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Mar: Sem 6 - Adv. Principles B > Complicated OB Part 2 > Flashcards

Complicated OB Part 2 Flashcards

1
Q

What term describes an umbilical cord that comes out of the uterus before the fetus?

A

Umbilical Cord Prolapse

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2
Q

What is the biggest presentation as a result of Umbilical Cord Prolapse

A

Fetal Bradycardia

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3
Q

Factors that contribute to Umbilical Cord Prolapse

A
  • Multiple gestations - higher incidence of abnormal presentation
  • Breech / shoulder- Increases risk of cord prolapse
  • May occur in twins after delivery of baby A
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4
Q

Management of Umbilical Cord Prolapse

A
  • Manual reduction/ Manual elevation of presenting part/ Knee to chest
  • Retrograde bladder filling (500-600 mL bolus)
  • Emergent → C-section
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5
Q

Anesthesia Management of Umbilical Cord Prolapse

A
  • Situational
  • If Fetal bradycardia present → C-section
  • Use In situ epidural → top up w/ Chloroprocaine/Lidocaine
  • General anesthesia as backup
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6
Q

Differentiate between Monozygotic Twins and Dizygotic twins

A
  • Monozygotic twins: one fertilized egg (ovum) splits and develops into two babies with exactly the same genetic information (identical twins).
  • Dizygotic twins: two eggs (ova) are fertilized by two sperm, producing two genetically unique children (fraternal twins).
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7
Q

Differentiate between a chorion and an amnion.

A
  • Chorion is the outer membrane that surrounds the embryo and the amnion.
  • Amnion is the inner membrane that surrounds the embryo
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8
Q

What type of placenta will have the lowest risk for twin-to-twin transfusion syndrome?

A

Dichorionic placenta

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9
Q

What type of placenta will have the highest risk for twin-to-twin transfusion syndrome?

A

Monochorionic placenta

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10
Q

Name the type of placentation

A

Monochorionic Monoamniotic

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11
Q

Name the type of placentation

A

Dichoriontic Diamniotic (fused placenta)

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12
Q

Name the type of placentation

A

Monochorionic Diamniotic

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13
Q

Name the type of placentation

A

Dichoriontic Diamniotic (separate placenta)

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14
Q

What will be the type of placentation for dizygotic twins?

A
  • Dichorionic Diamniotic
  • Can have either a fused or separate placenta
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15
Q

What two systems will experience the greatest physiological change during pregnancy?

A
  • Cardiovascular
  • Pulmonary
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16
Q

Cardiac Output during pregnancy increases by ______%.

A
  • 20% ↑ in CO d/t ↑ SV
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17
Q

What lung volumes decrease near-term gestation d/t uterine size?

A
  • ↓ TLC
  • ↓ FRC

The decrease lung volumes will increase risk of hypoxemia

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18
Q

During pregnancy, maternal weight gain increased faster after ____ weeks

A

30 weeks

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19
Q

What direction does the stomach displace during pregnancy?

A

Cephalad

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20
Q

A stomach displaced cephalad will _________ competence of LES and _________ aspiration risk.

A
  • Decrease competence of LES
  • Increase aspiration risk
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21
Q

Maternal blood volume = _________ mL/kg

A

105 mL/kg

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22
Q

How much does plasma volume increase during pregnancy?

A

750 mL

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23
Q

Delivery EBL approximation

A

about 500 mL

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24
Q

What complications will most monochorionic twins experience?

A
  • Vascular Anatomoses
  • ↑ Risk twin-to-twin transfusion
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25
Q

More than 50% of multiple gestation moms deliver before _______ weeks gestation.

A

Before 37 weeks

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26
Q

Twins are usually induced around __________ weeks

A

38 weeks

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27
Q

Triplets are usually induced around __________ weeks

A

35 weeks

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28
Q

Increased fetal weight & larger volume of amniotic fluid increase the risk of _________ compression & supine _________ syndrome.

A
  • Aortocaval
  • Hypotension
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29
Q

Multiple gestations can lead to uterine distention → Increase risk of ________ and ____________

A
  • PPH
  • Uterine atony

have Methergine and Hemabate on standby

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30
Q

Anesthesia management for Multiple Gestations

A
  • Double set-up (Vag and C-Section delivery)
  • Terbutaline 250 mcg IV or SQ for uterine relaxation
  • Alternative NTG for uterine relaxation (100-250 mcg IV or 400 mcg SL)
  • Facilitate podalic version of twin B for vaginal delivery
  • GETA as backup
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31
Q

What is the most common pregnancy-related disorder?

A

Pregnancy Induced Hypertension (PIH)

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32
Q

What is the most widely accepted definition/ parameters for PIH?

A
  • BP elevated > 139/89 mmHg x 2
  • After 20 weeks gestation
  • Most cases develop after 37 weeks gestation
  • Without proteinuria
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33
Q

What percentage of PIH patients will develop preeclampsia?

A

25%

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34
Q

When will PIH resolve?

A

12 weeks postpartum

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35
Q

Define preecmapsia

A
  • New Onset of HTN (>140/90) after 20 weeks
  • Renal insufficiency & proteinuria (>300 mg/day)
  • Creatinine >0.3
  • 1+ on urine dipstick specimen
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36
Q

Alternative Symptoms of Preeclampsia

A
  • Persistent epigastric / right upper quadrant pain
  • Persistent cerebral symptoms (blurry vision/ floaters)
  • IUGR
  • Thrombocytopenia / elevated liver enzymes
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37
Q

Parameters for Preeclampsia w/ severe features

A
  • BP ≥ 160/110 mmHg
  • Thrombocytopenia (plt < 100,000/mm3)
  • Serum [creatinine] > 1.1 mg/dL or > 2x baseline
  • Pulmonary edema
  • New onset cerebral or visual disturbances
  • Impaired liver function
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38
Q

What percentage of mothers who have chronic hypertension develop preeclampsia?

A

20-25%

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39
Q

Chronic Hypertension
Time of Onset:
Severity:
Proteinuria:
Serum Uric Acid > 5.5 mg/dL:
Hemoconcentration:
Thrombocytopenia:
Hepatic dysfunction:

A

Chronic Hypertension
Time of Onset: Before 20 weeks
Severity: Mild to severe
Proteinuria: Absent
Serum Uric Acid > 5.5 mg/dL: Rare
Hemoconcentration: Absent
Thrombocytopenia: Absent
Hepatic dysfunction: Absent

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40
Q

Gestational Hypertension
Time of Onset:
Severity:
Proteinuria:
Serum Uric Acid > 5.5 mg/dL:
Hemoconcentration:
Thrombocytopenia:
Hepatic dysfunction:

A

Gestational Hypertension
Time of Onset: After 20 weeks
Severity: Mild
Proteinuria: Absent
Serum Uric Acid > 5.5 mg/dL: Absent
Hemoconcentration: Absent
Thrombocytopenia: Absent
Hepatic dysfunction: Absent

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41
Q

Preecampsia
Time of Onset:
Severity:
Proteinuria:
Serum Uric Acid > 5.5 mg/dL:
Hemoconcentration:
Thrombocytopenia:
Hepatic dysfunction:

A

Preecampsia
Time of Onset: After 20 weeks
Severity: Mild to severe
Proteinuria: Typically present
Serum Uric Acid > 5.5 mg/dL: Almost all cases
Hemoconcentration: In severe cases
Thrombocytopenia: In severe cases
Hepatic dysfunction: In severe cases

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42
Q

Preeclampsia is a multisystem disease that includes placenta. No _______ is required to develop preeclampsia.

A

Fetus (molar pregnancy)

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43
Q

Preeclampsia can result in abnormal ___________ implantation.

A

placental

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44
Q

Impaired remodeling of spiral arteries as a result of preeclampsia will have what impact on the fetus?

A

Small & constricted blood vessels affect O2 & nutrient delivery to the fetus

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45
Q

How does preeclampsia cause diffuse endothelial dysfunction?

A

Injury from antiangiogenic proteins released by placenta

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46
Q

How does preeclampsia affect nitric oxide and prostacyclin?

A
  • Decrease Nitric Oxide
  • Decrease Prostacyclin
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47
Q

How does preeclampsia affect the sensitivity of angiotensin II?

A

Sensitivity to angiotensin II increases

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48
Q

How does preeclampsia affect oncotic pressure?

A

Preeclampsia → Hypoalbuminemia → Low Oncotic pressure (results in intravascular volume depletion and 3rd spacing)

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49
Q

What is considered early onset of preeclampsia?

A
  • Before 34 weeks gestation
  • Worse outcomes (usually results in C-section)
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50
Q

What is considered late onset of preeclampsia?

A
  • After 34 weeks
  • Typically already metabolically predisposed to preeclampsia (existing DM, HTN, obesity)
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51
Q

When can postpartum preeclampsia occur?
Presentation?

A
  • Within seven days postpartum
  • Proteinuria and Seizures
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52
Q

Prophylactic treatment for Preeclampsia

A
  • Initiate Aspirin 16 weeks or earlier for the best benefit
  • Aspirin will inhibit the synthesis of prostaglandins and biosynthesis of platelet thromboxane A2
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53
Q

Preeclampsia predictors of unfavorable outcomes

A
  • Early onset
  • Chest pain / dyspnea
  • Low SpO2
  • Thrombocytopenia
  • Elevated creatinine
  • Increased AST concentration
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54
Q

CNS presentation of Preeclampsia

A
  • Severe headache
  • Hyperexcitability (giddy)
  • Hyperreflexia
  • Coma
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55
Q

Visual changes involved with preeclampsia.

A
  • Scotoma (Blind Spot)
  • Amaurosis (Painless vision loss)
  • Blurred vision
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56
Q

How does preeclampsia affect cerebral vascular autoregulation?

A

Loss of cerebral vascular autoregulation → hyperperfusion → cerebral edema

Most common in posterior circulation resulting in Posterior reversible encephalopathy syndrome (PRES)

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57
Q

Clinical presentation of preeclampsia from an airway standpoint.

A
  • Normal pregnancy will result in capillary engorgement and decreased tracheal diameter
  • Preeclampsia → Pharyngo-laryngeal edema
  • Preeclampsia → Upper airway diameter decreased
  • Preeclampsia → Subglottic edema
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58
Q

Clinical presentation of preeclampsia from a CV standpoint.

A
  • Increased vascular tone
  • Increased sensitivity to vasoconstrictors & catecholamines
  • Severe vasospasm
  • Exaggerated hemodynamic response to catecholamines (ephedrine)
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59
Q

In severe preeclampsia, plasma volume can be decrease up to _________ %

A

Decrease 40%

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60
Q

How does Pre-eclampsia affect CO, SVR, and Left Ventricular Function?

A
  • CO will be normal to increase in the absence of pulmonary edema
  • Mild to moderately increased SVR w/ diastolic dysfunction
  • Hyperdynamic left ventricular function
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61
Q

What percentage of patients with preeclampsia develop pulmonary edema?

A

3%

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62
Q

What factors will increase the risk of pulmonary edema in preeclamptic patients?

A
  • Advanced maternal age
  • Preeclampsia superimposed on chronic HTN or
  • Renal disease
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63
Q

How does pulmonary edema develop in preeclamptic patients?

A
  • Plasma colloid osmotic pressure is greatly reduced
  • Results in increased pulmonary capillary permeability
  • Leads to increased intravascular hydrostatic pressure
  • Increase risk for pulmonary pressure
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64
Q

Clinical presentation of preeclampsia from a hematologic standpoint.

A
  • Thrombocytopenia is the most common hematologic abnormality
  • PLT <100,000/mm3 associated with increased disease severity or HELLP syndrome
  • ↑ risk of DIC

HELLP: Hemolysis, Elevated Liver enzyme levels, and Low Platelet levels.

65
Q

Coagulation state in a normal pregnancy

A

Hypercoagulable d/t a physiologically adaptive mechanism to prevent postpartum hemorrhage.

66
Q

What happens to the coagulation state in severe preeclampsia?

A
  • Relatively hypercoagulable
  • Platelets will activate and then degranulate, resulting in decreased platelet function
  • Decrease platelet count
67
Q

DIC can be present during these complications.

A
  • Severe liver involvement (pre-existing liver dz)
  • intrauterine fetal death (IUFD)
  • Placental abruption
  • PPH
68
Q

Pathophysiology of DIC

A
  • Consumption of procoagulants
  • Increased levels of fibrin degradation products
  • Microthrombi formation → end-organ damage
  • As procoagulants decrease this will result in a increase risk of spontaneous hemorrhage
69
Q

Clinical presentation of preeclampsia from a hepatic standpoint.

A
  • Periportal hemorrhage
  • Fibrin deposition in hepatic sinusoids
  • Presents as RUQ or epigastric pain
  • Risk of spontaneous hepatic rupture
70
Q

Clinical presentation of preeclampsia from a renal standpoint.

A
  • Persistent proteinuria is a defining characteristic
  • Impaired proximal tubular reabsorption
  • Glomerular filter change in pore size or charge selectivity
  • Smaller increase in GFR than normal pregnancy
  • Hyperuricemia d/t decrease renal clearance of uric acid
  • Oliguria (low urine output)
71
Q

Preeclampsia H/H Labs

A
  • Hemoconcentration indicative of preeclampsia d/t loss of intravascular plasma
  • Disease severity related to H/H
  • H/H decreased with hemolysis with disease progression
72
Q

What lab will require further coagulation tests for preeclamptic patients?

A
  • Plt less than 100K
  • assess PT and aPTT
  • Often times there will be a decrease in fibrinogen concentration
73
Q

Type & crossmatch for at least _____ PRBCs in thrombocytopenia or coagulation abnormalities

A

2 units

74
Q

Proteinuria = Preeclampsia NOT _____________

A

PIH (gestational HTN)

75
Q

When will antihypertensives be used to manage acute hypertension?

A
  • SBP > or = 160 mmHg
  • DBP > or = 110 mmHg
76
Q

Acute HTN Management decrease BP by __________%
Goal SBP:
Goal DBP:

A
  • Slow BP decreased by 15-25%
  • Goal SBP: 120-160 mmHg
  • Goal DBP: 80-105 mmHg

Rapid & drastic changes may negatively impact uteroplacental perfusion & O2 delivery to fetus

77
Q

Labetalol IV
Onset:
Dose:
Max Dose:

A

Labetalol IV
Onset: 5-10 mins
Dose: 20 mg IV → 40-80 mg IV q 10 mins
Max Dose: 220 mg IV

Realistically give 5-10 mg initially and see where to go from there

78
Q

Hydralazine IV
Onset:
Dose:
Max Dose:

A

Hydralazine IV
Onset: 10-20 mins
Dose: 5 mg IV q 20 mins
Max Dose: 20 mg

79
Q

Nifedipine PO
Onset:
Dose:
Max Dose:

A

Nifedipine PO
Onset: 10-20 mins
Dose: 10 mg q 20 mins
Max Dose: 50 mg

80
Q

Nicardipine IV infusion
Onset:
Dose:
Max Dose:

A

Nicardipine IV infusion
Onset: 10-15 mins
Dose: 5 mg/hr, ↑ 2.5 mg/hr q 5 mins
Max Dose: 15 mg/hr

81
Q

What medication is used for seizure prophylaxis in preeclamptic patients?

A
  • Magnesium Sulfate
  • Primarily used in parturients w/ severe features
82
Q

What are the pros and cons of using magnesium sulfate in parturients?

A
  • Pro: Decreases risk of developing eclampsia
  • Pro: Decreases risk of placental abruption
  • Con: Increases risk of maternal respiratory depression
  • Con: Increases risk of cesarean delivery
83
Q

Side effects of magnesium sulfate

A
  • Warm/flushed feeling
  • N/V
  • Headache
  • Muscle weakness / drowsiness / confusion
  • Hypotension / dizziness
84
Q

Fetal effects from magnesium sulfate

A
  • Decreased fetal HR, but Remains > 110 bpm
  • Decreased variability
85
Q

MOA of Magnesium Sulfate

A
  • No clear understanding of MOA
  • Decreased peripheral vascular resistance
  • Protects the blood-brain barrier
  • Decreases cerebral edema
  • Prevents rise in free intracellular Ca++ concentration
  • Competitive blockade at central NMDA receptors to raise seizure threshold
86
Q

Magnesium Sulfate Dosing for Preeclampsia and Eclampsia

A

Loading Dose: 4-6 gm over 20-30 mins
Infusion: 1-2 gm/hr

87
Q

Magnesium Sulfate Dosing for Recurrent Eclampsia

A

Loading Dose: 2 gm over 5 mins
Infusion: 1-2 gm/hr

88
Q

Magnesium limits the release of ________ at the NMJ

A

Acetylcholine

89
Q

Magnesium _________ (increases or decreases) sensitivity of NMJ to acetylcholine.

A

Decreases

90
Q

What does magnesium do to muscle fiber membrane?

A

Depresses excitability

91
Q

Effect of magnesium on depolarizing and NDMR?

A
  • Potentiate its action
  • Use a smaller dose and monitor peripheral nerve stimulator
92
Q

Effect of magnesium on neuraxial administered local anesthetic.

A
  • Increases the potency of local anesthetic
  • Risk of hypotension increases
93
Q

What is the therapeutic range of magnesium sulfate?

A

5-9 mg/dL

94
Q

How is magnesium eliminated in the body?

A

Renal Excretion

95
Q

Individuals with renal insufficiency/failure will have a Serum Cr > ________ and will tend to have higher serum magnesium levels.

A

1.2 mg/dL

96
Q

Hypermagnesemia S/E

A
  • Chest pain / tightness
  • Palpitations
  • Nausea
  • Blurred vision
  • Sedation
  • Transient hypotension
97
Q

At what magnesium serum level will a patient lose deep tendon (patellar) reflexes?

A

12 mg/dL

98
Q

At what magnesium serum level will a patient experience respiratory depression?

A

15-20 mg/dL

99
Q

At what magnesium serum level will a patient have a cardiac arrest (asystole)?

A

Greater than 25 mg/dL

100
Q

What is the normal serum magnesium level?

A

1.7 – 2.4 mg/dL

101
Q

What is the treatment of magnesium toxicity?

A
  • Calcium gluconate 1 gm over 3 - 10 minutes
  • Calcium chloride 10% 500 mg over 5 – 10 minutes
102
Q

What is the most common complication CNS feature from preeclampsia?

A

Reversible Cerebral Edema

103
Q

What is the leading cause of death in preeclampsia?

A

CVA

Hemorrhage more common than embolic CVA secondary to preeclampsia

104
Q

When does most hemorrhagic stroke occur during pregnancy?

A

Postpartum

105
Q

What percentage of parturients experience abruption secondary to preeclampsia?

A

2%

Incidence greater with chronic HTN
Abruption will lead to a greater risk of DIC

106
Q

HELLP Syndrome is a complication of preeclampsia. What do the acronyms stand for?

A
  • Hemolysis
  • Elevated levels of liver enzymes
  • Low platelet count

HELLP can be present w/o HTN or proteinuria.

107
Q

HELLP Syndrome increases the risk of these complications.

A
  • DIC
  • Placental abruption
  • Pulmonary edema
  • Acute renal failure
  • Liver hemorrhage/failure
  • ARDS
  • Sepsis
  • Stroke
  • Death
108
Q

Define Hemolysis

A

Destruction or breakdown of red blood cells, leading to the release of hemoglobin into the surrounding fluid (such as blood plasma).

Presence of Microangiopathic Hemolytic Anemia

109
Q

What symptoms may be present in a parturient if they are experiencing hemolysis?

A
  • RUQ or epigastric pain
  • N/V
  • Headache
  • HTN
  • Proteinuria
110
Q

Bilirubin levels in HELLP Syndrome

A

Bilirubin > 1.2 mg/dL

111
Q

Liver Enzyme levels in HELLP Syndrome

A

Increase AST > or = 70 IU/L
Increase LDH > 600 IU/L

112
Q

Plt levels in HELLP Syndrome

A

Plt count < 100K, but can decrease precipitously

113
Q

If a parturient has HELLP Syndrome, when will their plt count reach nadir?

A

Reaches nadir 2-3 days postpartum

114
Q

Which steroid can improve plt count?

A

Dexamethasone

115
Q

Plt count below this level during a C-section will covert to a GETA

A

less than 50K

116
Q

When will plt be transfused in a parturient?

A
  • Transfuse if plt count < 20,000
  • Transfuse if plt count < 40,000 & c-section planned

Hospital facility dependent

117
Q

Management for HELLP Syndrome

A
  • Delivery
  • Corticosteroid administration to improve fetal lung maturity
  • Magnesium sulfate for seizure prophylaxis
  • Antihypertensives
118
Q

What are the indications for inserting an A-line for a parturient?

A
  • Continuous BP monitoring during induction/emergence of GETA in severe disease with poorly controlled HTN
  • Planned use of rapid-acting vasodilators
  • ABGs in the presence of pulmonary edema
  • Estimate intravascular volume status
119
Q

What are the indications for inserting a central venous catheter/ pulmonary arterial catheter for a parturient?

A
  • In the setting of multiple organ failure
  • Underlying congenital/valvular heart disease
  • Critical cardiovascular instability
120
Q

Things to consider before placement of labor analgesia

A
  • Coagulation status
  • IV hydration injecting local anesthetics
  • Management of resultant hypotension
  • Use of epinephrine containing local anesthetics
121
Q

Neuraxial placement & platelet count parameters

A
  • > 80,000/mm3 – no concerns
  • 50,000-80,000/mm3 – weigh benefits/risks/alternatives
  • < 50,000/mm3 – no neuraxial
122
Q

Platelet count parameters for removing an epidural

A

Platelet count ≥ 75,000 - 80,000/mm3

123
Q

What drugs are used to manage hypotension secondary to labor analgesia?

A
  • Phenylephrine 25-50 mcg
  • Ephedrine 5-10 mg

Potential increased sensitivity to vasopressors

124
Q

GETA concerns for cesarean delivery

A
  • Potential difficulty with airway management
  • Risk of severe hypertension with tracheal intubation & emergence/extubation
  • Risk of cerebral hemorrhage & pulmonary edema
  • Magnesium sulfate effects on neuromuscular transmission
125
Q

For a GETA, BP needs to be reduced to around __________ mmHg before induction

A

140/90

126
Q

During laryngoscopy/intubation, maintain SBP between ___________ mmHg (range) and DBP between ___________ (range)

A
  • SBP: 140-160 mmHg
  • DBP: 90-100 mmHg
127
Q

Medication for HTN during a GETA Cesarean Delivery

A
  • Labetalol or Esmolol 2 mg/kg
  • Remifentanil 0.5 mcg/kg
  • Magnesium sulfate 30-40 mg/kg given after induction agent
128
Q

If HTN continues > 24 hrs postpartum, consider discontinuing this drug as it could be a potential contribution to HTN.

A

NSAIDs

129
Q

Preeclampsia usually resolves within ___ days postpartum

A

5 days

Marked Diuresis (mobilization of extracellular fluid, increase intravascular volume)
Risk of Pulmary Edema is the greatest

130
Q

When should antihypertensives be given postpartum?

A
  • SBP > 150 mmHg
  • DBP > 100 mmHg

Risk of CVA highest postpartum

131
Q

How is eclampsia defined?

A

New onset seizures / unexplained coma in pregnancy or postpartum in the presence of signs/sx of preeclampsia

132
Q

When is the most common onset of eclampsia?

A
  • Intrapartum
  • Within 48 hours postpartum
133
Q

Late eclampsia will have a seizure onset between _______ hours and _______ weeks postpartum

A

48 hours to 4 weeks postpartum

134
Q

Complications of Eclampsia

A
  • Aspiration
  • Pulmonary edema
  • CVA
  • VTE
  • Acute renal failure
  • Death
  • Placental abruption
  • Severe IUGR
  • Extreme prematurity
135
Q

Clinical Presentation of Eclampsia

A
  • Premonitory neuro sx in most of the parturients (HA, visual disturbances)
  • RUQ/ epigastric pain
  • Hyperreflexia
  • Abrupt onset of seizures (facial twitch → tonic phase 15-20 seconds)
136
Q

Patho of Eclampsia

A
  • Mechanism not fully understood
  • Loss of normal cerebral autoregulatory mechanism
  • Hyperperfusion → interstitial or vasogenic cerebral edema → decreased cerebral blood flow
  • Possibly manifestation of PRES

PRES: posterior reversible encephalopathy syndrome

137
Q

When does fetal bradycardia begin during eclampsia?

A

Fetal bradycardia begins during or immediately post-seizure.

Not a requirement for delviery unless prolonged

138
Q

Management of Eclampsia

A
  • Stop seizures
  • Maintain patent airway
  • Prevent complications (Hypoxemia, Aspiration)
  • Mag bolus & infusion to prevent more seizures
  • midazolam / diazepam to raise seizure threshold if recurrent
  • Manage increased intracranial pressure (propofol)
139
Q

Anesthetic management of eclampsia

A
  • Similar to parturient w/ preeclampsia w/ severe features
  • If in coma or posturing, decrease ICP
  • Restrict fluids to decrease the risk of exacerbating cerebral edema
  • Maintain SBP < 160 and DBP < 110
  • Labs, order coags
  • Avoid hypoxemia, hyperthermia, hyperglycemia
140
Q

Benefits of Propofol for eclampsia parturients

A

Decrease CMRO2 and CBF → Decrease ICP

141
Q

Why not hyperventilate to reduce ICP in eclampsia patients?

A

Hyperventilation will decrease CBF w/o change in CMRO2

142
Q

Why would you want to avoid hypoventilation in eclampsia patients?

A
  • Hypoventilation lowers the seizure threshold
  • Hypoventiation also increases ICP
143
Q

What is amniotic fluid embolism (AFE)?

A
  • Systemic inflammatory response resulting from the release of endogenous proinflammatory mediators (Arachidonic acid metabolites)
  • Amniotic fluid enters the mother’s bloodstream
144
Q

Describe Phase I of Amniotic Fluid Embolism

A
  • Proinflammatory mediators will cause transient period of pulmonary and systemic HTN
  • Acute pulmonary HTN → RV failure & dilation
  • Intraventricular septum deviates into LV
  • Decreased CO & V/Q mismatch → O2 desaturation
  • Release of endogenous catecholamines → brief systemic HTN & uterine tachysystole
145
Q

Describe Phase II of Amniotic Fluid Embolism

A
  • Phase II occurs 15 – 30 mins after initial event
  • Impingement of septum on LV → decreased CO
  • RV function improves, but LV failure predominates
  • Related to ischemic injury or direct myocardial depression
  • Decreased SVR
  • Decreased LV stroke index
  • Pulmonary edema
  • Cardiac arrest
146
Q

Describe Phase III of Amniotic Fluid Embolism

A
  • Phase III – may occur with CV collapse or after Coagulopathy
  • Tissue factor binds factor VII → activates extrinsic pathway
  • Triggers clotting by activating factor X → consumptive coagulopathy develops
  • Thromboplastin like-effect → platelet aggregation
  • Release of platelet factor III
  • Activates clotting cascade
147
Q

What labs are ordered for AFE?

A
  • Anemia & thrombocytopenia
  • Prolonged PT/PTT and decreased fibrinogen levels
  • Elevated fibrin split products
148
Q

AFE Phase 1 Management

A
  • Further RV failure results from increased pulmonary vascular resistance from hypoxia, hypercapnia, and acidosis
  • Consider dobutamine & milrinone to improve RV output
  • Inhaled NO, IV or inhaled prostacyclin, or sildenafil to improve vascular resistance
  • Hypotension → norepinephrine / vasopressin
149
Q

AFE Phase 2 Management

A
  • Avoid excess fluid administration → further dilates RV
  • Increase risk of MI & pulmonary edema
  • Improve LV contractility with dobutamine & milrinone
  • Maintain coronary perfusion pressure with vasopressors

Phase 2 = Left Ventricular Failure Stage

150
Q

AFE Phase 3 Management

A
  • Early assessment of clotting status
  • Activate massive transfusion protocol
  • Maintain platelet count > 50,000/mm3 & normal aPTT & INR
  • Tranexamic Acid (TXA)
  • Recombinant activated factor VII may be used but may have concern of excessive diffuse thrombosis & multiorgan failure
151
Q

What is the classic triad of AFE?

A
  • Hypoxia
  • Hypotension
  • Coagulopathy
152
Q

Presentation of AFE

A
  • Diagnosis based on clinical observations
  • Classic triad of hypoxia, hypotension, and coagulopathy
  • Anxiety, restlessness, confusion, sense of impending doom
  • Sudden onset dyspnea, decreased SpO2 → respiratory arrest
  • Severe hypotension, cardiac dysrhythmias → cardiac collapse & cardiac arrest
153
Q

AFE presentation on the fetal side

A
  • O2 rich blood shunted from uterus
  • Results in Decels / sustained bradycardia and loss of variability
  • Catecholamine induced uterine hypertonus
  • Continued decline in uterine perfusion
154
Q

AFE Treatment

A
  • OB ACLS – left uterine displacement if not delivered
  • Emergent delivery of fetus ≤ 5 mins after CV arrest improve maternal outcome & neonatal viability
  • Cardiopulmonary bypass / ECMO
155
Q

Anesthesia Management of AFE

A
  • Secure Airway
  • AOK (Atropine, Ondansetron, Ketorolac)
  • Anticipate massive hemorrhage
  • Activate MTP
  • Get Help
156
Q

Why is atropine used in AFE?

A
  • Atropine – vagolysis
  • Decreases vasoconstriction in pulmonary vasculature
  • Decreases incidence of bradycardia & heart blocks
157
Q

Why is ondansetron used in AFE?

A
  • Ondansetron contributes to vagotomy via 5-HT3 antagonism
  • Prevents CV collapse
158
Q

What is ketorolac used in AFE?

A
  • Ketorolac – block thromboxane production
  • Inhibits the formation of clots & the extension of clots in situ
  • Decreases cascade of inappropriate clotting
159
Q

AFE Flow Chart

A

Mar: Sem 6 - Adv. Principles B (14 decks)

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