obstetric emergency. amniotic fluid embolism-pathophysiology,clinical presentation, diagnosis, treatment, laboratory investigations and prognosis. cardiac arrest in preganacy and ACLS 2015 guidelines for CPR and new updates

1. AMNIOTIC FLUID EMBOLISM AND
CARDIAC ARREST IN
PREGNANCY
BY:-
DR. PRATEEK GUPTA (PG 2ND
YEAR ANESTHESIA)
MOD- DR. BEULAH ELANGO

2. INTRODUCTION
• Amniotic fluid embolism is a rare but
potentially lethal condition.
• First reported by Meyer in 1926, and
• First described by Steiner and Lushbaugh
in 1941
• Anaphylactoid syndrome of pregnancy

3. • AFE may lead to a mild degree of organ
dysfunction, coagulopathy, cardiovascular
collapse, and death.
• The syndrome typically occurs during
-labor,
-soon after vaginal or
-caesarean delivery, or
-during second trimester
dilation & evacuation procedures

4. EPIDEMIOLOGY
• Incidence of AFE is estimated to occur
between 1 in 8000 and 1 in 80,000
deliveries.
• The true incidence is unknown because
(1) AFE is a diagnosis of exclusion,
(2) there is no universally accepted
definition for identifying cases of AFE,
and
(3) Differing ascertainment methods
yield divergent rates of AFE.

5. RISK FACTORS
• MATERNAL FACORS
-Older maternal age.
-Multiparity.
-Intense contractions during labor.
-Abdominal trauma.
-Cesarean section.
-Induction of labor
-Placenta previa
-Eclampsia.
-Multiple pregnancy.
-Tears in the uterus or cervix.
-Early separation of the placenta from the
uterus wall.

6. • FETAL FACTORS
-Fetal distress.
-Fetal death.
-Male baby.

7. PATHOPHYSIOLOGY
• Disorderly labor, abnormal placentation,
surgical trauma, or any other breach of
the barrier between maternal blood and
amniotic fluid forces the entry of
amniotic fluid into the systemic
circulation and results in a physical
obstruction of the pulmonary circulation.
• There must be a pressure gradient that
favors transfer of fluid from the uterus
into the systemic circulation.

8. • The second and increasingly favored
hypothesis suggests that entry of
amniotic fluid into the maternal
circulation activates inflammatory
mediators, causing a humoral or
immunologic response.
• “ANAPHYLACTOID SYNDROME OF
PREGNANCY.”

10. STEINER AND LUSHBAUGH
(1941) (firsrt theory)
• Amniotic fluid was forced into the
maternal circulation during contractions
leading to the embolic event
• Maternal lung tissue revealed embolic
material of squamous cells, mucin,
meconium, and amorphous eosinophilic
material

11. BUT…..
• Uterine tachysystole are the least likely
times for maternoplacental exchange of
embolic material to occur as uterine blood
flow ceases.
• The passage of fetal squamous, lanugo hair,
and mucin into the maternal vasculature
appears to be a common event at term
• Fetal material has been identified in
pulmonary arterial samples aspirated from
critically ill women who did not have AFE.

12. SECOND THEORY
• Exact trigger unknown
- Rare pathologic fetal antigen bound to
IgE or
• Amniotic fluid contains vasoactive and
procoagulant products including platelet-
activating factor, cytokines, bradykinin,
thromboxane, leukotrienes, and
arachidonic acid
• The direct procoagulant property of
amniotic fluid may explain the prevalence
of DIC in AFE

13. • Maternal plasma endothelin
concentrations are increased
• Endothelin acts as a bronchconstrictor
as well as a pulmonary and coronary
vasoconstrictor, which may contribute
to respiratory and cardiovascular
collapse.
• Some have suggested that plasma
tryptase levels, a mast cell enzyme, may
be helpful in the diagnosis of AFE

14. • However, a series of case reports now
suggests that levels of tryptase and
histamine are not dramatically or
universally elevated among women
experiencing the AFE syndrome
• Although mast cell degranulation may
contribute to the pathophysiology of
AFE, this effect may be a secondary
product of the inflammatory cascade,
rather than causal

15. • Low levels of the C3 and C4 among women
diagnosed with AFE compared with controls,.
• Fetal squamous cells and syncytiotrophoblasts
display high concentrations of tissue factor and
phosphatidylserine.

16. • Tissue factor irreversibly aggregates
platelets, leading to platelet
degranulation, which releases TAX,
serotonin
-Serotonin is a potent pulmonary
vasoconstrictor that produces systemic
vasodilation and may lead to early right
heart failure
• TF binds factor VII, activates the extrinsic
pathway and triggers clotting by
activating factor X, with the subsequent
DIC.

17. • A second possible mechanism is that
amniotic fluid has a thromboplastin-like
effect, which induces platelet
aggregation, releases platelet factor III,
and activates the clotting cascade.
• Alternatively, the coagulopathy may be
related to fibrinolysis due to increased
levels of plasminogen activation inhibitor
1 in amniotic fluid.

19. CLINICAL FORMS
• Typical/Classic
• Atypical

20. TYPICAL
• THREE phases:
• Phase 1-respiratory and circulatory
disorders,
• Phase 2-coagulation disturbances of
maternal hemostasis,
• Phase 3-acute renal failure and acute
respiratory distress syndrome (ARDS),
and leading to cardiopulmonary collapse

21. ATYPICAL
• Cardiopulmonary collapse does not occur
in atypical embolism but the first
symptom is life threatening hemorrhage
due to DIC.
• Atypical embolism was observed during
-caesarean section or immediately
after it
-profound rupture of uterine
cervix,
-placenta abruption and
-induced mid-trimester abortion.

22. CLINICAL FEATURES
• Clark proposed a biphasic model
• Initial response is acute pulmonary
hypertension and vasospasm leading to
RVF, hypoxia, and cardiac arrest.
• PH is not sustained and replaced with
LVF and pulmonary edema & biomedical
mediators leading to DIC
• The typical presentation of AFE includes
a triad of sudden
-hypoxia,
-hypotension,
-coagulopathy,

23. • Cough
• Rapid decline in sPO2
• Sudden decrease in ETC02
• Hypotension
• Cyanosis
• Fetal bradycardia
• Encephalopathy: ranging from altered
mental state to seizures.
• Uterine atony
• Coagulopathy

25. INVESTIGATIONS
1) Continuous pulse oximetry and ABG to
determine the degree of hypoxemia.
ABG levels:
Decreased pH.
Decreased PO2 .
Increased PCO2 levels.
Base excess increased.
2) Serial CBC and coagulation studies.
-Thrombocytopenia is rare.
-PT is prolonged intervention is indicated
when the PT is 1.5 times the control value.
-aPTT may be within reference range or
shortened.
3) Fibrinogen level should be monitored.

26. 3) Blood type and screen in anticipation of
the requirement for a transfusion.
4) CXR PA/LAT
-diffuse B/L heterogeneous and
homogeneous areas of increased opacity,
which are indistinguishable from acute
pulmonary edema.

27. 5) A 12-lead ECG
-Tachycardia,
-ST-segment and T-wave changes,
-findings consistent with right
ventricle strain.
6) Lung scan
-areas of reduced radioactivity in the
lung field.
7) Increased serum tryptase, urinary
histamine concentrations and significantly
lower complement concentrations suggest
an anaphylactoid process.

28. 8) Decreased serum levels of C3 and C4
had sensitivities 88%-100% and a
specificity of 100%.
9) Monoclonal TKH-2 antibodies and zinc
coproporphyrin as rapid diagnostic
markers.????
10) Few studies have evaluated the
diagnostic accuracy of serum sialyl Tn
(STN), a fetal antigen present in
meconium and amniotic fluid, detected
through TKH-2 mab.
-serum levels >50 U/ml, the
sensitivities varies 78%-100% and the
specificities 97%-99%.

29. 11. Bedside TEE may aid early diagnosis
-acute pulmonary vasoconstriction,
-right ventricular dilation,
-collapsed left ventricle with
leftward deviation of the
intraventricular septum

30. • Zinc coproporphyrin-1 (ZnCP-1) is a
known component in meconium and
fetal urine.. It can be detected by
HPLC
• IGFBP-1 is a protein synthesized in
the decidua.. Higher levels in maternal
plasma can point towards AFE.
-A combination of maternal
serum IGFBP-1, alpha-fetoprotein,
and fetal fibronectin has been
postulated as a confirmatory test for
AFE

32. DD
• Aortic dissection.
• Cholesterol embolism.
• Myocardial infarction.
• Aspiration of gastric contents.

35. TREATMENT
• The key factors in the management of
AFE are early recognition, prompt
resuscitation, and delivery of the fetus.
• Management is primarily supportive and
resuscitative.
• Maternal resuscitation should focus on
three priorities:
(1) maintenance of oxygenation;
(2) hemodynamic support; and
(3) correction of coagulopathy

36. • OXYGENATION
-Control of the airway with tracheal
intubation and administration of 100%
O2 with positive pressure ventilation
should be performed

37. HYPOTENSION
• Large-bore IV access is warranted.
• Arterial line and CVP may facilitate
hemodynamic monitoring, blood sampling, and
vasopressor administration.
• Fluid resuscitation is imperative.
• Optimization of preload, with rapid volume
infusion of crystalloid and colloids solutions.
Although both can restore blood volume,
packed red blood cells is necessary to restore
oxygen carrying capacity
• TTE/TEE may guide fluid therapy with
evaluation of left ventricular filling.

38. COAGULOPATHY
• If platelets are <20,000/μL, or if
bleeding occurs and platelets are
20,000-50,000/μL, transfuse platelets
at 1-3 U/10 kg/day.
• Administer FFP to normalize the PT.
• If fibrinogen level is <100 mg/dL,
administer cryoprecipitate. Each unit of
cryoprecipitate raises the fibrinogen level
10 mg/dL.

39. PHARMACOLOGICAL INTERVENTION
• EPINEPHRINE may be the agent of choice as it is used in
other anaphylactoid reactions, in addition to the α-
adrenergic vasoconstrictor effects.
• PHENYLEPHRINE, is often an excellent choice early in the
treatment of AFE because at that time point systemic
vasodilation is the most prominent circulatory abnormality.
• DOPAMINE OR NORADRENALINE may be ideal agents,
which improve cardiac function.
• VASOPRESSIN may be used as primary therapy or as an
adjunct to other inotropic therapies and has the benefit of
sparing the pulmonary vasculature from vasoconstriction,
especially at low doses.
• MILRINONE or other PDE# should be considered In the face
of RHF
• DIGOXIN
• HYDROCORTISONE.

40. • OXYTOCIN: Decreases inflammation by
suppressing migration of polymorphonuclear
leukocytes and reversing increased capillary
permeability.
• METHERGINE causes a sustained tetanic
uterotonic effect that reduces uterine bleeding.
• CARBOPROST: produces myometrial
contractions, which reduces postpartum
bleeding
• RECOMBINANT FACTOR VIIa (rfVIIa) has been
a/w massive intravascular thrombosis.
• APROTININ has also been effective in reducing
hemorrhage with AFE.
• Other antifibrinolytic drugs, such as
aminocaproic acid and tranexamic acid, have
been described in the management of
obstetric hemorrhage and menorrhagia and
might also be considered during AFE.

41. WHAT ELSE??
• Exchange transfusion,
• ECMO,
• cardiopulmonary bypass,
• Right ventricular assist device,
• Uterine artery embolization,
• IABP with ECMO.
• Continuous hemofiltration,
• Cell-salvage combined with blood filtration and
serum protease inhibitors
• Hysterectomy may be required in patients with
persistent uterine hemorrhage to control blood
loss.
• Aerosolized prostacyclin and inhaled nitric oxide
(NO)

42. PROGNOSIS
• The prognosis after AFE is very poor, and
most women do not survive.
• If patient survives the embolism, most
survivors have neurologic deficits.
• The infant survival rate is 70%.
Neurologic status of the infant is directly
related to the time elapsed between
maternal arrest and delivery.
• Risk of recurrence is unknown. Successful
subsequent pregnancies have been
reported.

43. CARDIAC ARREST IN
PREGNANCY

44. PHYSIOLOGICAL CHANGES
• CARDIAC OUPUT
• SVR.
• The enlarging uterus can produce
increased afterload and decreased venous
return, starting at ≈12 to 14 weeks of
gestational age.
• As a result, the supine position, which is
most favorable for resuscitation, can lead
to hypotension.

45. • Uteroplacental blood flow increases from
50 to close to 1000 mL/min during
pregnancy, receiving up to a maximum
of 20% of maternal CO at term.
• Expanded intravascuar volume and a
decrease in uterine vascular resistance
facilitate sufficient uterine placental
blood.

46. • FRC
• Oxygen consumption increases
-The reduced functional residual
capacity reservoir and increased
consumption of oxygen are responsible
for the rapid development of hypoxemia
in response to hypoventilation or apnea
in the pregnant woman.
• Oxyhemoglobin dissociation curve

47. • Upper airway edema and friability occur
as a result of hormonal effects and may
reduce visualization during laryngoscopy
and increase the risk of bleeding.
• Progesterone relaxes gastroesophageal
sphincters and prolongs transit times
throughout the intestinal tract during
the second and third trimesters
predisposing the patient to aspiration of
stomach contents.

48. ESTIMATING GA
• Symphysis fundal height is the
measurement from the top of the
maternal pubic bone to the top of the
uterine fundus
• Gestational age is
-12 weeks if the uterus is palpable at
above the pubic symphysis,
-20 weeks if the uterus is palpable at
the level of the umbilicus,
-36 weeks if the uterus is palpable
at the level of the xiphisternum.

49. Risk stratification
A score ≥6 should trigger a call for support from the intensive care unit or rapid
response team and initiation of continuous monitoring of vital signs.

51. Pre-Event Planning
• Preparation for cardiac arrest:.
• Preparation for perimortem cesarean
delivery (PMCD):
• Preparation for management of obstetric
complications: Oxytocin and PGF2α.
• Decisions involving the resuscitation status
of the neonate:. The decision depends on the
gestational age and, to a significant degree,
the neonatal facilities available. This
information should be clearly documented

53. Unstable pregnant patient
• The patient should be placed in a full left
lateral decubitus
• Administration of 100% oxygen by face
mask to treat or prevent hypoxemia
• IV access should be established above the
diaphragm
• Precipitating factors should be
investigated and treated.

55. BLS

58. • Chest compressions should be performed
at a rate of at least 100 per minute at a
depth of at least 2 inches, allowing full
recoil,
• Compression-ventilation ratio of 30:2
• Interruptions should be limited to 10
seconds except for specific interventions
such as insertion of an advanced airway
or use of a defibrillator

59. • Continuous manual LUD should be
performed in whom the uterus is
palpated at or above the umbilicus
• Because an immediate cesarean
delivery (PMCD) may be the best way
to optimize the condition of the
mother and fetus this operation
should optimally occur at the site of
the arrest.

61. • A pregnant patient with in-hospital
cardiac arrest SHOULD NOT be
transported for cesarean delivery.
Management should occur at the site of
the arrest.
• Transport to a facility that can perform
a cesarean delivery may be required
when indicated (eg, for out-of-hospital
cardiac arrest or cardiac arrest that
occurs in a hospital not capable of
cesarean delivery).

62. • The same currently recommended
defibrillation protocol should be used in
the pregnant patient as in the non
pregnant patient.
• The patient should be defibrillated with
biphasic shock energy of 120 to 200 J.
• Compressions should be resumed
immediately delivery of the electric shock
• Anterolateral defibrillator pad
placement.,

63. ACLS

65. • The maternal cardiac arrest team would ideally be
composed of the following
• An adult resuscitation team (critical care physicians
and nurses, and/or emergency physicians and nurses,
and/ or internal medicine physicians and nurses, or
other service lines such as general surgery and
trauma, with respiratory therapy and pharmacy
representatives according to institutional policy, etc)
• Obstetrics: 1 obstetric nurse, 1 obstetrician
• Anesthesia care providers: obstetric anesthesiologist if
available or staff anesthesiologist; anesthesia assistant
or certified nurse anesthetist
• Neonatology team: 1 nurse, 1 physician, 1 neonatal
respiratory therapist

66. • In centers without
obstetric/neonatology services, it is
suggested that the cardiac arrest
committee and hospital emergency
services discuss contingency plans in
the event of maternal cardiac arrest.
•

67. • Leadership: Depends on where the arrest
occurs and may be specific to
institutional practices.
There should be a team leader for
obstetric care, and a team leader for
neonatal/fetal care.
• One approach to deal with multiple
subspecialties is for the usual cardiac
arrest team leader to delegate leadership
for obstetric, fetal, & airway
management.
• All team leaders must communicate
effectively together to make decisions

69. • Endotracheal intubation should be
performed by an experienced
laryngoscopist
– Starting with an ETT with a 6.0- to 7.0-
mm
– Optimally no more than 2 laryngoscopy
attempts
– Supraglottic airway placement is the
preferred rescue strategy
– If attempts at airway control and mask
ventilation fail, current guidelines for
emergency invasive airway access should be
followed

70. • Prolonged intubation attempts should be
avoided to prevent deoxygenation,
prolonged interruption in chest
compressions, airway trauma, and
bleeding.
• Cricoid pressure is NOT routinely
recommended

71. SURE???
• Continuous waveform capnography, in
addition to clinical assessment, is the
most reliable method of confirming and
monitoring correct placement of the ETT
• Findings consistent with adequate chest
compressions or ROSC include a rising
Petco2 level or levels >10 mm Hg

72. DRUGS ?
• For refractory (shock-resistant)
ventricular fibrillation and tachycardia,
amiodarone 300 mg rapid infusion
should be administered with 150mg
doses repeated as needed
• Doses do not require alteration In the
setting of cardiac arrest, NO medication
should be withheld because of concerns
about fetal teratogenicity

73. • Administering 1 mg epinephrine IV/IO
every 3 to 5 minutes during adult
cardiac arrest should be considered. In
view of the effects of vasopressin on the
uterus and because both agents are
considered equivalent, epinephrine should
be the preferred agent

74. FETUS
• Fetal assessment should NOT be
performed during resuscitation
• Fetal monitors should be removed or
detached as soon as possible to facilitate
PMCD without delay or hindrance
• In the event of multiple pregnancies, each
fetus should be resuscitated by a separate
resuscitation team

75. • Assisted vaginal delivery should be
considered when the cervix is dilated and
the fetal head is at an appropriately low
station

76. PMCD

77. • If the pregnant woman (with a fundus
height at or above the umbilicus) has not
achieved ROSC with usual resuscitation
measures with manual LUD,
• Decisions on the optimal timing of a
PMCD require consideration of factors
-cause of arrest,
-maternal pathology
-cardiac function,
-Gestational age, and resources
Shorter arrest-to-delivery time is
associated with better outcome

78. • PMCD should be strongly considered in
whom ROSC has not been achieved
after ≈4 minutes of resuscitative
efforts
• If maternal viability is not possible, the
procedure should be started
immediately;

79. • When PMCD is performed, the following
are recommended
-should not be transported to an
operating room
-should not wait for surgical
equipment to begin; only a scalpel is
required
-should not spend time on lengthy
antiseptic procedures.
-Continuous manual LUD should be
performed throughout the PMCD until
the fetus is delivered

80. If the uterus is difficult to
assess.
• In this situation, PMCD should be
considered at the discretion of the
obstetrician by using his or her best
assessment of the uterus. In these
patients, bedside ultrasound may help
guide decision making

82. ems

83. • If resources are available, EMS response
should include the appropriate staff to
ensure that BLS and ACLS actions can be
performed, including chest compressions,
LUD, defibrillation when indicated, and
management of the difficult airway
• If available, transport should be directed
toward a center that is prepared to
perform PMCD, but transport should not be
prolonged by >10 minutes to reach a center
with more capabilities
• EMS and the receiving emergency
department must establish optimal
communication for the transport of patient

90. What after…
• If still pregnant, should be placed in the
full left lateral decubitus position,
provided that this does not interfere
with additional management issues such
as airway control, and IV access. If not,
manual LUD should be maintained
continuously
• Transfer to ICU unless an operation is
required
• Optimal pre-event planning should be
ensured as discussed
• The cause of the arrest should continue
to be considered and treated accordingly

91. Targeted Temperature Management/Therapeutic
Hypothermia
• Should be considered in pregnancy on an
individual basis
• If used in pregnancy, targeted
temperature management should follow
the same current protocol as for the
non-pregnant patient
• Fetal monitoring should be performed
throughout targeted temperature
management

93. • thanks

95. • Maternal mortality is defined as the
death of a woman during pregnancy
and up to 42 days after delivery or
termination of pregnancy, provided
that the cause of death is related to
or aggravated by the pregnancy or
its manage- ment

96. • The initial respiratory reaction possibly
begins with a transient pulmonary
vasospasm. Vasospasm may be caused by
amniotic microemboli that trigger the
release of arachidonic acid metabolites and
leads to pulmonary hypertension,
intrapulmonary shunting,
bronchoconstriction, and severe hypoxia.
The second manifestation includes negative
inotropism and left ventricular failure
resulting in increasing pulmonary edema
and hypotension quickly leading to shock.
The third manifestation is a neurological
response to the respiratory and
hemodynamic injury, which may include
seizures, confusion, or coma