Exam 1: Complicated OB Part 2 Flashcards
(163 cards)
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
can do lidocaine or chloroprocaine boluses in the epidural as a backup if needed
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).
unknown how/why this happens - anacdotal twins, but not really a huge genetic component
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
Multiple gestation placental presentation
A
type of placentation determines probable presence of vascular communications
9
Q
What type of placenta will have the lowest risk for twin-to-twin transfusion syndrome?
A
Dichorionic placenta
10
Q
What type of placenta will have the highest risk for twin-to-twin transfusion syndrome?
A
Monochorionic placenta
11
Q
Name the type of placentation
A
Monochorionic Monoamniotic
12
Q
Name the type of placentation
A
Dichoriontic Diamniotic (fused placenta)
13
Q
Name the type of placentation
A
Monochorionic Diamniotic
14
Q
Name the type of placentation
A
Dichoriontic Diamniotic (separate placenta)
More in line with normal birth structure
15
Q
What will be the type of placentation for dizygotic twins?
A
- Dichorionic Diamniotic
- Can have either a fused or separate placenta
100% of the time, dizygotic twins will be diamniotic diamniotic
16
Q
What two systems will experience the greatest physiological change during pregnancy?
A
- Cardiovascular
- Pulmonary
17
Q
Cardiac Output during pregnancy increases by ____%.
A
- 20% ↑ in CO d/t ↑ SV
18
Q
What lung volumes decrease near-term gestation d/t uterine size?
A
- ↓ TLC
- ↓ FRC
The decrease lung volumes will increase risk of hypoxemia (especially with more gestations and multpile babies in the uterus)
19
Q
During pregnancy, maternal weight gain increased faster after ____ weeks
A
30 weeks
20
Q
What direction does the stomach displace during pregnancy?
A
Cephalad
21
Q
A stomach displaced cephalad will ____ competence of LES and ____ aspiration risk.
A
- Decrease competence of LES
- Increase aspiration risk
22
Q
Maternal blood volume = ____ mL/kg (during multiple gestation)
A
105 mL/kg
Corn says 100-110 mL/kg
23
Q
How much does plasma volume increase during multiple gestation pregnancy?
A
750 mL
24
Q
Delivery EBL approximation for multi gestation
A
about 500 mL greater than a single gestation
25
What complications will most monochorionic twins experience?
* Vascular Anatomoses
* ↑ Risk twin-to-twin transfusion
## Footnote
From deep AV vascular commications
26
Complications from the donor and recepient twin AV vascular communications
Donor: Smaller twin - complications, risk of IUGR and anemia
Recipient: plethoric, risk of volume overload and cardiac failure (RV)
27
More than 50% of multiple gestation moms deliver before ____ weeks gestation.
Before 37 weeks
28
Twins are usually induced around __________ weeks
38 weeks
29
Triplets are usually induced around __________ weeks
35 weeks
30
Increased fetal weight & larger volume of amniotic fluid increase the risk of ____ compression & supine ____ syndrome.
* Aortocaval
* Hypotension
31
Multiple gestations can lead to uterine distention → Increase risk of ____ and ____
* PPH
* Uterine atony
## Footnote
have Methergine and Hemabate on standby
32
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
33
What is the most common pregnancy-related disorder?
Pregnancy Induced Hypertension (PIH)
34
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
## Footnote
Proteinuria differentiates PIH and eclampsia
35
What percentage of PIH patients will develop preeclampsia?
25%
36
When will PIH resolve?
12 weeks postpartum
37
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**
38
Alternative Symptoms of Preeclampsia
* Persistent epigastric / right upper quadrant pain (but there also is an increased instance of cholecystitis in preggers)
* Persistent cerebral symptoms (blurry vision/ floaters/seizures)
* IUGR
* Thrombocytopenia / elevated liver enzymes
39
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
40
What percentage of mothers who have chronic hypertension develop preeclampsia?
20-25%
41
**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
42
**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
43
**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
44
Preeclampsia is a multisystem disease that includes placenta. No ____ is required to develop preeclampsia.
Fetus (molar pregnancy)
## Footnote
you can have preeclampsia after delivery and with a molar pregnancy too
45
Preeclampsia can result in abnormal ___________ implantation.
placental
46
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
47
How does preeclampsia cause diffuse endothelial dysfunction?
Injury from antiangiogenic proteins released by placenta
48
How does preeclampsia affect nitric oxide and prostacyclin?
* Decrease Nitric Oxide
* Decrease Prostacyclin
49
How does preeclampsia affect the sensitivity of angiotensin II?
Sensitivity to angiotensin II increases
## Footnote
Tiny tortourous vessels becoming vasoconstricted (worsening placental insufficiency)
50
How does preeclampsia affect oncotic pressure?
Preeclampsia → Hypoalbuminemia → Low Oncotic pressure (results in intravascular volume depletion and 3rd spacing)
**very low albumin levels**
- intravascuilar volume depletion and 3rd spacing of fluids
51
What is considered early onset of preeclampsia?
* Before 34 weeks gestation
* Worse outcomes (usually results in C-section)
## Footnote
Usually are admited to the anti-partum floor and likelyb will stay there for some time (or go on bed rest) - or until delivery
52
What is considered late onset of preeclampsia?
* After 34 weeks
* Typically already metabolically predisposed to preeclampsia (existing DM, HTN, obesity)
53
When can postpartum preeclampsia occur?
Presentation?
* Within seven days postpartum
* Proteinuria and Seizures
54
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
55
Preeclampsia predictors of unfavorable outcomes
* Early onset
* Chest pain / dyspnea
* Low SpO2
* Thrombocytopenia
* Elevated creatinine
* Increased AST concentration
56
CNS presentation of Preeclampsia
* Severe headache
* Hyperexcitability (giddy)
* Hyperreflexia (try to get baseline DTR)
* Coma
Sergio Excites Really Commonly
## Footnote
this is the progression
57
Visual changes involved with preeclampsia.
* Scotoma (Blind Spot)
* Amaurosis (Painless vision loss)
* Blurred vision (most common)
58
How does preeclampsia affect cerebral vascular autoregulation?
Loss of cerebral vascular autoregulation (vascular barotrauma) → hyperperfusion → cerebral edema
**Most common in posterior circulation resulting in Posterior reversible encephalopathy syndrome (PRES)**
- accumulation of all the s/s they are presenting with (manage the volume status and keep the BP within the normal autoregulation curve and you will be fine)
59
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
## Footnote
Cut ETT size down .5 to 1 size down
60
Clinical presentation of preeclampsia from a CV standpoint.
* Increased vascular tone
* **Increased sensitivity to vasoconstrictors & catecholamines** ( a little goes a long way, give less ephedrine or neo at first)
* but if they are on mag drip, there is a decreased response, pay attention to where they are treatment-wise
* Severe vasospasm
* Exaggerated hemodynamic response to catecholamines (ephedrine)
61
In severe preeclampsia, plasma volume can be decrease up to ____%
Decrease 40%
## Footnote
Its not gone from the body, but the majority of the 3rd space fluid is plasma
62
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
63
What percentage of patients with preeclampsia develop pulmonary edema?
3%
64
What factors will increase the risk of pulmonary edema in preeclamptic patients?
* Advanced maternal age
* Preeclampsia superimposed on chronic HTN or
* Renal disease
65
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
66
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.
67
Coagulation state in a normal pregnancy
Hypercoagulable d/t a physiologically adaptive mechanism to prevent postpartum hemorrhage.
68
What happens to the coagulation state in severe preeclampsia?
* Relatively hypocoagulable
* Platelets will activate and then degranulate, resulting in decreased platelet function
* Decrease platelet count
69
DIC can be present during these complications.
* Severe liver involvement (pre-existing liver dz)
* intrauterine fetal death (IUFD)
* Placental abruption
* PPH
70
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
71
Clinical presentation of preeclampsia from a hepatic standpoint.
* Periportal hemorrhage
* Fibrin deposition in hepatic sinusoids resulting in impaired circulation
* Presents as RUQ or epigastric pain
* Risk of spontaneous hepatic rupture
72
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
* BUN and creatinine stay in normal range if its not a severe case
* Hyperuricemia d/t decrease renal clearance of uric acid
* Oliguria (low urine output)
73
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
74
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
## Footnote
Lots of labs are "sent-out" labs, but don't sleep on POC testing like a TEG or ROTEM that can help you decide what they need
75
Type & crossmatch for at least ____ PRBCs in thrombocytopenia or coagulation abnormalities
2 units
76
Proteinuria = Preeclampsia NOT ____
PIH (gestational HTN)
77
When will antihypertensives be used to manage acute hypertension?
* SBP > or = 160 mmHg
* DBP > or = 110 mmHg
78
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 (remember no autoregulation in the uterus)
79
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
80
Hydralazine IV
Onset:
Dose:
Max Dose:
Hydralazine IV
Onset: 10-20 mins
Dose: 5 mg IV q 20 mins
Max Dose: 20 mg
81
Nifedipine PO
Onset:
Dose:
Max Dose:
Nifedipine PO
Onset: 10-20 mins
Dose: 10 mg q 20 mins
Max Dose: 50 mg
82
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
83
What medication is used for seizure prophylaxis in preeclamptic patients?
* Magnesium Sulfate
* Primarily used in parturients w/ severe features
84
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
85
Side effects of magnesium sulfate
* Warm/flushed feeling
* N/V
* Headache
* Muscle weakness / drowsiness / confusion
* Hypotension / dizziness
86
Fetal effects from magnesium sulfate
* Decreased fetal HR, but Remains > 110 bpm
* Decreased variability (this is good)
87
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
88
Magnesium Sulfate Dosing for Preeclampsia and Eclampsia
Loading Dose: 4-6 gm over 20-30 mins
Infusion: 1-2 gm/hr
89
Magnesium Sulfate Dosing for Recurrent Eclampsia
Loading Dose: 2 gm over 5 mins
Infusion: 1-2 gm/hr
90
Magnesium limits the release of ________ at the NMJ
Acetylcholine
91
Magnesium ____ (increases or decreases) sensitivity of NMJ to acetylcholine.
Decreases
92
What does magnesium do to muscle fiber membrane?
Depresses excitability
93
Effect of magnesium on depolarizing and NDMR?
* Potentiate its action
* Use a smaller dose and monitor peripheral nerve stimulator
94
Effect of magnesium on neuraxial administered local anesthetic.
* Increases the potency of local anesthetic
* Risk of hypotension increases
95
What is the therapeutic range of magnesium sulfate?
5-9 mg/dL
96
How is magnesium eliminated in the body?
Renal Excretion
97
Individuals with renal insufficiency/failure will have a Serum Cr > ____ and will tend to have higher serum magnesium levels.
1.2 mg/dL
98
Hypermagnesemia S/E
* Chest pain / tightness
* Palpitations
* Nausea
* Blurred vision
* Sedation
* Transient hypotension
99
At what magnesium serum level will a patient lose deep tendon (patellar) reflexes?
12 mg/dL
100
At what magnesium serum level will a patient experience respiratory depression?
15-20 mg/dL
101
At what magnesium serum level will a patient have a cardiac arrest (asystole)?
Greater than 25 mg/dL
102
What is the normal serum magnesium level?
1.7 – 2.4 mg/dL
103
What is the treatment of magnesium toxicity?
* Calcium gluconate 1 gm over 3 - 10 minutes
* Calcium chloride 10% 500 mg over 5 – 10 minutes
104
What is the most common complication CNS feature from preeclampsia?
Reversible Cerebral Edema
105
What is the leading cause of death in preeclampsia?
CVA
| Hemorrhage more common than embolic CVA secondary to preeclampsia
106
When does most hemorrhagic stroke from Pre-E occur during pregnancy?
Postpartum
107
Pre-E renal complications
Rare but....usually from hypoperfusion
- can have acute renal failure
- Prerenal: renal hypoprefusion
- Intrarenal: intrinsic renal parenchymal damage
- postrenal: obstructive uropathy
108
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
109
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.
110
HELLP Syndrome increases the risk of these complications.
* DIC
* Placental abruption
* Pulmonary edema
* Acute renal failure
* Liver hemorrhage/failure
* ARDS
* Sepsis
* Stroke
* Death
111
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
112
What symptoms may be present in a parturient if they are experiencing hemolysis?
* RUQ or epigastric pain
* N/V
* Headache
* HTN
* Proteinuria
113
Bilirubin levels in HELLP Syndrome
Bilirubin > 1.2 mg/dL
## Footnote
More specific for HELLP syndrome
114
Liver Enzyme levels in HELLP Syndrome
Increase AST > or = 70 IU/L
Increase LDH > 600 IU/L
115
Plt levels in HELLP Syndrome
Plt count < 100K, but can decrease precipitously
## Footnote
HELLP plt decrease is rapid, where pre-E is gradual
116
If a parturient has HELLP Syndrome, when will their plt count reach nadir?
Reaches nadir 2-3 days postpartum
117
Which steroid can improve plt count?
Dexamethasone
118
Plt count below this level during a C-section will covert to a GETA
less than 50K
119
When will plt be transfused in a parturient?
* Transfuse if plt count < 20,000
* Transfuse if plt count < 40,000 & c-section planned, or neuraxial
## Footnote
Hospital facility dependent - small facilties don't have platelets on hand (refer out likely)
120
Management for HELLP Syndrome
* Delivery
* Corticosteroid administration to improve fetal lung maturity
* Magnesium sulfate for seizure prophylaxis (increased risk of seizures with HELLP)
* Antihypertensives
121
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
122
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
## Footnote
Happens, but not really that much
123
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
* coload fluids
## Footnote
Do this early!
124
Neuraxial placement & platelet count parameters
* > 80,000/mm3 – no concerns
* 50,000-80,000/mm3 – weigh benefits/risks/alternatives
* < 50,000/mm3 – no neuraxial
125
Platelet count parameters for removing an epidural
Platelet count ≥ 75,000 - 80,000/mm3
126
What drugs are used to manage hypotension secondary to labor analgesia?
* Consider preloading/coloading with narrowed pulse pressure (but cautious with pulm. edema)
* Phenylephrine 25-50 mcg
* Ephedrine 5-10 mg
## Footnote
Potential increased sensitivity to vasopressors
127
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
* dont give fent for induction, esmolol would help to decrease this risk
* Magnesium sulfate effects on neuromuscular transmission
128
For a GETA, BP needs to be reduced to around __________ mmHg before induction
140/90
129
During laryngoscopy/intubation, maintain SBP between ___________ mmHg (range) and DBP between ___________ (range)
* SBP: 140-160 mmHg
* DBP: 90-100 mmHg
130
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
131
If HTN continues > 24 hrs postpartum, consider discontinuing this drug as it could be a potential contribution to HTN.
NSAIDs
132
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
133
At what pressure should antihypertensives be given postpartum?
* SBP > 150 mmHg
* DBP > 100 mmHg
## Footnote
Risk of CVA highest postpartum
134
How is eclampsia defined?
New onset seizures / unexplained coma in pregnancy or postpartum in the presence of signs/sx of preeclampsia
## Footnote
Eclampsia is rarely a surprise, most of these moms had Pre-E with severe s/s (exception is no prenatal care or less than diligent care)
135
When is the most common onset of eclampsia?
* Intrapartum
* Within 48 hours postpartum
136
Late eclampsia will have a seizure onset between _______ hours and _______ weeks postpartum
48 hours to 4 weeks postpartum
137
If you have a seizing pregnant woman, it is ____ until proven otherwise and you treat it with ____
If you have a seizing pregnant woman, it is **eclampsia** until proven otherwise and you treat it with **mag**
138
Complications of Eclampsia
* Aspiration
* Pulmonary edema
* CVA
* VTE (hypercoagulable state)
* Acute renal failure
* Death
* Placental abruption
* Severe IUGR
* Extreme prematurity
139
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)
140
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
141
When does fetal bradycardia begin during eclampsia?
Fetal bradycardia begins during or immediately post-seizure.
## Footnote
Not a requirement for delviery unless prolonged then we need to get the baby out with c-section
142
Management of Eclampsia
* Stop seizures (mag or benzos)
* 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)
143
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
## Footnote
increased risk of hemorrhage in these pts
144
Benefits of Propofol for eclampsia parturients
Decrease CMRO2 and CBF → Decrease ICP
145
Why not hyperventilate to reduce ICP in eclampsia patients?
Hyperventilation will decrease CBF w/o change in CMRO2
146
Why would you want to avoid hypoventilation in eclampsia patients?
* Hypoventilation lowers the seizure threshold
* Hypoventiation also increases ICP
147
What is amniotic fluid embolism (AFE)?
* Anaphylactoid syndrome of pregnancy
* Systemic inflammatory response resulting from the release of endogenous proinflammatory mediators (Arachidonic acid metabolites)
* Amniotic fluid enters the mother's bloodstream
## Footnote
This is actually a clotting problem, not a lung problem
- Activation of coagulation system related to platelet activaiton
- Fetal squamous cells have high tissue factor which irreversibly aggregates platelets causing degranulation
- *thromboxane and seotonin release*
148
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
149
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
150
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
151
What labs are ordered for AFE?
* Anemia & thrombocytopenia
* Prolonged PT/PTT and decreased fibrinogen levels
* Elevated fibrin split products
* CBC, coags, DIC panel
152
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
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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
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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
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What is the classic triad of AFE?
* Hypoxia
* Hypotension
* Coagulopathy
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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
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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
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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
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Anesthesia Management of AFE
* Secure Airway
* AOK (Atropine, Ondansetron, Ketorolac)
* Anticipate massive hemorrhage
* Activate MTP
* Get Help
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Why is atropine used in AFE?
* Atropine – vagolysis
* Decreases vasoconstriction in pulmonary vasculature
* Decreases incidence of bradycardia & heart blocks
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Why is ondansetron used in AFE?
* Ondansetron contributes to vagotomy via 5-HT3 antagonism
* Prevents CV collapse
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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
## Footnote
30-60mg
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AFE Flow Chart
