lecture 18 abnormalities of fetal membranes & amniotic fluid

Lecture 18Lecture 18

ABNORMALITIES OF ABNORMALITIES OF FETAL MEMBRANES & FETAL MEMBRANES &

AMNIOTIC FLUIDAMNIOTIC FLUID

Prof. Vlad TICA, MD, PhDProf. Vlad TICA, MD, PhD

ABNORMALITIES OF FETAL MEMBRANES & AMNIOTIC FLUID

MECONIUM STAINING

Staining of amniotic membrane within 1-3 hrs after meconium passage

Neonatal mortality rate

3.3% in the group with meconium-stained membrane compared with 1.7% in those without stng

Inflammation of fetal membrane is a manifestation of an intrauterine infection

Frequently associated with prolonged membrane rupture and long labor

(+) mononuclears & polymorphonuclear leukocytes infiltrating the chorion

CHORIOAMNIONITIS

DISORDERS OF THE AMNIOTIC FLUID VOLUME

HYDRAMNIOS

Defined as amniotic fluid index >24-25 cm

Mild → moderate degrees = 2-3 L

Incidence: 1 % of all pregnancies

2/3 - idiopathic

1/3 is associated with fetal anomalies, maternal DM or multifetal gestation

HYDRAMNIOSMild hydramnios

Defined as pockets measuring 8-11 cm in vertical dimension

Present in 85% of cases with excessive fluid

Moderate hydramnios

Defined as pockets containing only small parts & measured 12-15 cm deep

Present in 15 %

PATHOGENESIS

Early in pregnancyAmnionic cavity is filled with fluid

similar in composition to ECF

During 1st half of pregnancyTransfer of H2O & other small

molecules takes place not only across the amnion but thru the fetal skin

2nd trimesterFetus begin to urinate, swallow & inspire amnionic fluid

HYDRAMNIOS

SYMPTOMS

Severe dyspnea

Edema

DIAGNOSISClinical findings

Uterine enlargements in association with difficulty in palpating fetal small parts & in hearing FHT

By UTZ Large amounts of amnionic fluid can always be

demonstrated as an abnormally echo-free space between fetus & uterine wall or placenta

HYDRAMNIOS

PROGNOSIS

The more severe the hydramnios, the higher the perinatal mortality rate

Maternal complication associated with hydramnios

Placental abruption

Uterine dysfunction

Postpartum hge

HYDRAMNIOS

MANAGEMENT

Amniocentesis

Principal purpose is to relieve maternal distress

Amniotomy

Disadvantage is cord prolapse

HYDRAMNIOS

MANAGEMENT

Indomethacin therapy

Impairs lung liquid production or enhances absorption

Decrease fetal urine production

Increase fluid movement across fetal membrane

Dose: 1.5-3 mg/kg/day

Disadvantage:

Potential closure of fetal ductus arteriosus

HYDRAMNIOS

Defined as amniotic fluid index (AFI) < 5 cm

Risk:

Cord compression

OLIGOHYDRAMNIOS

CONDITIONS FREQUENTLY ASSOCIATED WITH OLIGOHYDRAMNIOS

OLIGOHYDRAMNIOS

Fetal

Chromosomal abnormalities

Congenital anomalies

Growth restriction

Demise

Postterm pregnancy

Ruptured membranes

Maternal

Uteroplacental insufficiency

Hypertension

Preeclampsia

DM

CONDITIONS FREQUENTLY ASSOCIATED WITH OLIGOHYDRAMNIOS

OLIGOHYDRAMNIOS

Placenta

Abruption

Twin-twin transfusion

Drugs

Prostaglandin synthetase inhibitors

ACE inhibitors

Idiopathic

EARLY-ONSET OLIGOHYDRAMNIOS

Almost always evident when there is obstruction of fetal urinary tract or renal agenesis

Exposure to ACE inhibitors

Fetal prognosis is poor

OLIGOHYDRAMNIOS

PULMONARY HYPOPLASIA

Incidence @ birth: 1.1 – 1.4 in 1000 infants

(+) when amnionic fluid is scant

3 possibilities that account for pulmonary hypoplasia:

Thoracic compression

Lack of fetal breathing movement decreases lung inflow

Failure to retain amnionic fluid or increase outflow with impaired lung growth and development

OLIGOHYDRAMNIOS

OLIGOHYDRAMNIOS IN LATE PREGNANCY

Amnionic fluid volume diminishes normally after 35 weeks

Significant oligohydramnios

Associated with increased risk of adverse perinatal outcomes

Fivefold increased cesarean delivery rate

OLIGOHYDRAMNIOS

1926 - Ricardo Meyer

1941 - Steiner & Luschbaugh autopsy series of 8 woman died of sudden shock during labor

Other studies revealed amniotic fluid debris in maternal kidney, liver, spleen, pancreas, brain

AMNIOTIC FLUID EMBOLISM

Amniotic fluid embolism (AFES) or anaphylactoid syndrome of pregnancy

Incidence: 1/8000 ~ 1/80000

Maternal mortality: 60 ~ 90 %

AFES & Pulmonary thromboembolism → 20% perinatal maternal mortality


PATHOPHYSIOLOGY Entrance of amniotic fluid to

maternal circulation:

Endocervical veins

Placental insertion site

Site of uterine trauma


PATHOPHYSIOLOGY Why Anaphylactoid Syndrome of Pregnancy?

1. A lag period

2. Amniotic debris in non-AFES mother

3. Variability of clinical signs & symptoms and its severity


PATHOPHYSIOLOGY Proposed Mechanisms:

1. Host immune responses

2. Abnormal amniotic fluid, atypical substance


CLINICAL PRESENTATION

Onset most commonly during labor & delivery

Nonspecific symptoms: chills, nausea, vomiting, agitation

Cardiorespiratory collapse occurred at presentation in the majority

Some have tonic-clonic seizure



Major clinical findings:

Hypoxia & respiratory failure

Cardiogenic shock

Disseminated intravascular coagulation (DIC)

Each of the above can be the dominant presentation



Signs & symptoms similar to anaphylactoid or septic shock

Risk factors unknown?

Etiology unkown?


HYPOXEMIA

Due to ventilation / perfusion mismatching

Some (15%) cases had bronchospasm

50% - 1st hour death were due to hypoxia and cardiogenic shock

May result in neurologic impairment


HYPOXEMIA

70% who initially survived developed pulmonary edema

May be cardiogenic / noncardiogenic

Evidence for endothelial-alveolar membrane damage → capillary leak →

1. High protein concentration in lung edema fluid

2. Amniotic fluid debris in sputum & alveoli


CARDIOGENIC SHOCK (CARDIOVASCULAR COLLAPSE)

Pulmonary artery & pulmonary capillary wedge pressures ↑

Cardiac output ↑

LV stroke index ↑

PA catheter data usually show CO↓ with relatively small increase in pulmonary vascular resistance

Arrhythmia, PEA, asystole may occur


DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

Major clinical findings:

Hypoxia & respiratory failure

Cardiogenic shock

80% AFES develop DIC

The temporal correlation is not constant among DIC, cardiogenic shock, hypoxia

When AFES occurs postpartum and DIC is the major early finding, diagnosis may be delayed due to s/s mimics hemorrhage!


DIAGNOSIS

Via symptoms & signs suspicion of AFES

Other causes of sudden cardiorespiratory failure:

1. Hemorrhage

2. Air or pulmonary embolism

3. Anesthetic complications

4. Anaphylaxis

5. Sepsis

6. Aspiration of gastric contents

7. Myocardial infarction


DIAGNOSIS

Some authors require the amniotic fluid debris (eg. squamous and trophoblastic cells, mucin, lanugo) from the distal port of a pulmonary artery catheter to make the diagnosis

But, amniotic fluid components commonly are present in the maternal circulation in women with no signs & symptoms of AFES


MANAGEMENT

Aggressive monitor

About maternal & fetal hypoxia

Pharmacologic therapy

Fluid support

Correct coagulopathy as needed


MANAGEMENT

Monitoring:

SpO2

EKG

Arterial line

Fetal monitor if onset prior to delivery

Echocardiography

CVP alone is not sufficient

Pulmonary artery catheterization


MANAGEMENT

Maternal Hypoxia

Secure airway

Intubation & Ventilation

Small tidal volume (6~8 ml/kg)

Normocapnia (~32 mmHg)

PEEP


MANAGEMENT

Fetal Hypoxia

65% fatal AFES present before delivery

Prevention of Fetal Hypoxia:

Maternal PO2 keep > 47 mmHg; best above 65 mmHg

Fetal umbilical vein PO2 >32 mmHg Fetal compensation by elevated Hb level &

cardiac output

Immediate delivery decreases fetal morbidity


MANAGEMENT

Pharmacologic Therapy

Inotropic & vasoactive agents:

Norepinephrine

Dopamine

Dobutamine (often use norepinephrine in combination)


MANAGEMENT

Fluid management

Pulmonary artery catheter insertion first, if possible

Avoid exacerbating pulmonary edema

Initial management with vasopressor is preferred

Correct coagulopathy with blood product as needed


DEFINITIONS

PROM is defined as amniorrhexis prior to the onset of labor at any stage of gestation

Amniorrhexis means spontaneous rupture of membranes as opposed to amniotomy

PPROM is used to defined that the patient who are preterm with ruptured membranes, whether or not they have contractions

PREMATURE RUPTURE OF THE MEMBRANES

ETIOLOGY AND RISK FACTORS

Vaginal and cervical infections

Abnormal membrane physiology

Incompetent cervix

Nutritional deficiencies


DIAGNOSIS

It is based on the history of vaginal loss of fluid and confirmation of amniotic fluid in the vaginal

A sterile vaginal speculum examination should be performed

Before labor, vaginal examination should not be performed

Carry out a complete ultrasonic examination


DIAGNOSIS

Confirmation of the diagnosis can be made by:

Testing the fluid with nitrazine paper, which will turn blue in the presence of the alkaline amniotic fluid

Placing a sample on a microscopic slide, air drying, and examining for ferning


MANAGEMENT

General considerations

Conservative expectant management

Management of chorioamnionitis

Tests of pulmonary maturity


MANAGEMENT

General considerations

Membranes are a natural barrier to prevent infections

PPROM has high risks of infections and sepsus

PPROM can lead to oligohydramnios


DIAGNOSIS OF OLIGOHYDRAMNIOS

Ultrasonic definition has been standardized

Criteria include:

1. Measure the amniotic fluid present in 4 quadrands by vertical axis

2. AFI: total being called the amniotic fluid index

3. A value < 5 cm is considered abnormal


OLIGOHYDRAMNIOS RESULTS IN:

Fetal crowding with thoracic compression

Restriction of fetal breathing

Disturbances of pulmonary fluid production and flow

Constaints placed on fetal movements in utero can also result in positional skeletal abnormalities, such as talipes equinovarus


MANAGEMENT

If PROM occurs at 36 weeks or later, condition of the cervix is favorable, no spontaneous contractions, labor should be induced after 6-12 hours

If PROM occurs prior to 36 weeks’ gestation, we should manage as followings:


LABORATORY TESTS

Complete blood cells

Gram stain and culture of amniotic fluid

Pulmonary maturation studies of amniotic fluid


MANAGEMENT

Conservative expectant management

The goal is to continue the pregnancy until the lung profile is mature

Take careful surveillance to diagnose subclinical infection and chorioamnionitis


CLINICAL SIGNS & SYMPTOMS OF CHORIOAMNIONITIS

Maternal temperature is > 38 0C

Fetal tachycardia

A tender uterus

Uterine irritability on nonstress testing

White blood cells elevates

Measure the amniotic fluid by ultranography


MANAGEMENT OF CHORIOAMNIONITIS

Use antibiotics depends on cultures and sensitivity

Once antibiotics have been started, labor should be induced

Vaginal delivery or cesarean section


MANAGEMENT

Tocolytic therapy

Corticosteriods

Labor and delivery

They are just the same with preterm labor !


MANAGEMENT

Tests of pulmonary maturity:

Lecithin/sphingomyelin (L/S) ratio maturity > 2

Lamellar body number density (LBND)

Maturity: > 46.000 LBND


MANAGEMENT

Surfactant therapy

It is effective

Expensive


THANKS !

lecture 18 abnormalities of fetal membranes & amniotic fluid

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