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OB > Embolism > Flashcards

Embolism Flashcards

1
Q

Among women who died after live birth the leading causes of death are

A

Embolism and PIH

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2
Q

Types of embolisms

A

Venous thromboembolism
PE
VAE
Amniotic fluid embolism

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3
Q

What is the risk of VTE with pregnancy

A

5-10x the risk

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4
Q

What physiological adaptions is VTE caused by

A

Venous stasis
Hypercoagulability
Damage to vessel wall
Virchows triad

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5
Q

Risk factors for VTE

A 
> 35 y.o
Higher parity
Obesity
Prolonged immobilization
Surgery during pregnancy aka CS
Family or personal history
Pre-eclampsia
Pelvic trauma
Hereditary thrombophilia protein C and S deficiency
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6
Q

Clinical signs of PE

A

Most common: tachypnea and sudden onset of dyspnea

Tachycardia, desaturation

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7
Q

Lab findings with a PE

A

Hypoxemia
Resp alkalosis
Normal chest x ray

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8
Q

EKG findings with a PE

A

RV strain
ST segment abnormality
T wave inversion
Supraventricular arrhythmias

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9
Q

Respiratory failure, pulmonary HTN for PE may result from

A

Respiratory failure occurs from the occlusion of the pulmonary vasculature (V/Q mismatch), and pulmonary edema due to increased hydrostatic forces and the disruption of normal capillary integrity
Pulmonary HTN results from direct vascular obstruction and results in RV overload

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10
Q

Invasive monitoring with a PE reveals

A

Normal to low PA occlusion pressures
Increased mean PAP
Increased CVP

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11
Q

Diagnostic tests used for pE

A

V/Q scans
MRA
Spiral CT
Pulm angio

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12
Q

Pulm angio is required in

A

Patients who have a negative V/Q scan but strong clinical suspicion of PE or in severe cases for confirmation of PE before thrombolysis

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13
Q

What is the radiation dose to the fetus with a combination of CXR, V/Q scan, pulm angio

A

0.5 rad

> 5 is significant for tetratogenesis

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14
Q

Supportive measures for PE/VTE

A

Improve Oxygenation and circulation, O2 administration and cardiorespiratory support with fluids inotropes and vasopressors
RA filling pressures should be maintained at a high level to maintain output from the failing RV

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15
Q

Specific therapy for VTE/PE

A

Anticoag (heparin, LMWH)

Thrombolysis

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16
Q

What thrombolytics can be used during pregnancy

A

Streptokinase or urokinase, and r-tpa

Urokinase is less antigenic and should have fewer side effects

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17
Q

Does not induce systemic fibrinolysis but is active when bound to thrombin so it is clot specific

A

R-TPA

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18
Q

Antepartum and intrapartum complications from thrombolysis includes

A

Maternal hemorrhage and placental abruption

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19
Q

Which is the therapy of choice between heparin and LMWH

A

Unfractionated heparin

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20
Q

Dosing with heparin

A

Iv bolus then an infusion for PTT 1.5 to 2x the upper level of control values for 10-14 days
Followed by subq injections 5k-10ku q8-12 hours throughout pregnancy

21
Q

When is heparin d/c

A

Shortly before delivery and restarted with warfarin

When the INR is between 2-3

22
Q

Controversial during pregnancy for thromboprophylaxis

A

LMWH

23
Q

Greater antithrombotic activity (factor xa) than anticoagulant activity (anti factor IIa)
it does not affect the aPTT

A

LMWH

24
Q

Why does the smaller structure of LMWH have advantages over heparin

A

Prolonged serum half life
Decreased daily dosing
Lower protein binding
Lower risk of bleeding, and platelet activation and thrombocytopenia

25
Q

How can air be demonstrated during CS

A

By precordial doppler auscultation

26
Q

Risk factors for VAE

A

Gradient of -5cm H2O between periphery and the heart would allow significant entry of air into venous circulation
Trendelenburg and exteriorizing the uterus during CS increases the gradient

27
Q

Uterine exteriorization predisposes to VAE by

A

Increasing the hydrostatic gradient by raising the incisional are above the level of the heart
By enlargement of the uterine sinuses providing more exposure to air

28
Q

What physiologic occurrence causes death from VAE is

A

Circ arrest from air entrapped in the RV outflow tract
5ml/kg of air lethal for air lock in RV or in pulmonary arterial circ
Can result in cardiogenic shock

29
Q

VAE with PA vasoconstriction can result in

A

Acute cor pulmonale

30
Q

Air on endothelial surfaces results in

A

Increased capillary permeability, platelet activation, and coagulopathy

31
Q

Massive VAE presents as

A

Hypotension, hypoxemia, cardiac arrest

32
Q

6 signs of air embolism

A 
Decreased end tidal 
Chest pain
Tachypnea, dyspnea
Cyanosis/mottled skin
Wheel mill murmur auscultated through steth
Tachycardia and hypotension
33
Q

Resuscitation steps for massive PE

A
  1. D/c nitrous and give 100% fio2
  2. Prevent further air entrapment flood surgical field, change position
  3. Support ventilation as needed
  4. Support circ
  5. Consider placement of central line to aspirate
  6. Expedite delivery
  7. Delayed emergence from GA consider neurodiagnostic imaging to r/o intracerebral air (arterial gas embolism) benefit from hyperbaric therapy within 5 hours
34
Q

The leading cause of mortality during labor and first few PP hours

A

AFE

35
Q

Maternal death with AFE occurs in one of three ways

A
  1. Sudden cardiac arrest
  2. DIC
  3. ARDS MOF
36
Q

Causes of AFE

A

Tear in amnion or chorion
Opens uterine and endocervical veins
Pressure is high to force amniotic fluid into venous circulation

37
Q

Risk factors for AFE

A 
Advanced age
Multiparity
Tumultuous labor
ROM
Fetal death
Trauma
Uterine overdistension
38
Q

Aminotic fluid components that are biochemical mediators causing major effects and anaphylactoid reaction and multi system involvement

A 
Surfactant
Endothelin
Leukotrienes C4 D4
Thromboxane A2
Prostaglandins
Arachidonic acid
Thromboplastin
Collagen tissue factor III
Phospholipase A2
PF III
39
Q

Suspension amniotic fluid components causing minor effects and mechanical obstruction

A 
Lanugo hair
Vernix caseosa
Fetal squames
Bile stained meconium
Fetal gut mucin
Trophoblasts
40
Q

Intermediate phase of anaphylactoid reaction to AFE

A 
Occurs when initially exposed
Respiratory distress
Cyanosis
Hemodynamic instability
Cerebral hypoperfusion with seizures, confusion, coma
41
Q

Second phase of anaphylactoid reaction to afe

A

Coagulopathy and hemorrhage

First and only presentation of AFE possibly

42
Q

Third phase of anaphylactoid reaction to AFE

A

Tissue injury is established

Die from lung or brain injury, MOF, or infection acquired during ICU

43
Q

Clinical manifestations of afe

A 
Nonspecific
1. Respiratory distress
2. Cyanosis
3. CV collapse
4. Coma
5. Hemorrhage
Hemorrhage and fetal distress initial symptoms
44
Q

Diagnosis of AFE

A

CXR maybe normal
EKG RV strain early on
ECHO - severe LV failure
Difficult to do specific testing d/t hemodynamic instability

45
Q

Past diagnosis of AFE

A

Autopsy by finding fetal squamous cells in maternal pulm circulation

46
Q

AFE treatment is supportive and directed towards

A 
Oxygenation
CO, SBP >90
Organ perfusion UO >25ml/hr
Coag corrections
Uterine toning
47
Q

Pharmacologic management if afe

A

Crystalloids, pressors, inotropic support
Restrict fluids after first hypotensive episode resolved to prevent pulm edema and ARDS
Corticosteroids hydrocort 500mg qh/hr
Heparin is controversial
CPB and thromboembolectomy

48
Q

T or F therapy for PE focuses on prevention of recurrent PEs

A

T

49
Q

T or F AFE may occur at any time during L and D

A

T

OB (10 decks)

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