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Lecture 18 ABNORMALITIES OF FETAL MEMBRANES & AMNIOTIC FLUID

Lecture 18 ABNORMALITIES OF FETAL MEMBRANES & AMNIOTIC FLUID. Prof. 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

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Lecture 18 ABNORMALITIES OF FETAL MEMBRANES & AMNIOTIC FLUID

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  1. Lecture 18 ABNORMALITIES OF FETAL MEMBRANES & AMNIOTIC FLUID Prof. Vlad TICA, MD, PhD

  2. 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

  3. CHORIOAMNIONITIS • 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

  4. 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

  5. HYDRAMNIOS • Mild 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 %

  6. HYDRAMNIOS PATHOGENESIS • Early in pregnancy • Amnionic cavity is filled with fluid similar in composition to ECF • During 1st half of pregnancy • Transfer of H2O & other small molecules takes place not only across the amnion but thru the fetal skin • 2nd trimester • Fetus begin to urinate, swallow & inspire amnionic fluid

  7. HYDRAMNIOS SYMPTOMS • Severe dyspnea • Edema DIAGNOSIS • Clinical 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

  8. HYDRAMNIOS PROGNOSIS • The more severe the hydramnios, the higher the perinatal mortality rate • Maternal complication associated with hydramnios • Placental abruption • Uterine dysfunction • Postpartum hge

  9. HYDRAMNIOS MANAGEMENT • Amniocentesis • Principal purpose is to relieve maternal distress • Amniotomy • Disadvantage is cord prolapse

  10. 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

  11. OLIGOHYDRAMNIOS • Defined as amniotic fluid index (AFI) < 5 cm • Risk: • Cord compression

  12. OLIGOHYDRAMNIOS CONDITIONS FREQUENTLY ASSOCIATED WITH OLIGOHYDRAMNIOS Maternal • Uteroplacental insufficiency • Hypertension • Preeclampsia • DM Fetal • Chromosomal abnormalities • Congenital anomalies • Growth restriction • Demise • Postterm pregnancy • Ruptured membranes

  13. OLIGOHYDRAMNIOS CONDITIONS FREQUENTLY ASSOCIATED WITH OLIGOHYDRAMNIOS Drugs • Prostaglandin synthetase inhibitors • ACE inhibitors Idiopathic Placenta • Abruption • Twin-twin transfusion

  14. OLIGOHYDRAMNIOS 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

  15. 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

  16. 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

  17. AMNIOTIC FLUID EMBOLISM • 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

  18. 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

  19. AMNIOTIC FLUID EMBOLISM PATHOPHYSIOLOGY • Entrance of amniotic fluid to maternal circulation: • Endocervical veins • Placental insertion site • Site of uterine trauma

  20. AMNIOTIC FLUID EMBOLISM PATHOPHYSIOLOGY • Why Anaphylactoid Syndrome of Pregnancy? • A lag period • Amniotic debris in non-AFES mother • Variability of clinical signs & symptoms and its severity

  21. AMNIOTIC FLUID EMBOLISM PATHOPHYSIOLOGY • Proposed Mechanisms: • Host immune responses • Abnormal amniotic fluid, atypical substance

  22. AMNIOTIC FLUID EMBOLISM 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

  23. AMNIOTIC FLUID EMBOLISM CLINICAL PRESENTATION • Major clinical findings: • Hypoxia & respiratory failure • Cardiogenic shock • Disseminated intravascular coagulation (DIC) • Each of the above can be the dominant presentation

  24. AMNIOTIC FLUID EMBOLISM CLINICAL PRESENTATION • Signs & symptoms similar to anaphylactoid or septic shock • Risk factors unknown? • Etiology unkown?

  25. AMNIOTIC FLUID EMBOLISM 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

  26. AMNIOTIC FLUID EMBOLISM HYPOXEMIA • 70% who initially survived developed pulmonary edema • May be cardiogenic / noncardiogenic • Evidence for endothelial-alveolar membrane damage → capillary leak → • High protein concentration in lung edema fluid • Amniotic fluid debris in sputum & alveoli

  27. AMNIOTIC FLUID EMBOLISM 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

  28. AMNIOTIC FLUID EMBOLISM 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!

  29. AMNIOTIC FLUID EMBOLISM DIAGNOSIS • Via symptoms & signs  suspicion of AFES • Other causes of sudden cardiorespiratory failure: • Hemorrhage • Air or pulmonary embolism • Anesthetic complications • Anaphylaxis • Sepsis • Aspiration of gastric contents • Myocardial infarction

  30. AMNIOTIC FLUID EMBOLISM 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

  31. AMNIOTIC FLUID EMBOLISM MANAGEMENT • Aggressive monitor • About maternal & fetal hypoxia • Pharmacologic therapy • Fluid support • Correct coagulopathy as needed

  32. AMNIOTIC FLUID EMBOLISM MANAGEMENT • Monitoring: • SpO2 • EKG • Arterial line • Fetal monitor if onset prior to delivery • Echocardiography • CVP alone is not sufficient • Pulmonary artery catheterization

  33. AMNIOTIC FLUID EMBOLISM MANAGEMENT • Maternal Hypoxia • Secure airway • Intubation & Ventilation • Small tidal volume (6~8 ml/kg) • Normocapnia (~32 mmHg) • PEEP

  34. AMNIOTIC FLUID EMBOLISM 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

  35. AMNIOTIC FLUID EMBOLISM MANAGEMENT • Pharmacologic Therapy • Inotropic & vasoactive agents: • Norepinephrine • Dopamine • Dobutamine (often use norepinephrine in combination)

  36. AMNIOTIC FLUID EMBOLISM 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

  37. PREMATURE RUPTURE OF THE MEMBRANES 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

  38. PREMATURE RUPTURE OF THE MEMBRANES ETIOLOGY AND RISK FACTORS • Vaginal and cervical infections • Abnormal membrane physiology • Incompetent cervix • Nutritional deficiencies

  39. PREMATURE RUPTURE OF THE MEMBRANES 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

  40. PREMATURE RUPTURE OF THE MEMBRANES 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

  41. PREMATURE RUPTURE OF THE MEMBRANES MANAGEMENT • General considerations • Conservative expectant management • Management of chorioamnionitis • Tests of pulmonary maturity

  42. PREMATURE RUPTURE OF THE MEMBRANES MANAGEMENT General considerations • Membranes are a natural barrier to prevent infections • PPROM has high risks of infections and sepsus • PPROM can lead to oligohydramnios

  43. PREMATURE RUPTURE OF THE MEMBRANES DIAGNOSIS OF OLIGOHYDRAMNIOS • Ultrasonic definition has been standardized • Criteria include: • Measure the amniotic fluid present in 4 quadrands by vertical axis • AFI: total being called the amniotic fluid index • A value < 5 cm is considered abnormal

  44. PREMATURE RUPTURE OF THE MEMBRANES 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

  45. PREMATURE RUPTURE OF THE MEMBRANES 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:

  46. PREMATURE RUPTURE OF THE MEMBRANES LABORATORY TESTS • Complete blood cells • Gram stain and culture of amniotic fluid • Pulmonary maturation studies of amniotic fluid

  47. PREMATURE RUPTURE OF THE MEMBRANES 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

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