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
2
Q
What is the biggest presentation as a result of Umbilical Cord Prolapse
A
Fetal Bradycardia
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
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
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
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).
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
8
Q
What type of placenta will have the lowest risk for twin-to-twin transfusion syndrome?
A
Dichorionic placenta
9
Q
What type of placenta will have the highest risk for twin-to-twin transfusion syndrome?
A
Monochorionic placenta
10
Q
Name the type of placentation
A
Monochorionic Monoamniotic
11
Q
Name the type of placentation
A
Dichoriontic Diamniotic (fused placenta)
12
Q
Name the type of placentation
A
Monochorionic Diamniotic
13
Q
Name the type of placentation
A
Dichoriontic Diamniotic (separate placenta)
14
Q
What will be the type of placentation for dizygotic twins?
A
- Dichorionic Diamniotic
- Can have either a fused or separate placenta
15
Q
What two systems will experience the greatest physiological change during pregnancy?
A
- Cardiovascular
- Pulmonary
16
Q
Cardiac Output during pregnancy increases by ______%.
A
- 20% ↑ in CO d/t ↑ SV
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
18
Q
During pregnancy, maternal weight gain increased faster after ____ weeks
A
30 weeks
19
Q
What direction does the stomach displace during pregnancy?
A
Cephalad
20
Q
A stomach displaced cephalad will _________ competence of LES and _________ aspiration risk.
A
- Decrease competence of LES
- Increase aspiration risk
21
Q
Maternal blood volume = _________ mL/kg
A
105 mL/kg
22
Q
How much does plasma volume increase during pregnancy?
A
750 mL
23
Q
Delivery EBL approximation
A
about 500 mL
24
Q
What complications will most monochorionic twins experience?
A
- Vascular Anatomoses
- ↑ Risk twin-to-twin transfusion
25
More than 50% of multiple gestation moms deliver before _______ weeks gestation.
Before 37 weeks
26
Twins are usually induced around __________ weeks
38 weeks
27
Triplets are usually induced around __________ weeks
35 weeks
28
Increased fetal weight & larger volume of amniotic fluid increase the risk of _________ compression & supine _________ syndrome.
* Aortocaval
* Hypotension
29
Multiple gestations can lead to uterine distention → Increase risk of ________ and ____________
* PPH
* Uterine atony
## Footnote
have Methergine and Hemabate on standby
30
Anesthesia management for Multiple Gestations
* 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
31
What is the most common pregnancy-related disorder?
Pregnancy Induced Hypertension (PIH)
32
What is the most widely accepted definition/ parameters for PIH?
* BP elevated > 139/89 mmHg x 2
* After 20 weeks gestation
* Most cases develop after 37 weeks gestation
* Without proteinuria
33
What percentage of PIH patients will develop preeclampsia?
25%
34
When will PIH resolve?
12 weeks postpartum
35
Define preecmapsia
* New Onset of HTN (>140/90) after 20 weeks
* Renal insufficiency & proteinuria (>300 mg/day)
* Creatinine >0.3
* 1+ on urine dipstick specimen
36
Alternative Symptoms of Preeclampsia
* Persistent epigastric / right upper quadrant pain
* Persistent cerebral symptoms (blurry vision/ floaters)
* IUGR
* Thrombocytopenia / elevated liver enzymes
37
Parameters for Preeclampsia w/ severe features
* 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
38
What percentage of mothers who have chronic hypertension develop preeclampsia?
20-25%
39
**Chronic Hypertension**
Time of Onset:
Severity:
Proteinuria:
Serum Uric Acid > 5.5 mg/dL:
Hemoconcentration:
Thrombocytopenia:
Hepatic dysfunction:
**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
40
**Gestational Hypertension**
Time of Onset:
Severity:
Proteinuria:
Serum Uric Acid > 5.5 mg/dL:
Hemoconcentration:
Thrombocytopenia:
Hepatic dysfunction:
**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
41
**Preecampsia**
Time of Onset:
Severity:
Proteinuria:
Serum Uric Acid > 5.5 mg/dL:
Hemoconcentration:
Thrombocytopenia:
Hepatic dysfunction:
**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
42
Preeclampsia is a multisystem disease that includes placenta. No _______ is required to develop preeclampsia.
Fetus (molar pregnancy)
43
Preeclampsia can result in abnormal ___________ implantation.
placental
44
Impaired remodeling of spiral arteries as a result of preeclampsia will have what impact on the fetus?
Small & constricted blood vessels affect O2 & nutrient delivery to the fetus
45
How does preeclampsia cause diffuse endothelial dysfunction?
Injury from antiangiogenic proteins released by placenta
46
How does preeclampsia affect nitric oxide and prostacyclin?
* Decrease Nitric Oxide
* Decrease Prostacyclin
47
How does preeclampsia affect the sensitivity of angiotensin II?
Sensitivity to angiotensin II increases
48
How does preeclampsia affect oncotic pressure?
Preeclampsia → Hypoalbuminemia → Low Oncotic pressure (results in intravascular volume depletion and 3rd spacing)
49
What is considered early onset of preeclampsia?
* Before 34 weeks gestation
* Worse outcomes (usually results in C-section)
50
What is considered late onset of preeclampsia?
* After 34 weeks
* Typically already metabolically predisposed to preeclampsia (existing DM, HTN, obesity)
51
When can postpartum preeclampsia occur?
Presentation?
* Within seven days postpartum
* Proteinuria and Seizures
52
Prophylactic treatment for Preeclampsia
* Initiate Aspirin 16 weeks or earlier for the best benefit
* Aspirin will inhibit the synthesis of prostaglandins and biosynthesis of platelet thromboxane A2
53
Preeclampsia predictors of unfavorable outcomes
* Early onset
* Chest pain / dyspnea
* Low SpO2
* Thrombocytopenia
* Elevated creatinine
* Increased AST concentration
54
CNS presentation of Preeclampsia
* Severe headache
* Hyperexcitability (giddy)
* Hyperreflexia
* Coma
55
Visual changes involved with preeclampsia.
* Scotoma (Blind Spot)
* Amaurosis (Painless vision loss)
* Blurred vision
56
How does preeclampsia affect cerebral vascular autoregulation?
Loss of cerebral vascular autoregulation → hyperperfusion → cerebral edema
## Footnote
Most common in posterior circulation resulting in Posterior reversible encephalopathy syndrome (PRES)
57
Clinical presentation of preeclampsia from an airway standpoint.
* Normal pregnancy will result in capillary engorgement and decreased tracheal diameter
* Preeclampsia → Pharyngo-laryngeal edema
* Preeclampsia → Upper airway diameter decreased
* Preeclampsia → Subglottic edema
58
Clinical presentation of preeclampsia from a CV standpoint.
* Increased vascular tone
* Increased sensitivity to vasoconstrictors & catecholamines
* Severe vasospasm
* Exaggerated hemodynamic response to catecholamines (ephedrine)
59
In severe preeclampsia, plasma volume can be decrease up to _________ %
Decrease 40%
60
How does Pre-eclampsia affect CO, SVR, and Left Ventricular Function?
* CO will be normal to increase in the absence of pulmonary edema
* Mild to moderately increased SVR w/ diastolic dysfunction
* Hyperdynamic left ventricular function
61
What percentage of patients with preeclampsia develop pulmonary edema?
3%
62
What factors will increase the risk of pulmonary edema in preeclamptic patients?
* Advanced maternal age
* Preeclampsia superimposed on chronic HTN or
* Renal disease
63
How does pulmonary edema develop in preeclamptic patients?
* Plasma colloid osmotic pressure is greatly reduced
* Results in increased pulmonary capillary permeability
* Leads to increased intravascular hydrostatic pressure
* Increase risk for pulmonary pressure
64
Clinical presentation of preeclampsia from a hematologic standpoint.
* Thrombocytopenia is the most common hematologic abnormality
* PLT <100,000/mm3 associated with increased disease severity or HELLP syndrome
* ↑ risk of DIC
## Footnote
HELLP: Hemolysis, Elevated Liver enzyme levels, and Low Platelet levels.
65
Coagulation state in a normal pregnancy
Hypercoagulable d/t a physiologically adaptive mechanism to prevent postpartum hemorrhage.
66
What happens to the coagulation state in severe preeclampsia?
* Relatively hypercoagulable
* Platelets will activate and then degranulate, resulting in decreased platelet function
* Decrease platelet count
67
DIC can be present during these complications.
* Severe liver involvement (pre-existing liver dz)
* intrauterine fetal death (IUFD)
* Placental abruption
* PPH
68
Pathophysiology of DIC
* 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
Clinical presentation of preeclampsia from a hepatic standpoint.
* Periportal hemorrhage
* Fibrin deposition in hepatic sinusoids
* Presents as RUQ or epigastric pain
* Risk of spontaneous hepatic rupture
70
Clinical presentation of preeclampsia from a renal standpoint.
* 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
Preeclampsia H/H Labs
* 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
What lab will require further coagulation tests for preeclamptic patients?
* Plt less than 100K
* assess PT and aPTT
* Often times there will be a decrease in fibrinogen concentration
73
Type & crossmatch for at least _____ PRBCs in thrombocytopenia or coagulation abnormalities
2 units
74
Proteinuria = Preeclampsia NOT _____________
PIH (gestational HTN)
75
When will antihypertensives be used to manage acute hypertension?
* SBP > or = 160 mmHg
* DBP > or = 110 mmHg
76
Acute HTN Management decrease BP by __________%
Goal SBP:
Goal DBP:
* Slow BP decreased by 15-25%
* Goal SBP: 120-160 mmHg
* Goal DBP: 80-105 mmHg
## Footnote
Rapid & drastic changes may negatively impact uteroplacental perfusion & O2 delivery to fetus
77
Labetalol IV
Onset:
Dose:
Max Dose:
Labetalol IV
Onset: 5-10 mins
Dose: 20 mg IV → 40-80 mg IV q 10 mins
Max Dose: 220 mg IV
## Footnote
Realistically give 5-10 mg initially and see where to go from there
78
Hydralazine IV
Onset:
Dose:
Max Dose:
Hydralazine IV
Onset: 10-20 mins
Dose: 5 mg IV q 20 mins
Max Dose: 20 mg
79
Nifedipine PO
Onset:
Dose:
Max Dose:
Nifedipine PO
Onset: 10-20 mins
Dose: 10 mg q 20 mins
Max Dose: 50 mg
80
Nicardipine IV infusion
Onset:
Dose:
Max Dose:
Nicardipine IV infusion
Onset: 10-15 mins
Dose: 5 mg/hr, ↑ 2.5 mg/hr q 5 mins
Max Dose: 15 mg/hr
81
What medication is used for seizure prophylaxis in preeclamptic patients?
* Magnesium Sulfate
* Primarily used in parturients w/ severe features
82
What are the pros and cons of using magnesium sulfate in parturients?
* 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
Side effects of magnesium sulfate
* Warm/flushed feeling
* N/V
* Headache
* Muscle weakness / drowsiness / confusion
* Hypotension / dizziness
84
Fetal effects from magnesium sulfate
* Decreased fetal HR, but Remains > 110 bpm
* Decreased variability
85
MOA of Magnesium Sulfate
* 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
Magnesium Sulfate Dosing for Preeclampsia and Eclampsia
Loading Dose: 4-6 gm over 20-30 mins
Infusion: 1-2 gm/hr
87
Magnesium Sulfate Dosing for Recurrent Eclampsia
Loading Dose: 2 gm over 5 mins
Infusion: 1-2 gm/hr
88
Magnesium limits the release of ________ at the NMJ
Acetylcholine
89
Magnesium _________ (increases or decreases) sensitivity of NMJ to acetylcholine.
Decreases
90
What does magnesium do to muscle fiber membrane?
Depresses excitability
91
Effect of magnesium on depolarizing and NDMR?
* Potentiate its action
* Use a smaller dose and monitor peripheral nerve stimulator
92
Effect of magnesium on neuraxial administered local anesthetic.
* Increases the potency of local anesthetic
* Risk of hypotension increases
93
What is the therapeutic range of magnesium sulfate?
5-9 mg/dL
94
How is magnesium eliminated in the body?
Renal Excretion
95
Individuals with renal insufficiency/failure will have a Serum Cr > ________ and will tend to have higher serum magnesium levels.
1.2 mg/dL
96
Hypermagnesemia S/E
* Chest pain / tightness
* Palpitations
* Nausea
* Blurred vision
* Sedation
* Transient hypotension
97
At what magnesium serum level will a patient lose deep tendon (patellar) reflexes?
12 mg/dL
98
At what magnesium serum level will a patient experience respiratory depression?
15-20 mg/dL
99
At what magnesium serum level will a patient have a cardiac arrest (asystole)?
Greater than 25 mg/dL
100
What is the normal serum magnesium level?
1.7 – 2.4 mg/dL
101
What is the treatment of magnesium toxicity?
* Calcium gluconate 1 gm over 3 - 10 minutes
* Calcium chloride 10% 500 mg over 5 – 10 minutes
102
What is the most common complication CNS feature from preeclampsia?
Reversible Cerebral Edema
103
What is the leading cause of death in preeclampsia?
CVA
| Hemorrhage more common than embolic CVA secondary to preeclampsia
104
When does most hemorrhagic stroke occur during pregnancy?
Postpartum
105
What percentage of parturients experience abruption secondary to preeclampsia?
2%
## Footnote
Incidence greater with chronic HTN
Abruption will lead to a greater risk of DIC
106
HELLP Syndrome is a complication of preeclampsia. What do the acronyms stand for?
* Hemolysis
* Elevated levels of liver enzymes
* Low platelet count
## Footnote
HELLP can be present w/o HTN or proteinuria.
107
HELLP Syndrome increases the risk of these complications.
* DIC
* Placental abruption
* Pulmonary edema
* Acute renal failure
* Liver hemorrhage/failure
* ARDS
* Sepsis
* Stroke
* Death
108
Define Hemolysis
Destruction or breakdown of red blood cells, leading to the release of hemoglobin into the surrounding fluid (such as blood plasma).
## Footnote
Presence of Microangiopathic Hemolytic Anemia
109
What symptoms may be present in a parturient if they are experiencing hemolysis?
* RUQ or epigastric pain
* N/V
* Headache
* HTN
* Proteinuria
110
Bilirubin levels in HELLP Syndrome
Bilirubin > 1.2 mg/dL
111
Liver Enzyme levels in HELLP Syndrome
Increase AST > or = 70 IU/L
Increase LDH > 600 IU/L
112
Plt levels in HELLP Syndrome
Plt count < 100K, but can decrease precipitously
113
If a parturient has HELLP Syndrome, when will their plt count reach nadir?
Reaches nadir 2-3 days postpartum
114
Which steroid can improve plt count?
Dexamethasone
115
Plt count below this level during a C-section will covert to a GETA
less than 50K
116
When will plt be transfused in a parturient?
* Transfuse if plt count < 20,000
* Transfuse if plt count < 40,000 & c-section planned
## Footnote
Hospital facility dependent
117
Management for HELLP Syndrome
* Delivery
* Corticosteroid administration to improve fetal lung maturity
* Magnesium sulfate for seizure prophylaxis
* Antihypertensives
118
What are the indications for inserting an A-line for a parturient?
* 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
What are the indications for inserting a central venous catheter/ pulmonary arterial catheter for a parturient?
* In the setting of multiple organ failure
* Underlying congenital/valvular heart disease
* Critical cardiovascular instability
120
Things to consider before placement of labor analgesia
* Coagulation status
* IV hydration injecting local anesthetics
* Management of resultant hypotension
* Use of epinephrine containing local anesthetics
121
Neuraxial placement & platelet count parameters
* > 80,000/mm3 – no concerns
* 50,000-80,000/mm3 – weigh benefits/risks/alternatives
* < 50,000/mm3 – no neuraxial
122
Platelet count parameters for removing an epidural
Platelet count ≥ 75,000 - 80,000/mm3
123
What drugs are used to manage hypotension secondary to labor analgesia?
* Phenylephrine 25-50 mcg
* Ephedrine 5-10 mg
## Footnote
Potential increased sensitivity to vasopressors
124
GETA concerns for cesarean delivery
* 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
For a GETA, BP needs to be reduced to around __________ mmHg before induction
140/90
126
During laryngoscopy/intubation, maintain SBP between ___________ mmHg (range) and DBP between ___________ (range)
* SBP: 140-160 mmHg
* DBP: 90-100 mmHg
127
Medication for HTN during a GETA Cesarean Delivery
* Labetalol or Esmolol 2 mg/kg
* Remifentanil 0.5 mcg/kg
* Magnesium sulfate 30-40 mg/kg given after induction agent
128
If HTN continues > 24 hrs postpartum, consider discontinuing this drug as it could be a potential contribution to HTN.
NSAIDs
129
Preeclampsia usually resolves within ___ days postpartum
5 days
## Footnote
Marked Diuresis (mobilization of extracellular fluid, increase intravascular volume)
Risk of Pulmary Edema is the greatest
130
When should antihypertensives be given postpartum?
* SBP > 150 mmHg
* DBP > 100 mmHg
## Footnote
Risk of CVA highest postpartum
131
How is eclampsia defined?
New onset seizures / unexplained coma in pregnancy or postpartum in the presence of signs/sx of preeclampsia
132
When is the most common onset of eclampsia?
* Intrapartum
* Within 48 hours postpartum
133
Late eclampsia will have a seizure onset between _______ hours and _______ weeks postpartum
48 hours to 4 weeks postpartum
134
Complications of Eclampsia
* Aspiration
* Pulmonary edema
* CVA
* VTE
* Acute renal failure
* Death
* Placental abruption
* Severe IUGR
* Extreme prematurity
135
Clinical Presentation of Eclampsia
* 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
Patho of Eclampsia
* Mechanism not fully understood
* Loss of normal cerebral autoregulatory mechanism
* Hyperperfusion → interstitial or vasogenic cerebral edema → decreased cerebral blood flow
* Possibly manifestation of PRES
## Footnote
PRES: posterior reversible encephalopathy syndrome
137
When does fetal bradycardia begin during eclampsia?
Fetal bradycardia begins during or immediately post-seizure.
## Footnote
Not a requirement for delviery unless prolonged
138
Management of Eclampsia
* 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
Anesthetic management of eclampsia
* 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
Benefits of Propofol for eclampsia parturients
Decrease CMRO2 and CBF → Decrease ICP
141
Why not hyperventilate to reduce ICP in eclampsia patients?
Hyperventilation will decrease CBF w/o change in CMRO2
142
Why would you want to avoid hypoventilation in eclampsia patients?
* Hypoventilation lowers the seizure threshold
* Hypoventiation also increases ICP
143
What is amniotic fluid embolism (AFE)?
* Systemic inflammatory response resulting from the release of endogenous proinflammatory mediators (Arachidonic acid metabolites)
* Amniotic fluid enters the mother's bloodstream
144
Describe Phase I of Amniotic Fluid Embolism
* 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
Describe Phase II of Amniotic Fluid Embolism
* 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
Describe Phase III of Amniotic Fluid Embolism
* 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
What labs are ordered for AFE?
* Anemia & thrombocytopenia
* Prolonged PT/PTT and decreased fibrinogen levels
* Elevated fibrin split products
148
AFE Phase 1 Management
* 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
AFE Phase 2 Management
* 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
## Footnote
Phase 2 = Left Ventricular Failure Stage
150
AFE Phase 3 Management
* 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
What is the classic triad of AFE?
* Hypoxia
* Hypotension
* Coagulopathy
152
Presentation of AFE
* 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
AFE presentation on the fetal side
* 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
AFE Treatment
* 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
Anesthesia Management of AFE
* Secure Airway
* AOK (Atropine, Ondansetron, Ketorolac)
* Anticipate massive hemorrhage
* Activate MTP
* Get Help
156
Why is atropine used in AFE?
* Atropine – vagolysis
* Decreases vasoconstriction in pulmonary vasculature
* Decreases incidence of bradycardia & heart blocks
157
Why is ondansetron used in AFE?
* Ondansetron contributes to vagotomy via 5-HT3 antagonism
* Prevents CV collapse
158
What is ketorolac used in AFE?
* Ketorolac – block thromboxane production
* Inhibits the formation of clots & the extension of clots in situ
* Decreases cascade of inappropriate clotting
159
AFE Flow Chart
