the uterine wall during labor. It may also occur with entry into the uterus during a C-section delivery.

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TreatmentTreatment

• The course of expectant treatment depends on – The amount of abnormal uterine bleeding– Whether the fetus is developed enough to survive

outside the uterus– The amount of placenta over the cervix– The position of the fetus– The parity (number of previous births) for the mother– The presence or absence of labor.

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TreatmentTreatment

• Early in pregnancy, transfusions may be given to replace maternal blood loss.

• Medications may be given to prevent premature labor, prolonging pregnancy to at least 36 weeks.

• Beyond 36 weeks, the benefits of additional infant maturity have to be weighed against the potential for major hemorrhage.

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TreatmentTreatment

• In selecting the optimum time for delivery, tests of fetal lung maturation are invaluable adjuvants.

• Cesarean section is the method for delivery. It has proven to be the most important factor in reducing maternal and infant death rates.

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Expectations (prognosis)Expectations (prognosis)

• The maternal prognosis (probable outcome) is excellent when managed appropriately. – This is done by hospitalizing those at risk who

are exhibiting signs and symptoms, and by performing C-section delivery.

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ABRUPTIO ABRUPTIO PLACENTAEPLACENTAE

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Definition

• Abruptio Placentae( placental abruption):

premature separation of the normally implanted placenta from the uterine wall.

Incidence: 1/77-89 deliveries

Severe form (resulting in fetal death)1/500-750

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Classification

• Concealed separation: no vaginal bleeding

• Apparent separation :vaginal bleeding will be

• Mixed separation : vaginal bleeding will be apparent

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Classification

• Concealed form (20%)– Detachment of the placenta may be complete– Complications are often severe. About 10%

with DIC.

• External form (80%)– Placenta detachment is more likely to be

incomplete– Complications are fewer and less severe.

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Etiology

• Mechanism: hemorrhage into the decidua basalis, leading to premature placental separation and further bleeding.

Associated factors:

• Maternal hypertension

• Sudden decompression of the uterus

• Maternal age and multiparity

• trauma

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Pathophysiology and pathologyPathophysiology and pathology

• Local vascular injury that results in vascular rupture into the decidua basalis, bleeding, and hematoma formation.– Preeclampsia-eclampsia, chronic hypertension, DM, chronic ren

al disease

• An abrupt rise in uterine venous pressure transmitted to the intervillous space.– Vasodilatation secondary to shock, compensatory hypertension

and the paralytic vasodilation of conduction anesthesia.

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Pathophysiology and pathologyPathophysiology and pathology

• Uteroplacental apoplexy– Extensive intramyometrial bleeding, resulting i

n a purplish and copper-colored, ecchymotic, indurated organ that all but loses its contractile power because of disruption of muscle bundles.

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Pathophysiology and pathologyPathophysiology and pathology

Coagulation abnormalities• Hypofibrinogenemia• Increaseing levels of fibrin degradation pro

ducts• decreasing platelet count • Increasing prothrombin time and partial thr

omboplastin time• Decreasing other serum clotting factors

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DiagnosisClassic clinical presentation:

• vaginal bleeding 80%

• Tender uterus 2/3

• Uterine contractions 1/3

• Fetal distress 50%

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• Ultrasonography:

• Placental examination

The extent of placental abruption of the maternal surface of the placenta on which a clot is detect at the time of delivery.

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ComplicationDICShockAmniotic fluid embolismAcute renal dysfunction

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ManagementManagement

Maintain hemodynamic stabilization ( Transfusion therapy)

• Crystalloid transfusion

• Whole blood therapy

• Component therapy

• Correct coagulation status

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Delivery

• When the fetus is mature, vaginal delivery is preferable unless there is evidence of fetal distress or hemodynamic instability.

• When the fetus is not mature and placental abruption is limited, observation with close monitoring of both fetal and maternal status.

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DeliveryDelivery

• Cesarean section is indicated:– Fetus exhibits persistent evidence of distress.– Situation is not favorable for rapid delivery.– Uncontrollable hemorrhage– A rapid expanding uterus with hemorrhage.– Uterine apoplexy

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