Amniotic Fluid Embolism
(AFE)
September 2019
epidemiology
 The incidence of clinically detectable AFE is low
 estimated to be 1 in 20,000 to 80,000 live births.
 Maternal mortality approaches 80%.
 Of patients with AFE, 50% die within the first hour
of onset of symptoms.
 Of survivors of the initial cardiorespiratory phase,
50% develop a coagulopathy.
 Neonatal survival is 70%.
Definition of AFE
 AFE is a rare obstetric emergency in
which amniotic fluid, fetal cells, hair, or
other debris enter the maternal
circulation, causing cardiorespiratory
collapse.
 Current data suggest that the process is
more similar to anaphylaxis than to
embolism
 term anaphylactoid syndrome of
pregnancy has been suggested
Major causes and factors
 occurs during labor
 multiparous woman with a large baby
 a short tumultuous labor
 use of uterine stimulants
 occurred during abortion
 amnioinfusion
 Amniocentesis
 caesarian section
 placenta accreta
 ruptured uterus
Amniotic Fluid Embolism Sept 2019.ppt
Amniotic Fluid Embolism Sept 2019.ppt
pathology
 Amniotic fluid and fetal cells enter the maternal
circulation, possibly triggering an anaphylactic
reaction to fetal antigens.
(1) Clinical symptoms result from mast cell
degranulation with the release of histamine and
tryptase,
(2) Clinical symptoms result from activation of the
complement pathway.
Progression usually occurs in 2 phases.
Phase I:
 pulmonary artery vasospasm with
pulmonary hypertension and elevated right
ventricular pressure cause hypoxia.
 Hypoxia causes myocardial capillary
damage and pulmonary capillary damage, left
heart failure, and acute respiratory distress
syndrome.
 Women who survive these events may enter
Phase II.
 This is a hemorrhagic phase characterized
by massive hemorrhage with uterine atony
and DIC
 however, fatal consumptive coagulopathy
may be the initial presentation.
Presentation
 The clinical presentation of AFE is
generally dramatic
 in the late stages , acutely dyspnea and
hypotension with rapid progression to
cardiopulmonary arrest
 In 40% of cases, followed by some
degree of consumptive coagulopathy,
 Hypotension: Blood pressure may drop
significantly with loss of diastolic measurement.
 Dyspnea: Labored breathing and tachypnea may
occur.
 Seizure: The patient may experience tonic-clonic
seizures.
 Cough: This is usually a manifestation of dyspnea.
 Cyanosis: As hypoxia/hypoxemia progresses,
circumoral and peripheral cyanosis and changes in
mucous membranes may manifest.
 Pulmonary edema: identified on chest
radiograph.
 Cardiac arrest
 Uterine atony:
 Fetal bradycardia: In response to the hypoxic
 Uterine atony usually results in excessive
bleeding after delivery.
Differentials
 Anaphylaxis
 Aortic Dissection
 Cholesterol Embolism
 Myocardial Infarction
 Pulmonary Embolism
 Septic Shock
Lab Studies
 Arterial blood gas (ABG) levels: Expect
changes consistent with hypoxia/hypoxemia
.
 Decreased pH levels
 Decreased PO2 levels
 Increased PCO2 levels
 Base excess increased
 Hemoglobin and hematocrit
/Thrombocytopenia is rare
 Prothrombin time (PT)
 Activated partial thromboplastin time
(aPTT)
 fibrinogen (Fg)
 Blood type
 Chest radiograph
 A 12-lead ECG
Treatment
 Administer oxygen to maintain normal
saturation.
 Initiate cardiopulmonary resuscitation
(CPR) if the patient arrests.
 Treat hypotension with crystalloid and blood
products.
 Consider pulmonary artery catheterization
in patients who are hemodynamically
unstable.
 Treat coagulopathy with fresh frozen
plasma(FFP) for a prolonged aPTT,
 cryoprecipitate for a fibrinogen level less
than 100 mg/dL, and
 transfuse platelets for platelet counts less
than 20,000/mL.
 Continuously monitor the fetus.
 Delivery quickly (forceps)
 Surgical Care: Perform emergent cesarean
delivery in arrested mothers who are
unresponsive to resuscitation.
 hemorrhage controlled with bilateral
uterine artery embolization.
Management of AFE
In the ICU
 To assess the effectiveness of treatment and
resuscitation, it is prudent to continuously
monitor ECG, pO2, CO2, and urine output.
To ICU
Management of AFE
In the ICU
 Central venous pressure monitoring is important to
diagnose right ventricular overload and guide fluid
infusion and vasopressor therapy. Blood can also be
sampled from the right heart for diagnostic purposes.
 Pulmonary artery and capillary wedge pressures and
echocardiography are useful to guide therapy and
evaluate left ventricular function and compliance.
 An arterial line is useful for repeated blood sampling
and blood gases to evaluate the efficacy of
resuscitation.
Management of AFE
Coagulopathy
• DIC results in the depletion of fibrinogen, platelets, and
coagulation factors, especially factors V, VIII, and XIII.
The fibrinolytic system is activated as well.
• Most patients will have hypofibrinogenemia, abnormal
PT and aPTT and low Platelet counts
• Treat coagulopathy with FFP (fresh frozen plasma) for a
prolonged aPTT, cryoprecipitate for a fibrinogen level
less than 100 mg/dL, and transfuse platelets for platelet
counts less than 20,000/mm3.
Restoration of uterine tone
 Uterine atony is best treated with massage, uterine
packing, and oxytocin or prostaglandin analogues.
 Improvement in cardiac output and uterine
perfusion helps restore uterine tone.
 Extreme care should be exercised when using
prostaglandin analogues in hypoxic patients, as
bronchospasm may worsen the situation.
Sympathomimetic Vasopressor agent
Dopamine
• Dopamine increases myocardial contractility and systolic BP with
little increase in diastolic BP. Also dilates the renal vasculature,
increasing renal blood flow and GFR.
• DOSE: 2-5 mcg/kg/min IV; titrate to BP and cardiac output.
• Contraindications: ventricular fibrillation, hypovolemia,
pheochromocytoma.
• Precautions: Monitor urine flow, cardiac output, pulmonary wedge
pressure, and BP during infusion; prior to infusion, correct
hypovolemia with either whole blood or plasma, as indicated;
monitoring central venous pressure or left ventricular filling
pressure may be helpful.
Maternal Mortality in AFE
• Maternal death usually occurs in one of three ways:
 (1) sudden cardiac arrest,
 (2) hemorrhage due to coagulopathy, or
 (3) initial survival with death due to acute respiratory
distress syndrome (ARDS) and multiple organ failure.
• For women diagnosed as having AFE, mortality rates
ranging from 26% to as high as 86% have been reported.
• The variance in these numbers is explained by dissimilar
case definitions and possibly improvements in intensive care
management of affected patients.
Further issues in the
Management
 Transfer: Transfer to a
level 3 hospital may be required once the patient is stable.
 Deterrence/Prevention: Amniotic fluid
embolism is an unpredictable event.
 Risk of recurrence is unknown. The recommendation for
elective cesarean delivery during future pregnancies in an
attempt to avoid labor is controversial.
 Perimortem cesarean delivery: After 5 minutes
of unsuccessful CPR in arrested mothers, abdominal
delivery is recommended.
Medical/Legal Pitfalls
• Failure to respond emergently is a pitfall.
• AFE is a clinical diagnosis.
• Steps must be taken to stabilize the patient as soon as
symptoms manifest.
• Failure to perform perimortem cesarean delivery in a
timely fashion is a pitfall.
• Failure to consider the diagnosis during legal abortion
is a pitfall.
• A review of the literature indicates that most case
reports of AFE have occurred during late second-
trimester abortions.
SUMMARY
• AFE is a sudden and unexpected rare but life threatening
complication of pregnancy.
• It has a complex pathogenesis and serious implications for
both mother and infant
• Associated with high rates of mortality and morbidity.
• Suspect AFE when confronted with any pregnant patient
who has sudden onset of respiratory distress, cardiac
collapse, seizures, unexplained fetal distress, and abnormal
bleeding
• Obstetricians should be alert to the symptoms of AFE and
strive for prompt and aggressive treatment.
The End
Uterine Rupture
Uterine Rupture
 is one of the most feared complications of
pregnancy
 the fetus, placenta, and a lot of blood
extruding into the mother's abdomen
 from a weak spot in the uterine wall or
uterus scar
epidemiology
 the risk of uterine rupture was 1 per 625 women
who chose repeat cesarean without labor,
 1 per 192 women who went into labor and tried for
VBAC, 1 per 129 for those who had their labor
induced without prostaglandins (usually with
Pitocin)
 1 per 41 when prostaglandin medications were
used for induction
 When the uterus did rupture, 1 in 18 babies died,
and 1 in 23 of the women required a hysterectomy.
Causes and factors
 previous surgery on the uterus
 Prior classical cesareans, where the incision
is near the top of the uterus
 prior removal of fibroid tumors
 any other uterine surgery that went through
the full depth of the muscular portion of the
uterus,
 multiple (three or more) prior low transverse
cesareans
 having had more than five full-term
pregnancies
 having an overdistended uterus (as with
twins or other multiples),
 abnormal positions of the baby such as
transverse lie
 the use of Pitocin and other labor-inducing
medications like prostaglandins
presentation
 Most uterine ruptures occur without
symptoms and do not cause problems for
the mother or fetus.
 This mild type is only noticed when surgery
is required for other reasons.
 In the most severe form , the laceration is
large or cuts across the uterine blood vessels
 the mother may hemorrhage and require a
blood transfusion
 the uterus may not be repairable and must
be surgically removed (hysterectomy)
 Many women will be advised not to get
pregnant again, due to the risk of repeated
rupture
 the baby may not survive
 the mother's life cannot be saved
Signs of uterine rupture
 severe, localized pain
 abnormalities of the fetal heart rate
 vaginal bleeding
 the vaginal examination may show that the
baby is not as low in the birth canal as he
had been earlier.
Preventing and Treatment
 Some uterine ruptures occur before labor and are
considered unpreventable.
 Sudden severe abdominal pain in later pregnancy
should be reported
 Women with risk factors ( prior classical
cesareans, deep fibroid excisions, and other major
uterine surgeries )should not attempt labor
 should be scheduled for cesarean usually between
36 and 39 weeks' gestation.
 If trying for vaginal birth after low transverse
cesarean(VBAC), fetal monitoring is important
 When uterine rupture is diagnosed during
labor, an emergency cesarean is performed.
 Usually the baby's life can be saved.
Amniotic Fluid Embolism Sept 2019.ppt

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Amniotic Fluid Embolism Sept 2019.ppt

  • 2. epidemiology  The incidence of clinically detectable AFE is low  estimated to be 1 in 20,000 to 80,000 live births.  Maternal mortality approaches 80%.  Of patients with AFE, 50% die within the first hour of onset of symptoms.  Of survivors of the initial cardiorespiratory phase, 50% develop a coagulopathy.  Neonatal survival is 70%.
  • 3. Definition of AFE  AFE is a rare obstetric emergency in which amniotic fluid, fetal cells, hair, or other debris enter the maternal circulation, causing cardiorespiratory collapse.
  • 4.  Current data suggest that the process is more similar to anaphylaxis than to embolism  term anaphylactoid syndrome of pregnancy has been suggested
  • 5. Major causes and factors  occurs during labor  multiparous woman with a large baby  a short tumultuous labor  use of uterine stimulants  occurred during abortion  amnioinfusion  Amniocentesis  caesarian section  placenta accreta  ruptured uterus
  • 8. pathology  Amniotic fluid and fetal cells enter the maternal circulation, possibly triggering an anaphylactic reaction to fetal antigens. (1) Clinical symptoms result from mast cell degranulation with the release of histamine and tryptase, (2) Clinical symptoms result from activation of the complement pathway.
  • 9. Progression usually occurs in 2 phases. Phase I:  pulmonary artery vasospasm with pulmonary hypertension and elevated right ventricular pressure cause hypoxia.  Hypoxia causes myocardial capillary damage and pulmonary capillary damage, left heart failure, and acute respiratory distress syndrome.
  • 10.  Women who survive these events may enter Phase II.  This is a hemorrhagic phase characterized by massive hemorrhage with uterine atony and DIC  however, fatal consumptive coagulopathy may be the initial presentation.
  • 11. Presentation  The clinical presentation of AFE is generally dramatic  in the late stages , acutely dyspnea and hypotension with rapid progression to cardiopulmonary arrest  In 40% of cases, followed by some degree of consumptive coagulopathy,
  • 12.  Hypotension: Blood pressure may drop significantly with loss of diastolic measurement.  Dyspnea: Labored breathing and tachypnea may occur.  Seizure: The patient may experience tonic-clonic seizures.  Cough: This is usually a manifestation of dyspnea.  Cyanosis: As hypoxia/hypoxemia progresses, circumoral and peripheral cyanosis and changes in mucous membranes may manifest.
  • 13.  Pulmonary edema: identified on chest radiograph.  Cardiac arrest  Uterine atony:  Fetal bradycardia: In response to the hypoxic  Uterine atony usually results in excessive bleeding after delivery.
  • 14. Differentials  Anaphylaxis  Aortic Dissection  Cholesterol Embolism  Myocardial Infarction  Pulmonary Embolism  Septic Shock
  • 15. Lab Studies  Arterial blood gas (ABG) levels: Expect changes consistent with hypoxia/hypoxemia .  Decreased pH levels  Decreased PO2 levels  Increased PCO2 levels  Base excess increased
  • 16.  Hemoglobin and hematocrit /Thrombocytopenia is rare  Prothrombin time (PT)  Activated partial thromboplastin time (aPTT)  fibrinogen (Fg)  Blood type  Chest radiograph  A 12-lead ECG
  • 17. Treatment  Administer oxygen to maintain normal saturation.  Initiate cardiopulmonary resuscitation (CPR) if the patient arrests.  Treat hypotension with crystalloid and blood products.  Consider pulmonary artery catheterization in patients who are hemodynamically unstable.
  • 18.  Treat coagulopathy with fresh frozen plasma(FFP) for a prolonged aPTT,  cryoprecipitate for a fibrinogen level less than 100 mg/dL, and  transfuse platelets for platelet counts less than 20,000/mL.  Continuously monitor the fetus.  Delivery quickly (forceps)
  • 19.  Surgical Care: Perform emergent cesarean delivery in arrested mothers who are unresponsive to resuscitation.  hemorrhage controlled with bilateral uterine artery embolization.
  • 20. Management of AFE In the ICU  To assess the effectiveness of treatment and resuscitation, it is prudent to continuously monitor ECG, pO2, CO2, and urine output. To ICU
  • 21. Management of AFE In the ICU  Central venous pressure monitoring is important to diagnose right ventricular overload and guide fluid infusion and vasopressor therapy. Blood can also be sampled from the right heart for diagnostic purposes.  Pulmonary artery and capillary wedge pressures and echocardiography are useful to guide therapy and evaluate left ventricular function and compliance.  An arterial line is useful for repeated blood sampling and blood gases to evaluate the efficacy of resuscitation.
  • 22. Management of AFE Coagulopathy • DIC results in the depletion of fibrinogen, platelets, and coagulation factors, especially factors V, VIII, and XIII. The fibrinolytic system is activated as well. • Most patients will have hypofibrinogenemia, abnormal PT and aPTT and low Platelet counts • Treat coagulopathy with FFP (fresh frozen plasma) for a prolonged aPTT, cryoprecipitate for a fibrinogen level less than 100 mg/dL, and transfuse platelets for platelet counts less than 20,000/mm3.
  • 23. Restoration of uterine tone  Uterine atony is best treated with massage, uterine packing, and oxytocin or prostaglandin analogues.  Improvement in cardiac output and uterine perfusion helps restore uterine tone.  Extreme care should be exercised when using prostaglandin analogues in hypoxic patients, as bronchospasm may worsen the situation.
  • 24. Sympathomimetic Vasopressor agent Dopamine • Dopamine increases myocardial contractility and systolic BP with little increase in diastolic BP. Also dilates the renal vasculature, increasing renal blood flow and GFR. • DOSE: 2-5 mcg/kg/min IV; titrate to BP and cardiac output. • Contraindications: ventricular fibrillation, hypovolemia, pheochromocytoma. • Precautions: Monitor urine flow, cardiac output, pulmonary wedge pressure, and BP during infusion; prior to infusion, correct hypovolemia with either whole blood or plasma, as indicated; monitoring central venous pressure or left ventricular filling pressure may be helpful.
  • 25. Maternal Mortality in AFE • Maternal death usually occurs in one of three ways:  (1) sudden cardiac arrest,  (2) hemorrhage due to coagulopathy, or  (3) initial survival with death due to acute respiratory distress syndrome (ARDS) and multiple organ failure. • For women diagnosed as having AFE, mortality rates ranging from 26% to as high as 86% have been reported. • The variance in these numbers is explained by dissimilar case definitions and possibly improvements in intensive care management of affected patients.
  • 26. Further issues in the Management  Transfer: Transfer to a level 3 hospital may be required once the patient is stable.  Deterrence/Prevention: Amniotic fluid embolism is an unpredictable event.  Risk of recurrence is unknown. The recommendation for elective cesarean delivery during future pregnancies in an attempt to avoid labor is controversial.  Perimortem cesarean delivery: After 5 minutes of unsuccessful CPR in arrested mothers, abdominal delivery is recommended.
  • 27. Medical/Legal Pitfalls • Failure to respond emergently is a pitfall. • AFE is a clinical diagnosis. • Steps must be taken to stabilize the patient as soon as symptoms manifest. • Failure to perform perimortem cesarean delivery in a timely fashion is a pitfall. • Failure to consider the diagnosis during legal abortion is a pitfall. • A review of the literature indicates that most case reports of AFE have occurred during late second- trimester abortions.
  • 28. SUMMARY • AFE is a sudden and unexpected rare but life threatening complication of pregnancy. • It has a complex pathogenesis and serious implications for both mother and infant • Associated with high rates of mortality and morbidity. • Suspect AFE when confronted with any pregnant patient who has sudden onset of respiratory distress, cardiac collapse, seizures, unexplained fetal distress, and abnormal bleeding • Obstetricians should be alert to the symptoms of AFE and strive for prompt and aggressive treatment.
  • 31. Uterine Rupture  is one of the most feared complications of pregnancy  the fetus, placenta, and a lot of blood extruding into the mother's abdomen  from a weak spot in the uterine wall or uterus scar
  • 32. epidemiology  the risk of uterine rupture was 1 per 625 women who chose repeat cesarean without labor,  1 per 192 women who went into labor and tried for VBAC, 1 per 129 for those who had their labor induced without prostaglandins (usually with Pitocin)  1 per 41 when prostaglandin medications were used for induction  When the uterus did rupture, 1 in 18 babies died, and 1 in 23 of the women required a hysterectomy.
  • 33. Causes and factors  previous surgery on the uterus  Prior classical cesareans, where the incision is near the top of the uterus  prior removal of fibroid tumors  any other uterine surgery that went through the full depth of the muscular portion of the uterus,  multiple (three or more) prior low transverse cesareans
  • 34.  having had more than five full-term pregnancies  having an overdistended uterus (as with twins or other multiples),  abnormal positions of the baby such as transverse lie  the use of Pitocin and other labor-inducing medications like prostaglandins
  • 35. presentation  Most uterine ruptures occur without symptoms and do not cause problems for the mother or fetus.  This mild type is only noticed when surgery is required for other reasons.
  • 36.  In the most severe form , the laceration is large or cuts across the uterine blood vessels  the mother may hemorrhage and require a blood transfusion  the uterus may not be repairable and must be surgically removed (hysterectomy)  Many women will be advised not to get pregnant again, due to the risk of repeated rupture  the baby may not survive  the mother's life cannot be saved
  • 37. Signs of uterine rupture  severe, localized pain  abnormalities of the fetal heart rate  vaginal bleeding  the vaginal examination may show that the baby is not as low in the birth canal as he had been earlier.
  • 38. Preventing and Treatment  Some uterine ruptures occur before labor and are considered unpreventable.  Sudden severe abdominal pain in later pregnancy should be reported  Women with risk factors ( prior classical cesareans, deep fibroid excisions, and other major uterine surgeries )should not attempt labor  should be scheduled for cesarean usually between 36 and 39 weeks' gestation.
  • 39.  If trying for vaginal birth after low transverse cesarean(VBAC), fetal monitoring is important  When uterine rupture is diagnosed during labor, an emergency cesarean is performed.  Usually the baby's life can be saved.