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ADV PRIN II Test 3 > Complex OB > Flashcards

Complex OB Flashcards

1
Q

Effects of pregnancy on:

plasma volume?

total blood volume?

hemoglobin?

fibrinogen?

serum cholinesterase activity?

A
  • plasma volume- increase 40-50%
  • total blood volume- increase 25-40%
  • hemoglobin- dilutional decrease. 11-12 g/dL normal in pregnancy
  • fibrinogen- increase 100%
  • serum cholinesterase activity- decrease 20-30%
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2
Q

Effect of pregnancy on:

SVR?

CO?

systemic blood pressure?

A
  • SVR- decrease 50%
  • CO- increase 30-50%
  • Systemic blood pressure- decrease (slight)
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3
Q

Respriatory effects of pregnancy on

Functional residual capacity?

Minute ventilation?

Alveolar ventilation

Oxygen consumption

Carbon dioxide production

arterial carbon dioxide tension

minimum alveolar concentration

A
  • Functional residual capacity- decrease 20-30%
  • Minute ventilation- increase 50%
  • Alveolar ventilation- increase 70%
  • Oxygen consumption- increase 20%
  • Carbon dioxide production- increase 35%
  • arterial carbon dioxide tension- decrease 10 mmHg
  • arterial oxygen tension- increase 10 mmHg
  • minimum alveolar concentration- decrease 30-40%
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4
Q

CV changes in pregnancy?

A
  • Normal findings
    • S1 and S3 toward end pregnant
    • Left axis deviation
    • Left ventricular hypertrophy
  • Abnormal:
    • chest pain,
    • syncope,
    • high grade murmur, arrythmias,
    • HR symptoms,
    • clinical sig SOB → further assessment
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5
Q

Effect of pregnancy on blood volume/composition?

A

Increase intravascular fluid volume in 1st trimester

  • Rising progesterone levels → increased RAAS
    • more Na reabsorption → H2O retention

Albumin – 25 % dec

Total protein- 10% dec

  • decrease colloidal osmotic pressure
    • 50% increase in plasma volume → prepare for BL during delivery
    • Blood volume normalize 6-9 Postpartum
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6
Q

GI effects in pregnant women?

A

increase GI displacement

full stomach @ 12 week

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7
Q

Hemodynamic changes in pregnancy?

A
  • CO highest right after delivery
    • Increase 80-100% to prelabor values
      • d/t autotransfusion of empty uterus that now contracts and release of aorta-caval compression (baby not on IVC now)
        • RISKY time for CV hx pts (ex: fixed valvular stenosis/pHTN) → huge sudden increase in CO
  • SVR sig decrease but CO INCREASE
    • Change in BP not very sig, but slight change
      • S/D/MAP decrease 5-10% by 20 wks
        • More drop in diastolic d/t SVR drop
      • Grad increases while closer to term preg
  • CVP/Pulm capillary wedge pressure – no change
    • Increase plasma volume + drop venous capacity → offsets change
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8
Q

What is the impact of aortocaval compression during pregnancy?

A
  • Uterus sitting on IVC → decrease BP
    • Supine hypoTN syndrome – decrease MAP > 15 mmHg w/ increase HR > 20bpm
      • CV sig changes: diaphoresis, N/V, mental status change
    • Tx: LUD position (elevate R hip 10-15 cm w/ wedge/tilt)
      • Prevent hypoTN and increase fetal BF
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9
Q

Airway changes during pregnancy?

A
  • Capillary engorgement
  • DAW
    • Avoid instruments
    • Most expert
    • Small ETT
    • Position optimal
    • Decrease FRC… → reserve dec
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10
Q

Coagulation changes during pregnancy?

A
  • Hypercoagulable state → increase fibrinogen, factor 7
  • Factor 11 & 13 decreased
  • ATIII, Protein S- decreased
  • Protein C- unchanged
  • Plt normal- but dec 10% d/t dilutional effect
    • Gestational thrombocytopenia -d/t hemodilution and rapid plt turnover
      • r/o: ITP, hemolysis, elevated liver enzymes, HELLP → do TEG on at risk pt
      • PLT usually not < 70k unless problem
    • Normal pregnancy: PT and aPTT decreased by 20%
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11
Q

Effect of pregnnacy on MAC?

A

unknown mech

  • Progesterone ??
  • MAC Reduced up to 40%
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12
Q

Effect of LA during pregnancy?

A

more sensitive

  • Neuraxial req reduced by 40% at term
    • Epidural veins distended
    • Volume of epidural fat increases
      • → increases size of epidural space/volume of CSF in SA space → more spread
  • DOSE: DECREASED
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13
Q

What are the stages of labor?

A
  • First
    • Start: regular painful contractions
    • End: complete cervical dilation
      • Length: ~ 2 - 20 hours
  • Second
    • Start: complete cervical dilation
    • End: birth
  • Third
    • Start: Birth
    • End: Placenta delivery
  • Fourth (New)
    • Placenta to hemostatic stabilization
      • (1 -4 hours after delivery)
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14
Q

Labor pain in 1st versus 2nd stage

A
  • 1st Stage - visceral
    • Cervical distention and stretching of lower uterine segment
      • Latent phase: T10 – T12
      • Active Phase: T10 – L1
    • Non-specific nociceptor – unmyelinated C fibers
      • Visceral afferent fibers travel with sympathetic nerve fibers to uterine & cervical plexus and then through hypogastric & aortic plexus
  • 2nd Stage – somatic
    • Mediation:
      • Pudendal nerve (S2-4)
      • Somatic afferent fibers – myelinated A delta
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15
Q

Meperidine use in labor?

A
  • Dose 25 mg IV
  • Onset 5-10 min
  • DUration 2-4 hours
  • Active metabolite normeperidine can affect neonate if delivery occurs between 1-3 hours after administration
  • F/M ratio >1 @ 2 hours, ,1 @ 4 hours
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16
Q

Morphine use in labor?

A
  • Dose 2-5 mg
  • Onset 5 min IV
  • Duration 3-4 hours
  • Infrequently used- greater respiratory depression than with meperidine
  • F./M ratio 0.92
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17
Q

Fentanyl use in labor?

A
  • Dose 25-50 mcg IV
  • Onset 2-3 minutes
  • Duration 30-60 min
  • Short acting, accumulates over time
  • highly protein bound
  • F/M ratio 0.57
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18
Q

Sufentanil use in labor?

A
  • 5-10 mcg IV
  • Onset 2-3 min
  • Duration 2-3 hours
  • Potent respiratory depressant- use with caution
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19
Q

Remifentanil use in labor?

A
  • 0.25- 1 mcg/kg
  • Onset 1-2 min
  • Duration 3-5 min
  • Sedation, respiratory depression
  • crosses placenta- rapidly metabolized by fetus
    • esterases are fully develops @ birth
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20
Q

Nubain use in labor?

A
  • Dose 5-10 mg IV
  • Onset 2-3 min
  • Duration 3-4 hours
  • Opioid agonist/antagonist
  • sedating, ceiling on respiratory depression
  • F/M ratio 0.97
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21
Q

Ketamine use in labor?

A
  • 10-15 mg IV
  • Onset 1-3 min
  • Duration 10-15 min
  • Possiblity of delirium and hallucination
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22
Q

Nitrous oxide use in labor?

A
  • <50%
  • Onset immediate
  • duration minutes
  • minimal effect on mother/fetus, may only be partially effective
    • Impact on B12 synthesis
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23
Q

Regional anesthesia options for labor pain?

A
  1. Spinal opioids alone
    • Single vs intermittent injection
    • Good in high-risk patients – cardiac patients
  2. Local anesthetic +/- opioids
    • **Epidural
      • Local only vs. local + opioids**
    • Dural puncture epidural can inadvertently do CSE and do wet tap and do this technique unintentionally
      • Place epidural – puncture dura with spinal needle
      • Bolus epidural
        • Risks: typically these are result of wet-tap (unintentional tech)
    • Combined spinal epidural (CSE)frequent technique for quick analgesia and follow up with epidural for continued labor
      • Walking epidural – low dose local +/- opioid intrathecal
      • Thread epidural catheter – initiate epidural at later moment
        • Uses: quick analgesia and need bolus epidurals after
    • Saddle block – pudendal nerve (somatic pain)
      • Bupivacaine 2.5 mg and fentanyl 25 mcg
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24
Q

Considerations for fetal heart rate monitoring? tachycardia? Bradycardia?

A
  • Follow:
    • Baseline HR (120-160 bpm)
    • beat to beat variability
    • FHR pattern
  • Baseline
    • Normal varies between 120 -160 BPM
  • Fetal Tachycardia- fetal distress
    • > 160 BPM
      • Fetal hypoxia
      • maternal fever
      • sympathomimetic drugs
      • fetal anemia
      • fetal cardiac anomalies
  • Fetal Bradycardia (more ominous)
    • < 100 BPM
      • Fetal head compression
      • umbilical cord compression
      • sympatholytic drugs
      • prolonged hypoxia
      • fetal cardiac anomalies
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25
Q

What are some various fetal heart rate patterns?

A
  • A. Early Decelerations
    • Fetal head compression → baroreceptor activation
      • Uniform in nature – mirrors contraction
      • ~ 10 – 40 beat/min –NOT associated w/ fetal distress
  • B. Late Decelerations
    • Uteroplacental insufficiency
      • Decrease FHR at or following peak of uterine contraction
      • Decrease varies b/t 10 – 20 beats/min
      • Gradual and smooth return to baseline
      • can be concerning
  • C. Variable Decelerations
    • Most common fetal pattern
      • Variable in onset, duration, and magnitude
        • > 30 BPM
      • R/t cord compression
      • Associated with: FETAL HYPOXIA
        • FHR declines < 60 BPM
        • lasts > 60 seconds
        • persists > 30 minutes

Late decels and ominous variable decels → emergent c/s

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26
Q

Category I FHR intepretation system?

A

All of the following:

  • Baseline rate 110-160 bpm
  • Baseline FHR variability moderate
  • Late or variable decels- absent
  • early decel present or absent
  • accelerations: present or absent
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27
Q

Category II FHR Interpretation?

A
  • Categroy II FHR tracings include all FHR tracings not categorized as category I or Category III
  • Category II tracings may represent an appreciable fraction of those encountered in clinical care
  • Examples include any of the following:
    • baseline rate
      • bradycardia not accompanied by absent baseline variability
      • tachycardia
    • baseline FHR variability
      • minimal baseline variability
      • absent baseline variability not accompanied by recurrent decelerations
      • marked baseline variaiblity
    • accelerations
      • absence of induced accelerations after fetal stimulation
    • periodic or episodic decels
      • recurrent varaibile decels- accompanied by minimal or moderate baseline variability
      • prolonged decelerations >2 minutes but <10 minutes
      • recurrent late decelerations with moderate baseline variaiblity
      • variable decelerations with other characteristics such as slow return to baseline “overshot” or “shoulders”
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28
Q

Category III FHR interpretations systme?

A
  • Absent baseline FHR varaibility and any of the following:
    • recurrent late decels
    • recurrent varaibile decels
    • bradycardia
    • sinusoidal pattern
  • concerning and need to go to OR
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29
Q

Preop considerations for elective c-section (from coexist)

A
  • Preoperatively
    1. History /Physical
      • Airway evaluation
    2. Informed Consent
    3. LUD (left uterine displacement)
      • > 20 weeks – Aortic Caval Syndrome
    4. IV access (free flowing 18-16 gauge)
    5. Hydration (minimal 500 mL)
    6. Aspiration prophylaxis (bicitra, metoclopramide, ranitidine)
    7. Supplemental O2
    8. Anesthetic plan/ postoperative analgesia plan
  • Choice of anesthetic depends on
    1. Indications for surgery
    2. Degree of urgency
    3. Maternal status
    4. Condition of fetus
    5. Desires of the patient
      • Sometimes too emergent → put to sleep
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30
Q

What is first line for bleeding postpartum?

A

Rule of 3’s

  • Oxytocin 3 units (prepack syringe in 5 ml)
  • 3 min evaluation intervals
  • 3 total doses
  • Oxytocin infusion 3 units/hr maintenance
    • 3 units are given as a slow bolus
    • Uterine tone reassessed at 3 and 6 minutes
    • If inadequate, additional 3 doses are given after each reassessment
    • If uterine atony persists after 3 dosesà switch to another drug
    • After establishment of uterine tone, infuse 3 units/hr X 5 hours
  • Oxytocin as a rapid IV bolus:
    • Direct SM relaxant à SVR, hypotension, and tachycardia (going in too fast)
      • Hypotension may result in CV collapse
      • Chest pain, myocardial ischemia may develop (can give op)
      • Water intoxication and hyponatremia (Structural similarities b/t oxytocin and vasopressin)
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31
Q

2nd line for bleeding postpartum? (coexist)

A
  • Methylergonovine (Methergine-ergot alkaloid)
    • Dosage: 0.2 mg IM
    • Onset: 10 min
    • Duration: 2-4 hours
    • Can it be given IV: NOT RECOMMENDED
      • Intense vasoconstriction, acute HTN, seizures, retinal detachment, coronary artery spasms, CVA
    • May be repeated x1 after 30 min
    • Contraindications: HTN, preeclampsia, CAD
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32
Q

3rd line for bleeding postpartum (coexist)

A
  • 15-Methylprostaglandin F2a (carboprost - Hemobate)
    • Dose: 250 mcg IM
    • May repeat every 15 min x 8 doses (2 mg)
      • SE: fever, chills, n/v, diarrhea, and bronchoconstriction

***Who should not receive this drug? Asthmatics

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33
Q

Indications for emergenct c-section?

A
  • Immediate danger to life of mother or fetus
    • OB Code/Crash with failed intubation
      • Why more difficult- can’t wake up patient
      • What options are available to you?- emergency airway management. OB uses local/infiltration technique
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34
Q

Anesthetic plan for preop/induction emergent c-section? (coexist)

A
  • Preop assessment of airway
  • Large bore IV
  • Aspiration prophylaxis (Non-particulate antacid, H2-blocker, Reglan)
  • Monitors/suction/ emergency airway cart
  • Optimal airway positioning/ LUD
  • Preoxygenate! (3 min or longer)
  • Prep + drape –surgeon ready
  • RSI w/cricoid (10 N while awake; inc to 30 N after LOC) → start putting force before even asleep
    • Agents available
      • Ketamine (used with maternal hypotensive crisis) 1 mg/kg
      • Etomidate 0.3 mg/kg
      • Propofol 2-2.5 mg/kg
      • Succinylcholine 1-1.5 mg/kg
        • Preferred muscle relaxant
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35
Q

Intubation considerations for emergent c-section? What happens immediately following intubation?

A
  • Intubate
    • Expect difficult intubation
    • Proper positioning
    • Short handled laryngoscope (Datta) recommended
    • Use minimal amount of time; first attempt best attempt
    • Smaller ETT 6.0 or 6.5
    • Use caution…friable tissues and decreased airway size
  • Verify placement of ETT → tell surgeon!
    • Then…Surgeon makes skin incision (after tube placement verified)
  • Ventilate with 50% O2/50% N2O & VA (~1 MAC) → overpressure!
    • Don’t forget to turn on gas! Tremendous recall
  • Secure ETT, tape eyes, OGT
  • ****Critical interval of 3 minutes between uterine incision and delivery of fetus
    • Tremendous recall risk → medications waring down and youre busy (mom remembers)
  • Delivery of baby
    • PCA pump (bc didn’t do spinal)
    • As soon as baby is delivered→ can give Versed, Fent, etc.
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36
Q

What happens after delivery in emergent c-section (coexist)

A
  • AFTER DELIVERY:
    • Reduce VA (.75 MAC) → may increase N2O to 70%, and give opioids and benzodiazepine
      • Reduce MAC → don’t want to vasodilate & bleed out
  • Possible NDMR
  • Delivery of placenta
  • Then can add oxytocin to IV → start contracting of uterus so that mom doesn’t hemorrhage
  • At end:
    • Suction OGT
    • Reverse NDMR if necessary
    • Extubate AWAKE
      • Emergence and recovery is a critical period for anesthesia-related deaths from airway factors!
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37
Q

Maternal mortality statistics?

A
  • Profound decrease b/t 1991- 2002
    • Decreased morbidity/mortality from GA and increased from neuraxial (preg = DAW)
      • move from always GA to neuraxial, esp good with increased risk DAW in pregnancy
  • Most often related to cesarean delivery
    • Failed intubations = 23%
    • Respiratory failure = 20%
    • High spinal/epidural = 16%
    • Others:
      • LAST
      • PDPHa
      • Nerve injury
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38
Q

What is gestational HTN?

A
  • Most frequent cause of HTN during pregnancy
  • Incidence:
    • ~ 7% parturients
  • Characterizations:
    • Elevated BP after 20 weeks gestation (bp >140/90)
      • Without proteinuria
    • Most cases develop > 37 weeks’ gestation
    • Self-limiting: Resolves by 12 weeks postpartum
    • ~ ¼ will develop preeclampsia
      • True diagnosis only made after delivery when chronic hypertension can be ruled out
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39
Q

What is chronic hypertension of pregnancy?

A
  • Systolic BP > 140 and/or diastolic BP > 90
    • Starts before pregnancy or PRIOR to 20 weeks
  • Elevated blood pressure that fails to resolve after delivery
  • Consequences:
    • Develops into preeclampsia ~ 1/5- ¼ affected patients
    • Still an important risk factor for unfavorable maternal and fetal pregnancy outcomes
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40
Q

What is chronic hypertension with preeclampsia?

A
  • Occurs when preeclampsia develops in a woman with chronic HTN
    • Dx: proteinuria onset
    • Or sudden increase in proteinuria, blood pressure, or both
  • Morbidity increased for both the mother and fetus compared to preeclampsia
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41
Q

What is preeclampsia?

A
  • Preeclampsia is a multisystem disease unique to human pregnancy
  • Occurs in 3 - 8% of all pregnancies
  • Accounts for 15 – 19% of maternal deaths in the US and UK
  • Doubled in the last decade
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42
Q

What is mild pre-eclampsia?

A
  • BP > 140/90 after 20 wks gestation
  • Proteinuria
    • 300 mg/24 hours
    • 1+ on dipstick
    • protein/creatine ratio > 0.3
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43
Q

What is severe pre-eclampsia?

A
  • BP > 160/110
  • Proteinuria
    • > 5g/24 hours
    • >3+ on dipstick)
  • Thrombocytopenia
    • platelet < 100,000
  • Serum creatinine
    • > 1.1 mg/dl (or 2x’s baseline)
  • Pulmonary edema
  • New onset cerebral or visual disturbances
  • Impaired liver function
  • Epigastric pain
  • Intrauterine growth restriction
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44
Q

What are some coexisting and obstetric factors that increase risk for pre-eclampsia?

A
  • Coexisting
    • Chronic renal disease
    • Lupus
    • Protein S deficiency
    • Increased pulse pressure during 1st trimester
  • Obstetric Factors
    • African American
    • Nulliparity
    • Advanced age (> 40)
    • Smoking
    • Obesity
    • Diabetes
    • Multiple gestation
    • History of pre-eclampsia
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45
Q

Pathogenesis of preeclampstia?

A
  • Unknown Exact pathogenic mechanism
    • Hypothesis: Immune maladaptation → leads to inflammation
  • Focus on the placenta
    • Delivery of placenta resolves preeclampsia
    • Can occur in absence of a fetus (molar pregnancy)
  • 2 stage disorder
    • 1st stage = asymptomatic
    • 2nd stage = symptomatic
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46
Q

What occurs during the first stage of preeclampsia?

A
  • Impaired remodeling of spiral arteries
    • End branch of the uterine artery that supplies placenta
  • Normally
    • Cytotrophoblasts invade the spiral arteries changing them to low resistance and high flow vessels
      • Adrenergic denervation
  • Preeclampsia
    • Invasion is incomplete leaving small and constricted vessels that are responsive to adrenergic stimuli
    • basically vessels to uterus do not undergo necessary remodeling, so it leaves a high pressure system. still have response to adrenergic stimuli
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47
Q

What occurs during the second stage of pre-eclampsia?

A
  • Widespread endothelial dysfunction that is organ specific develops
  • Insufficient placental BF → leads to placental hypoxia
    • → IUGR
  • Increased production of free radicals and lipid peroxides
  • Imbalances
    • Vasoconstrictors: (thromboxane A2 = ⇧)
    • Vasodilators (prostacyclin’s = ⇩)
  • Hypoxia →
    • increase antiangiogenic factors (sFlt-1 and soluble endoglin) factors → decrease vascular endothelial growth factors and placental growth factors.
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48
Q

Pathophys of preeclampsia?

A
  • unknown cause
  • leads to endothelial damage
  • Cascade of events
    • Plt aggregation
    • Dec production of vasodilatory substances
    • Increase vascular sensitivity to vasoconstrictive sub (Angiotension, NE) → vasospasms
  • Consequences:
    • Increase capillary permeability
      • → proteinuria
    • Hemolytic anemia
    • Increase Liver enzymes
      • HELLP
        • Increase SVR
        • Decrease aldosterone escapre
        • Increase Na/H2O retention →
          • HTN
          • Edema → preeclampsia/eclampsia
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49
Q

Neurolgoic and CV pathologic alterations in preeclampsia?

A

Neurological

  • Headache
  • Visual disturbances
  • Hyperreflexia
  • Seizures (*eclampsia)
  • Cerebral edema
    • Increased risk

Cardiovascular

  • Increased BP
  • Decreased intravascular volume (d/t contraction of vascular space)
  • Increased arteriolar resistance
  • Heart failure
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50
Q

Respiratory changes in preeclampsia

A
  • Respiratory changes
    • Pharyngeal and laryngeal edema → airway management difficult
      • Potentially WORSE d/t Na/H2O retention
    • Pulmonary edema
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51
Q

Hepatic and renal changes in preeclampsia?

A
  • Hepatic
    • Impaired function
    • Elevated enzymes
    • Hematomas
    • Ruptures
  • Renal
    • Proteinuria
    • Na retention
    • Decreased GFR
    • Oliguria
    • Increased serum uric acid – decreased urate clearance
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52
Q

Hemetalogic alterations in preeclampsia?

A
  • Coagulopathy
    • Thrombocytopenia (both)
      • Quantitative: number
      • Qualitative: function
    • Platelet dysfunction
    • Prolonged PTT
      • *risk of cerebral hemorrhage → so need to tx HTN
        • Tx: (SBP >160) w/ labetolol, Hydralazine, nifedipine
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53
Q

General managmenet of preeclampsia?

A
  • Lots of overlap between obstetricians and anesthesia

General Overview

  1. Timing of delivery
    • R/o regional technique d/t coagulopathy?
  2. Fetal and maternal surveillance
  3. Treatment of hypertension
  4. Seizure prophylaxis
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54
Q

Timing of delivery in preeclampsia?

A
  • Delivery only cure
    • > 37 weeks
      • Induction of labor
    • > 34 weeks with severe symptoms
    • < 34 weeks
      • Expectant management
      • Delay delivery for 24 – 48 hours
      • Administer steroids to facilitate fetal lung function
        • Ex: betamethasone- mature fetal lungs
      • Should be undertaken at facilities with neonatal and maternal intensive care resources
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55
Q

What is involved in surveillance of preeclampsia?

A
  • S/S of end organ damage
    • Ex: renal, liver
  • Laboratory
    • CBC
      • PLT count (most important)
      • > 100,000
      • <100,000 – additional tests
        • PT/PTT/INR
    • Chemistry
    • Urine protein/creatinine
    • LFTs
    • Uric acid testing – conflicting evidence
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56
Q

What are some guidelines for treatment of HTN in preeclampsia?

A
  • Control BP- important
    • Considerations:
      • Rapid maternal perfusion pressure changes can adversely affect uteroplacental perfusion pressure
        • → uteroplacental perfusion pressure form arteries are already maximally dilated
        • *If drop BP rapidly → negatively affect perfusion to placenta
  • Targets:
    • 15 – 25% reduction BP
      • Initial BP > 160 (labetalol, Hydralazine, nifedipine)
    • Systolic: 120 – 160 mmHg
    • Diastolic: 80 – 105 mmHg
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57
Q

What are some first line agents for treating HTN in preeclampsia?

A
  • Labetalol
    • Crosses placenta but does NOT cause fetal bradycardia
    • B:A of 7:1
    • Dose:
      • 1st: 20 mg IV
      • 2nd: 40 mg q10min
        • Max: 220 mg
  • Hydralazine
    • MOA: Potent direct vasodilator
      • decreases MAP and SVR
      • increasing HR and CO
    • Dose: 5 mg IV q20 minutes
      • Max: 20 mg
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58
Q

What are second line anti-HTN to treat HTN in preeclampsia?

A
  • Nifedipine
    • Dose: 10 mg PO q20 min
      • Max: 50 mg
  • Nicardipine
    • Dose: 1– 6 mg/hr
    • CAUTION:
      • Combo Ca+ blockers + Mg+ è
        • profound hypoTN
        • myocardial depression
  • Others: sodium nitroprusside and nitroglycerine
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59
Q

What meds should you use with caution in patients with preeclampsia?

A
  • Methergine- any form of HTN in peripartum period
    • Lead to HTN crisis
  • Sensitive to exogenous and endogenous catecholamines (adrenergic agents)
  • Magnesium- utilized for preeclampsia
    • Leads to uterine atony → increased PP bleeding
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60
Q

Seizure prophylaxis in preeclampsia?

A
  • Magnesium Sulfate
    • Bolus: 4 – 6 grams over 10 - 30 minutes
    • Maintenance of 1 -2 gm’s/hour
      • Continued for 24 hours following delivery
    • Maternal Side-effects:
      • flushing, HA, dizziness
      • skeletal muscle weakness, decreased deep tendon reflex
      • respiratory depression
      • hypotension
      • pulmonary edema
      • uterine atony (pp) → increase bleeding risk
    • Fetal side effects:
      • neonatal hypotonia
      • respiratory depression
61
Q

What is normal serum magenisum?

Therapeutic level for preeclampsia?

When are EKG changes seen?

Loss of DTR with Mg level?

Respiratoyr arrest?

Cardiac arrest?

Treatment for mg toxicity?

A
  • Normal: 1.7 – 2.4 mg/dl
  • Therapeutic: 5 – 9 mg/dl (prevent szs)
  • EKG changes: 6 – 12 mg/dl
  • Loss of DTR: 11 – 12 mg/dl
  • Respiratory arrest: 15 – 20 mg/dl
  • Cardiac arrest: > 25 mg/dl

Treatment- Mag toxicity

  • Calcium gluconate: 1 gm over 10 minutes
  • Calcium chloride: 300 mg over 10 minutes
    • Ex: stop mag → admin Ca → monitor for EKG changes
62
Q

Airway managmenet in patietn with preeclampsia?

A
  • Generalized edema → obscure anatomical landmarks
  • Be prepared for a difficult airway, even more so than normal pregnant pt due to edema
  • Increased vascularity of Nasopharynx
    • Tissue swollen/friable → tendency to bleed
63
Q

Hemodynamic monitoring in patient with preeclampsia?

A
  • Noninvasive blood
    • Mild and uncomplicated severe
  • A-line- for sick/uncontrolled HTN
    • Need for frequent ABG measurement
    • Continuous monitoring during induction/emergence in poorly controlled hypertension
    • Calculated systolic pressure variation
  • Central- severe
    • Careful considerations and placement
  • TEE- severe
  • Useful technique for assessing cardiopulmonary status
  • AW swollen/vascular as is → CAREFUL w/ probe
64
Q

Labor management of preeclampsia?

A

neuraxial (CLE or CSE)

  • Preferred method of pain control
    • Recommendation → EARLY placement
      • Ex: analgesia → dec level catecholamines/stress hormones circulating → increase uterine BF, less CV effects
  • Advantages:
    • Provision of high quality analgesia
    • Decreased levels of catecholamines and stress hormones
    • Conversion of analgesia to anesthesia - avoids general anesthesia
    • Increase uterine blood flow
  • Considerations:
    • Coagulation status (Plt**)
    • Intravascular volume status
      • Contracted intravascular space → need volume prior to placement
    • HypoTN tx
      • Change in autoreg curve
    • Use of epinephrine containing solutions (ex: 2% Lido w/ 1:200,000 epi for loading dose)
      • Impact on BP?
65
Q

Impact of preeclampsia on platelets? considerations?

A
  • Coagulation: Plts
    • > 100,000 = traditional level
    • > 80,000 = currently acceptable w/o other risk factors
    • < 50,000 = unacceptable risk
    • 50,000 – 80,000
      • risk vs benefits of regional vs. general anesthesia
  • Considerations
    • Platelet count trends over last 24 – 48 hours
      • If platelet count is decreasing – may want to place epidural catheter early
    • Coexisting coagulopathies
      • Evaluate
        • Coagulation studies
        • LFTs
        • TEG and platelet function analysis
          • unproved technology in thrombocytopenia in pregnant patients
          • d/t multifactorial issues in preg
66
Q

What are some recommendations when choosing neuraxial technique in patients with Plt <100k?

A
    1. Most skilled provider
    1. Single shot technique
    1. Use of a flexible, wire-embedded epidural catheter
      * Less trauma
    1. Monitor S/S of neurological complication (ex: epidural hematoma)
    1. Check plt count before removal
      * NEED: > 75 – 80,000 BEFORE REMOVING
    1. Imaging studies should be obtained immediately if question to neuro fx
      * CT
      * MRI
67
Q

IV fluid mgmt in neuraxial anesthesia in patient with preeclampsia?

A
  • Preloading vs co-loading = equivocal outcomes
    • *Do not delay initiation of neuraxial techniques simply to administer a fixed volume of fluids
  • Considerations:
    • Restrictive fluid management: small 250 ml fluid boluses
      • Do not want to fluid overload → pulm edema
68
Q

Vasopressor use in preeclampsia?

A
  • Exaggerated response to endo/exogenous catecholamines (in preeclamptic pts)
    • Small doses!!
      • Ephedrine (5 – 10 mg)
      • Phenylephrine (25 – 50 mcg)
  • Careful titration – severe preeclamptics may have exaggerated response
  • Epinephrine in labor epidural = equivocal
    • Absence of malignant HTN (>160/110)
      • → epinephrine unlikely pose sig HTN crisis risk
      • But AVOID:
        • Reduction of uterine BF in animals
        • Preeclamptics exaggerated vasoactive response
    • Used for decades in obstetric anesthesia
  • Prudent to avoid epinephrine containing solutions
    • Reduced chronotropic response during pregnancy
    • Maternal heart rate variability during contractions
    • Reduction of uterine blood flow in animal models
  • Patients with preeclampsia may have increased vasoactive response
69
Q

C section in patient with preeclampsia?

A
  • Preferred Anesthesia → Neuraxial
  • Spinal vs epidural
    • Initially – spinal anesthetics were avoided in patients with severe preeclampsia
    • Now, not supported by the evidence
      • Hypotension did occur – only 1 minute longer and easily treated ephedrine/phenylephrine
      • No significant difference in neonatal outcomes
    • Epidural
      • Initiated with 2% lidocaine or 3% 2-chloroprocaine
70
Q

General anesthesia consideratiosn in patient with preeclampsia?

A
  • Airway considerations
    • Edema
  • Hypertensive response to laryngoscopy
    • *Laryngoscopy most sympathetic response!
    • < 160/110 before induction and extubation
    • Maintain:
      • 140 - 160/90-100 throughout
    • Tx: HTN
      • Labetalol
      • Remifentanil (0.5 mcg/kg)
        • Good drug: esterases fetus already mature → able to metabolize at same rate as mom
  • Muscle relaxants
    • Continue muscle relaxants throughout surgery
    • Considerations:
      • Very small doses
      • Monitor with nerve stimulator
        • Esp w/ Mag admin → decrease muscle tone/delay NMF
      • NM & Mag
        • Steriodal: DOA and potency increased d/t magnesium
          • Ex: rocuronium, vecuronium, and mivacurium
        • Succinylcholine: DOA NOT affected by magnesium
    • Reversal agents – including sugammadex is acceptable once baby out
71
Q

Considerations for emergent c-seciton in preeclamptic patient?

A
  1. Place radial arterial line if BP severe
  2. Verify difficult airway equipment & smaller sized tubes available (6.0, 6.5)
  3. Administration of H2 blocker or reglan 30 – 60 minutes before
  4. Sodium citrate 30 ml’s prior to induction
  5. De-nitrogenate
  6. Labetalol 10 mg iv boluses to get BP to <160/110
  7. Monitor FHR- s/s fetal distress
  8. Consider remifentanil 0.5 mcg/kg or other adjuncts to help blunt
  9. RSI with Propofol/succinylcholine or etomidate/succinylcholine
  10. Maintain with ½ MAC volatile and 50% N2O
    1. After delivery →
      1. Decrease VA
      2. Admin:
        1. Benzo- Versed
        2. Opioid
        3. Propofol
  11. Small doses of opioids and avoid muscle relaxants if possible (bc Mag)
  12. Reverse muscle relaxants and administer more labetalol/hydralazine to prevent hypertension on extubation
72
Q

What are some risk factors for eclampsia? s/s eclampsia?

A
  • Life threatening emergency
    • 0.1 – 5.9 per 10,000 pregnancies
  • Most often occurs 2nd half of pregnancy
    • > 20 wks gestation
  • Risk factors:
    • young maternal age
    • nulliparity
    • multiple gestation
    • pre-existing HTN
    • preeclampsia
  • 80% develop premonitory signs:
    • Headache
    • visual disturbances
    • photophobia
    • altered mental status
    • epigastric pain
73
Q

Characteristics of eclamptic seizure?

Complications of eclampsia?

A
  • Eclampsia (Seizure) onset:
    • Abrupt onset of facial twitching → then tonic phase → followed by clonic phase (often with apnea)
      • ~ lasts about 1 minute
  • Complications:
    • Aspiration
    • cerebral hemorrhage
    • kidney failure
    • cardiac arrest
    • placental abruption
    • extreme prematurity
74
Q

Treatment of eclampsia?

A
  • Stop the convulsions
    • Benzodiazepine
    • Propofol
    • Magnesium
  • Establish an airway
  • Turn patient to left side
  • Administer 100% oxygen
  • Apply VS monitors - frequent assessment
  • Check BP frequently – control hypertension (DBP < 110 mmHg)
    • Labetolol
    • Hydralazine
    • Nifedipine
  • Ensure adequate IV access
  • Ensure adequate ventilation/oxygenation
  • Maintain circulation
  • Deliver the baby expeditiously
75
Q

Anesthesia considerstaions in stable vs unstable eclamptic patient?

A
  • Stable
    • Epidural and spinal acceptable
  • Unstable
    • GA preferred
    • Techniques for patients with increased intracranial pressure
      • Propofol- positive effects on cerebral BF
      • Maintain cerebral perfusion pressure
        • MAP – ICP (MAP up, ICP down)
      • Avoid anything decreasing CPP
        • Hypoxemia
        • Hypoventilation
        • hyperglycemia
    • Persistent neurological evaluations
76
Q

What is HELLP syndrome?

A
  • Defined:
    • Hemolysis
    • Elevated levels of liver enzyme
    • Low platelets
      • Maybe a variant of severe preeclampsia
  • Associated with: DIC, abruption, pulmonary edema, acute renal failure, liver failure, sepsis, & death
    • 70% deliver pre-term
77
Q

What are the lab variations seen in HELLP syndrome?

A
  • Hemolysis
    • Microangiopathic hemolytic anemia
    • Abnormal peripheral blood smear
      • Schistocytes
      • burr cells
      • echinocytes
    • Bilirubin > 1.2 mg/dl
  • Elevated Liver Enzymes
    • AST > 70 IU/L
    • LDH > 600 IU/L
  • Low Platelets
    • < 100,000
    • Platelet transfusion
      • < 20,000 or significant bleeding in all paturients
  • < 40,00 scheduled for cesarean section
78
Q

What is a life threatnening complications of HELLP syndrome?

A
  • Rupture of subcapsular hematoma of liver (possibility)
    • Life threatening complication of HELLP syndrome
    • S/S:
      • abdominal pain
      • N/V
      • Headache
      • enlarged liver
      • hypotension
    • Dx - Ultrasound or CT scan
    • Tx – emergency surgery- delivery of fetus
      • volume resuscitation
      • coagulation management
79
Q

What are some reasons why pregnancy has increased bleeding and clotting risk?

A
  • Thrombocytopenia- 10% pregnancies
  • Etologies:
    • > 20 wks → can be sign of HELLP
    • Typically benign → Gestational Thrombocytopenia
  • Plts
    • Normal: Plts # decrease 10%
    • Threshold
      • ~100,000 safe (varies)
      • 70-100,000
      • NO < 50,000
    • Coexisting bleeding disorders → increased risk
      • Ex: VWF Deficiency → risk of peripartum hemorrhage
  • Increased risk of clotting
    • DVT/PE → d/t hormone changes
      • Preexisting factor 5 leiden, Protein S/C/AT/Antiphospholipid deficiencies → increase risk clotting
        • Tx: anticoag therapy → impacts delivery plan
80
Q

What is the leading cause of maternal death worldwide?

A
  • Antepartum hemorrhage- Leading cause maternal mortality
  • # /Need of blood transfusions → morbidity indicator
  • blood loss
    • typically underestimated
    • delay to treat– since magnitude of loss is underapprecieated
81
Q

What is placenta previa?

A
  • Present if placenta implants in advance of fetal presenting part of fetus
    • Dx: (Miller)
      • Placenta low in uterus
      • in front of presenting fetus
      • Either covering or encroaching on cervical os
  • Occurs in 0.4 -1% of pregnancies (0.5%)
82
Q

What are the various classifications of placenta previa?

A
  • Marginal
    • Lies close to, but does not cover the cervical os
  • Partial
    • Partially covers the cervical os
  • Complete
    • Placenta completely covers the cervical os
83
Q

What are some risk factors for placenta previa?

A
  • Previous cesarean section (prior scar tissue)
  • Prior placental previa
  • Multiparity
  • advanced maternal age
  • assisted pregnancy
  • smoking
84
Q

Diagnosis and OB managmeent of placenta previa?

A
  • Diagnosis:
    • Painless vaginal bleeding during the 2nd or 3rd semester
      • Self-limited
    • Transvaginal ultrasound
    • Digital or speculum exam requires “double set-up”
  • OB Management
    • Bed rest
    • Between 24 and 34 weeks – betamethasone
      • → accelerate fetal lung maturity/surfactant development
    • C-Section delivery
85
Q

Preop considerations for management of placenta previa?

A
  • All patients admitted with vaginal bleeding should be evaluated by anesthesia on arrival to the labor deck
  • Increased risk for intraoperative BL
    • Placenta maybe injured during incision
    • Lower uterine segment may not contract as well
    • Increased risk for placenta accreta
  • Prepare for massive BL
    • 2 large bore IV’s, fluid warmer, blood tubing, rapid infuser, invasive monitoring equipment, a-line
86
Q

What are some considerations for choice of aneshtetic management for patient with placenta previa?

A
  • Choice of anesthetic technique depends on:
    • urgency of delivery
    • maternal vital signs
    • pregnancy history
  • Without active bleeding & normal vital signs
    • Epidural or CSE acceptable (one RCT showed epidural superior to GA)
  • Active bleeding or altered vital signs (d/t prolonged bleeding)
    • RSI- CV instability
    • Induction agent based on hemodynamic status
      • Low dose Propofol or etomidate & ketamine all have been used
    • Maintenance
      • Depends on hemodynamic status
      • Benzodiazepine/ketamine vs nitrous/volatile
    • Bleeding management (Uterotonics)
      • Oxytocin
      • Hemabate
      • Methergine
      • D/C VA if bleeding continues
        • → Increase N2O [] + midaz or low dose Propofol/ketamine infusion
      • Activate massive transfusion protocol
87
Q

What is placenta abruption? s/s?

A
  • Defined:
    • Complete or partial separation of placenta from the uterine wall (decidua basalis) > 20 wks gestation but before delivery of fetus
  • S/S:
    • Vaginal bleeding
      • Significant BL trapped behind placenta (remain in uterus)
        • → Coagulopathy!!
    • PAINFUL/tenderness w/ examination
      • ​placenta previa is painless
  • Fetal compromise occurs
    • Loss of placental surface area
      • → Oxygen tissue exchanging surfaces area reduced → fetal distress
88
Q

Risk factors placenta abruption?

A
  • advanced maternal age
  • Chorioamnionitis
  • PROM
  • Hx of abruption
  • multiparity
  • preeclampsia
  • hypertension
  • substance abuse- cocaine *
  • ETOH/tobacco use
  • direct/indirect trauma *
89
Q

Diagnosis of placenta abruption?

A
  • Vaginal bleeding (clotted dark blood)
  • Coagulopathies
  • uterine tenderness
  • hypotension
  • increased uterine activity
    • Bleeding may be concealed and gross underestimation of hemorrhage can occur
  • Fetus:
    • Non-reassuring FHR
    • Bradycardia
    • loss of variability
  • Ultrasound examination
90
Q

OB management of placenta abruption?

A
  • Delivery of infant and placenta
  • Degree of compromise determines timing and route
    • Expectant
    • Vaginal
    • Emergent cesarean section
91
Q

Anesthetic management of placenta abruption?

A
  • Labor
    • Epidural
  • Cesarean delivery
    • Stable – adequate volume resuscitation and normal coagulation
      • Epidural, Spinal, CSE
    • Severe ( >50% placenta detached) – fetal death rate approaches 50%
      • Crash GA
        • ketamine/etomidate and succinylcholine
      • Multiple large bore IV’s – place a-line/CVP
      • Volume resuscitation – 1:1:1 ratio
      • Monitor for DIC
      • Monitor for uterine atony (uterotonics*)
92
Q

What is uterin rupture?

A
  • Uterine wall defect with maternal hemorrhage and/or fetal compromise
    • require emergency C-section or postpartum laparotomy(after delivery)
      • Disastrous for mother and fetus
93
Q

What are some conditions that are associated with uterine rupture?

A
  • Obstetric:
    • Prior uterine surgery
    • induction of labor
    • high dose oxytocin
    • Trial of labor after cesarean (TOLAC)
      • Scar dehiscence
  • Trauma:
    • OB:
      • Forceps application
      • internal podalic version
      • excessive fundal pressure
    • Non-OB: Blunt or penetrating trauma
94
Q

Diagnosis of uterine rupture?

A
  • Abnormal FHR and fetal distress – most common sign
  • Abdominal pain (sudden & severe), abnormal FHR, and vaginal bleeding (<9%)
  • Hypotension, vaginal bleeding, change in uterine contour, and changes in contraction pattern – cessation of labor
  • Breakthrough pain and need for frequent redosing of neuraxial labor
95
Q

OB management of uterine rupture?

A
  • Antepartum – emergent laparotomy with delivery
  • Uterine repair
  • Arterial ligation – may not control bleeding and delay definitive treatment
  • Hysterectomy
96
Q

Anesthetic managmeent in stable versus unstalbe patient with uterine rupture?

A
  • Stable
    • May proceeded with preexisting epidural for labor analgesia
  • Unstable
    • Emergency cesarean section and laparotomy
    • Aggressive volume resuscitation
97
Q

What is placenta accreta?

Classifications?

A
  • When placenta abnormally adheres to uterus
  • Types: (3)
    • Placenta accreta vera
      • Adherence of the basal plate directly to the uterine myometrium without an intervening decidual layer
      • Miller: Abnormal adherence to myometrium w. absent decidual line of separation (w/o entering decidual layer)
    • Placenta increta
      • When the chronic villi invade the myometrium
      • Miller: Abnormal implantation and growth of placenta into myometrium
    • Placenta percreta
      • Invasion through the myometrium into the serosa and adjacent organs
      • Miller: Growth of placenta through uterine wall (myometrium) with placental implantation onto surrounding tissue (bladder, bowel, ovaries, etc)
98
Q

What increases risk for placenta accreta?

A
  • ​Mirrors the cesarean section rate
  • Previous cesarean delivery or other uterine surgery increase the risk
  • # C/S deliveries → Increase risk!!
    • 0 = 3%
    • 1 = 11%
    • 2 = 40%
    • 3 = 61%
    • 4 or > = 67%
99
Q

What is the labor mgmt plan for patient with placenta accreta syndrome?

A
  • Plan:
    • Planned preterm c/s and hysterectomy with placenta left in situ
      • → removing likely to initiate massive hemorrhage
    • Goal: Gestation > 34 weeks
    • Most often at institutions that manage complex OB patients
  • However must be prepared for emergency delivery and hysterectomy at any institution the care for parturients
    • Crash GA
      • RSI
    • Blood loss can be massive
    • Prepare for massive transfusion
    • Efforts to stop bleeding:
      • Internal iliac artery balloon catheters
      • resuscitative endovascular balloon occlusion of aorta
100
Q

What is retained placenta?

Conesequence?

Aneshtesia interventions?

A
  • Placenta that has not undergone expulsion w/in 30 min of birth
    • whole placenta
    • placenta parts
  • Consequences: post-partum hemorrhage
  • Therapy:
    • Epidural = top up +/- conscious sedation
    • Intravenous = nitroglycerine 1 mcg/kg
      • May also try sublingual spray 400 mcg
    • GA with high dose volatiles
  • All the risks that go with general anesthesia
101
Q

What is uterine inversion? Risk factors? S/S?

A
  • The uterus inverts through the cervix into the vagina
    • Rare – 1: 2,000 – 10,000 deliveries
  • Risk factors:
    • Pulling on the umbilical cord
    • uterine atony
    • placenta previa
    • connective tissue disorders
  • S/S:
    • postpartum hemorrhage
    • hypotension
    • *Bradycardia – traction on uterine ligament
102
Q

Treatment of uterine inversion?

A
  • Immediate uterine relaxation followed by uterine contraction
    • Nitroglycerine
      • 50 – 200 mcg IV
      • 400 mcg sublingual
    • GETA with high dose VA
    • Monitor fluid volume status
      • Uterine contraction
        • Oxytocin
        • Hemabate
        • methergine
103
Q

What is normal blood loss during vaginal delivery? c section?

What defines post partum hemorrhage?

A
  • Normal Blood Loss
    • Vaginal delivery = 500 ml
    • Cesarean section = 800 – 1000 ml’s
      • Well tolerated d/t physiological increase plasma volume (compensates)
  • Post-partum hemorrhage
    • American College of Obstetrician and Gynecologists
      • > 1,000 ml’s
      • Signs and symptoms of hypovolemia
      • Within 24 hours of birth
      • US rate = 3%
        • Most common cause of maternal mortality world wide
104
Q

What is most common cause of severe post-partum hemorrhage?

A

Uterine Atony

  • Most common cause of severe post-partum hemorrhage
    • 80% of cases
  • Patho:
    • Uterine atony results from inability of uterus to contract and constrict uterine vessels
105
Q

Risk factors for uterine atony?

A
  • OB:
    • Multiple gestation
    • Polyhydramnios
    • high parity
    • prolonged labor
    • choriamnionitis
    • induced/augmented labor
    • c-section
  • Maternal:
    • advanced maternal age
    • hypertension
    • diabetes
  • Other:
    • tocolytic drugs – slows down labor
      • ex: Magnesium
    • high VA []
106
Q

What is commonly administered for uterine atony prophylaxis? side effects?

A

Oxytocin

  • First line drug therapy for uterine atony prophylaxis
  • Synthetic preparation with 6 minute half life
  • Rapidly metabolized by the liver and cleared in the urine and bile
  • Dosage:
    • 20 units/L crystalloid @ 200 – 500 ml/hour – (uncomplicated c/s)
      • can double if ineffective 40 Units
    • Some newer protocols:
      • Ex: 3 unit boluses of oxytocin, rest on infusion pump
  • Side Effects:
    • Vasodilation
    • Hypotension
    • Tachycardia
    • coronary vasoconstriction (don’t push large doses)
    • hyponatremia (with large dosages)
107
Q

What is second line for uterine atony? Side effects? CI?

A

Ergot alkaloids

  • Methylergonovine or ergonovine (methergine)
    • Dose: 0.2 mg IM Q 30 minutes x’s 1
    • Relative contraindications:
      • Hypertensive
      • CAD
      • preeclampsia
    • Side effects: Nausea/vomiting, increased blood pressure, chest pain, blurred vision and headache, seizure,
108
Q

What are 3rd line uterine atony treatment? side effects? C/I?

A

Prostaglandins

  • 15-Methylprostaglandin (carboprost) – Hemabate
    • Dose: 0.25 mg IM Q 15 min to 2 mg
    • Relative contraindications:
      • Reactive airway disease (asthma)
      • pulmonary hypertension
      • hypoxemia
    • Side effects: Bronchoconstriction, nausea, vomiting, diarrhea,
  • Misoprostol
    • Dose: 600 – 1000 mcg PR
    • Relative contraindications: None
    • Side effects: fever, chills, nausea, vomiting, & diarrhea
109
Q

Other treamtnets (besides medications) for uterine atony?

A
  1. Manual message
  2. Intrauterine balloon tamponade
  3. Uterine compression sutures
  4. Embolization of arteries supplying the uterus
  5. Cesarean hysterectomy
110
Q

What is considered Stage I uterine atony? Treatment?

A
  • BL:
    • > 500 ml vaginal
    • > 1000 ml cesarean
  • VS: Normal
  • Labs: Normal
  • Treatment:
    • Place 100% oxygen
    • Start large bore IV
    • increase IV fluids
    • T/C 2 units
111
Q

What is stage 2 for uterine atony? treatment?

A
  • BL:
    • > 1500 ml’s or
    • > 2 uterotonics
  • VS: Normal
  • Labs: Normal
  • Treatment:
    • Call for help
    • Start 2nd large bore IV
    • Draw stat labs (CBC, coags, fibrinogen)
    • Obtain 2 units RBC’s and FFP (1:1) → anticipate OR if not there already
      • Type specific better than O-negative
    • Provide analgesia
    • Prepare OR
112
Q

What is stage 3 uterine atony? treatment?

A
  • BL:
    • > 1500 ml’s EBL
    • > 2 units PRBC’s admin
  • VS/labs: abnormal
    • oliguria

Treatment:

  • Move to OR – mobilize additional resources
  • Initiate massive transfusion protocol
    • Fixed ratio transfusion (1:1:1)
    • Add cryoprecipitate, TXA, and calcium
      • TXA: crosses placenta
        • Recommendation: wait until cord clamped to admin
      • Cell salvage- possible
  • Factor VIIa - not recommended for routine use
  • Admin per TEG studies
113
Q

What is stage 4 uterine atony?

A

CV collapse

114
Q

What are goals of massive transfuion in OB patient?

A
  • Lactate- Decrease
  • Base excess- Normalize
  • Hemoglobin: > 7 g/dl
  • Platelets: > 50,000/mm3
  • Fibrinogen: > 200 mg/dl
  • INR: < 1.5 times normal
115
Q

What are some abnormal presentations of the fetus that can be seen during labor?

A

Breech

Transverse or Shoulder

  • Shoulder Dystocia
    • Emergency
    • Occurs after delivery of head, the shoulders cannot be delivered secondary to impaction on maternal pelvis
    • A/w:
      • Prolonged gestation
      • Labor induction
      • Obesity
      • High fetal wt
      • Prolonged dilation from 8-10 cm
      • Epidural analgesia
116
Q

What are some additional physiologic changes seen in patients with multiple gestations?

A
  • Approximately 1:150 births
  • Physiological changes
    • Accelerate and exaggerate physiological changes of pregnancy
    • Increased uterine size
    • Pulmonary
      • Reduced TLC and FRC
      • Aspiration risk - Increased
      • Tracheal intubation (Difficult)- Increased
    • CV
      • Additional 750 ml plasma volume increase
      • 20% greater increase in CO
        • SV 15%
        • HR 3%
      • Greater aortocaval compression
117
Q

Anesthetic management for labor and vaginal delivery of twins

A
  • Epidural – great flexibility and optimal analgesia
    • Low threshold to replace equivocal epidural
  • Move to OR for delivery
    • Establish 2nd large bore IV → increased risk for uterine atony and bleeding
  • Be ready to convert epidural from analgesia to anesthesia- supplement
  • In case of uterine inversion:
    • Nitroglycerin
      • 400 mcg sublingual or
      • 150 – 250 mcg IV
118
Q

Plan for vaginal twin A and operative twin B?

A
  • Vaginal Twin A/Operative Twin B
    • Epidural = same as vaginal devliery
    • May require rapid conversion to general anesthesia with high concentration of volatile anesthetic
119
Q

Planned cesarean delivery with twins?

A
  • Spinal vs CSE
  • Mean umbilical venous/arterial lidocaine [] were 35 – 53% higher in twin newborns compared to singletons (increased sensitivity to LA)
    • Increased plasma volume combined with a decreased plasma protein volume
    • Clinical relevance of these findings remain unclear (Chestnut – Chapter 34)
120
Q

What is preterm labor?

A
  • Regular contractions occurring b/t 20 – 37 wks gestation
    • Result: dilation or effacement of cervix
      • Approximately 8% - 10% of births in US
      • Indicated in 50 -80% of perinatal deaths
  • Survivability depends on:
    • gestational age
    • maturity of organ systems
    • weight
121
Q

Risk factors for preterm labor?

A
  • History of preterm delivery,
  • preterm rupture of membranes,
  • age (< 18 or >35),
  • trauma
  • , infection, s
  • moking,
  • drug history,
  • multiple gestation,
  • low socioeconomic status,
  • acute illness,
  • abdominal surgery during pregnancy &
  • abnormal uterine or cervical anatomy.
122
Q

Treatment of preterm labor?

A
  • Bedrest with FHR monitoring
  • Corticosteroids for fetal lung development (Betamethasone)
  • Tocolytics (suppression of uterine activity)
123
Q

What tocolytic agents are used during preterm labor? moa of each? s/e?

A
  • Magnesium
    • Same as before
  • Calcium channel blockers
    • Inhibit influx of calcium
      • Nifedipine PO
  • SE: Hypotension, flushing, dizziness, nausea

Tocolytics

  • Cyclooxygenase inhibitors
    • Blocks arachidonic conversion
    • Ex: Indomethacin
      • Maternal SE: Nausea/vomiting
      • Fetal SE:
        • constriction of ductus arteriosus
        • pulmonary HTN
        • renal dysfunction
        • intraventricular hemorrhage
  • Beta-agonists
    • Ex: Terbutaline
    • Smooth muscle relaxation (increase CAMP – activates protein kinase – inactivating myosin light chain kinase – decreasing contraction)
      • SE: Tachycardia, cerebral vasospasm, chest pain, arrhythmias, palpitations, hyperglycemia, hypokalemia, pulmonary edema
      • Fetal SE: tachycardia, hypoglycemia, hypocalcemia & hypotension
124
Q

Delivery durign preterm labor?

A
  • Goal is a slow controlled delivery with minimal pushing
  • Large episiotomy and low forceps are often used
  • Spinal/general
    • Complete pelvic relaxation
    • Better Apgar scores than with general
    • Minimize fluids with beta agonists – pulmonary edema
  • General
  • Fetus is more vulnerable to sedative effects of opioids and anesthetics
125
Q

What is an amniotic fluid embolism?

A
  • Rare but often fatal complication that can occur during labor
  • Pathophysiology remains poorly understood
  • Epidemiology
    • No universally accepted definition for identifying cases
    • Differing ascertainment methods yield different rates
    • Ultimately a diagnosis of exclusion
  • Society for Maternal-Fetal Medicine and Amniotic Fluid Foundation
    • Sudden onset of cardiovascular arrest or both hypotension and respiratory arrest
    • Documentation of overt DIC, after the appearance of initial signs or symptoms.
      • The coagulopathy must be detected before sufficient blood loss is lost to account for dilutional or shock related to consumptive coagulopathy.
    • Clinical onset during labor or within 30 minutes of delivery of the placenta
    • No fever during labor
126
Q

When do you need to notify the US amniotic fluid embolism registry?

A
  • Acute Hypotension or cardiac arrest
  • Acute hypoxia (dyspnea, cyanosis, or respiratory arrest)
  • Onset during labor, cesarean delivery, dilation & evacuation, or within 30 minutes post partum
  • Absence of an alternative explanation of the observed signs and symptoms
127
Q

Risk factors for amniotic fluid embolism?

A
  • Older age
  • Obstetric factors
    1. Abnormal placenta
    2. Placental abruption
    3. Eclampsia
    4. Multiple gestation
    5. Induction of labor
    6. Operative delivery
128
Q

Pathophysiology of amniotic fluid embolism?

A
  • Appears to be a systemic inflammatory response associated with inappropriate release of endogenous inflammatory mediators and platelet activation
  • Exact trigger is unknown
  • A rare pathologic fetal antigen
  • Usual antigen presented in an unusual way – amount, timing, or frequency of entry into circulation
  • Fetal cells, lanugo hair, and mucin into the maternal pelvic vasculature is a common event
    • However, pulmonary artery aspirates of patients without AFE have shown fetal material in it
  • Systemic inflammatory response:
    • arachidonic acid metabolites like thromboxane, prostaglandins, leukotrienes, and endothelins.
    • Fetal squamous cells release tissue factor which activates platelets to release thromboxane and serotonin
129
Q

Presentation of amniotic fluid embolism?

A
  • Presentation
    • Initial – Prior to delivery
    • Seizure, loss of consciousness, and profound dyspnea
    • Maternal symptoms appear BEFORE abrupt onset of variable decelerations and fetal bradycardia
  • Presentation Around Delivery
    • Acute cardiovascular collapse
    • Pulmonary hypertension
      • Right ventricular dilation, decreased CO & profound V/Q mismatch
      • ABG’s 30 minutes on 100% FiO2 = < 30 mmHg
    • Cardiovascular
      • Vary = ST segment/T wave abnormalities to arrhythmias or asystole
      • ECHO = dilated, akinetic RV with progressive dilation
      • Right ventricle dilation leads to decreased LV function and decreased CO
    • Massive hemorrhage & DIC
      • Thrombocytopenia and significant hypofibrinogenemia
130
Q

Treatment of amniotic fluid embolism?

A
    1. Maintain Oxygenation
      * Intubate and administer 100% oxygen
    1. Hemodynamic Support
      * Place a-line and central line as necessary
      * Administer fluids and vasopressors as necessary
      • Ensure left uterine displacement
        * TEE to guide fluid replacement therapy
        * Chest compressions as needed
    1. Correction of coagulation
      * Activate massive transfusion protocol
      * Serial laboratory assessments
      * Coagulopathy support: TXA, recombinant Factor VIIa, prothrombin complex concentrates, or fibrinogen concentrate
131
Q

Newer treatment strategies for AFE?

A
  • Cardiopulmonary bypass
  • Extracorporeal membrane oxygenation
  • Continuous hemofiltration
  • Medication regime (A-OK)
    • Atropine 1 mg
      • Blocks vagal reflex → blocks systemic hypoTN
    • Ondansetron 8 mg
      • Blocks serotonin pathway → ultimately decrease pulm vasoconstriction
    • Ketorlac 30 mg
      • Blocks thromboxane → typically releases inflam mediators
132
Q

Non-OB surgery in parturient patient?

A
  • Incidence of surgery → estimated at 0.75 – 2.2%
  • Indications: cervical incompetence, ovarian cysts, appendicitis, cholecystitis, malignancies, and trauma
  • Timing of surgery – Swiss Study
    • First trimester: 42%
    • Second: 35% (preferred- but not elective. Less risk)
    • Third: 23%
  • Practical considerations
    • Surgery should not be denied because of trimester considerations
    • Second trimester is preferred because of lowest risk of spontaneous abortion and preterm labor
    • Emergency surgery – primary goal is to preserve the life of the mother
133
Q

Fetal considerations during non-OB surgery in paturitent patient?

A
  • Teratogenicity
    • Most structural abnormalities result from exposure during organogenesis
      • 31 – 71 days after first day of last menstrual period
    • Physiological derangements
    • Diagnostic procedures
    • Drugs
      • No anesthetic agents is proven teratogenic in humans
      • Most anesthesia providers AVOID:
        • Nitrous oxide (inhibits methionine synthase)
        • Benzodiazepines – cleft lip/palate risk
134
Q

Preop considerations and choice of anesthesia in paturient patient undergoing non OB surgery?

A
  • Preoperative
    • Multi-disciplinary team available
    • Good airway exam (multiple different plans)
    • Pharmacological prophylaxis against acid aspiration (H2 blocker, reglan, bicitria)
      • > 12 weeks
  • Choice of Anesthesia
    • Local
    • Regional
    • Neuraxial
    • General – only if necessary (avoid if can)
135
Q

Monitoring and prevention of compression in paturient pt for non-ob surgery?

A
  • Monitoring
    • When fetus is viable (20 -24 weeks) and technically feasible
    • OB provider available for diagnosis and intervention
  • Prevention of compression
    • Beginning at 18 -20 weeks
    • Good left uterus displacement
      • When mom supine → significant hypoTN
136
Q

Anesthesia management of paturient patient in non-OB surgery?

A
  • De-nitrogenation
    • d/t dec FRC
  • RSI with cricoid pressure
  • Volatile, muscle relaxants, opioids, and reversals acceptable
  • No difference in maternal/fetal outcomes based on anesthetic agents
  • Maintain PaCO2 in normal pregnancy range
    • 28 – 32 mmHg
  • Avoid hypoxemia, hypotension, acidosis and hyperventilation
  • Use low pneumoperitoneum pressure and Trendelenburg position
  • Avoid NSAIDS – close PDA
137
Q

What is advanced maternal age?

A
  • Mothers > 35 years of age
    • > 35 = 20%
    • > 40 = 4 %
  • Higher morbidity and mortality for both mother and fetus
  • Increased risk for miscarriage, congenital anomalies, preterm delivery, placental abruption & c-section (2x’s more likely to request)
  • Focus patients co-morbid conditions
    • 38% had pre-existing condition
138
Q

What is TOLAC?

C/I? Risk?

A
  • Trial of Labor After Cesarean Section
  • C-section rate was 32% in 2016
  • Trial
    • Based on c-section type (classic vs low transverse)
    • 60 – 80% successful
  • Contraindications
    • Multiple gestations, two previous sections, severe preeclampsia, obesity, previous stalled labor
  • Risk
    • Uterine rupture
    • Uterine atony
    • Blood transfusions
139
Q

What is primary dysfunctional labor?

A
  • Failure of labor to progress normally
    • < 0.5 cm dilation during 1st stage of labor after active labor is established
    • > 2 hours pushing after full dilation and no change of station
  • Due to:
    • Ineffective uterine contraction
    • Arrest of cervical dilation
  • Treatment
    • Oxytocin
    • C-section
140
Q

What is chorioamnionitis? s/s? tx?

A
  • Intra-amniotic infection
  • S/S
    • Maternal leukocytosis
    • Maternal tachycardia
    • Fetal tachycardia
    • Uterine tenderness
    • Foul smelling odor
  • Tx
    • Antibiotics
    • Delivery
141
Q

Heart disease in pregnancy?

A
  • Affects up to 1.6% of all pregnancies
  • Leading non-obstetric cause of maternal mortality
  • Optimal management begins at conception
    • Consult cardiology early
      • Most already know about
    • Tailor anesthetic plan to exact lesion
      • ​severe AS, not good candidate neuraxial anesthetic
  • Regional anesthesia is good
    • Analgesia = decrease pain and lowers catecholamine release
      • Epidural = slow onset – easier to maintain hemodynamic parameters
        • better choice
    • Careful fluid administration
  • Always provide supplemental oxygen
  • SBE prophylaxis = consult with OB
142
Q

Diabetes and pregnnacy?

A
  • Occurs in about 3% of pregnancies
  • Blood sugar goal: 60 -120 mg/dl
  • Problems:
    • placental insufficiency
    • preeclampsia
    • hypertension
  • No evidence that one anesthetic technique is superior to another
  • Consequences:
    • Maternal: DKA, HHNC, hypoglycemia, macro/microvascular disease, stiff joint syndrome, diabetic nephropathy,
    • Fetal: large for gestational age (shoulder dystocia/birth trauma) and structural malformations
143
Q

Obesity in pregnancy?

A
  • Higher rates of chronic hypertension, gestational diabetes, preeclampsia and UTI
  • Increased risk of
    • premature labor,
    • low birth weight,
    • fetal/neonatal demise
  • Increased cesarean section rates, post partum hemorrhage, and hospital stays
  • Good preanesthetic evaluation
    • Particular to airway evaluation
    • Have multiple airway adjunct available
  • Establish IV access early
  • Apply supplemental O2
  • Establish epidural early – high failure rate
    • LA → lower dose req (smaller epidural space)
    • Ensure LUD
144
Q

Tobacco use in pregnancy?

A
  • Most common abused substance in pregnancy = 18%
  • Nicotine causes vasoconstriction and may decrease placental blood flow and oxygenation
  • Associated with
    • miscarriages,
    • IUGR,
    • placental previa,
    • abruptio placentae,
    • preterm delivery &
    • SIDS.
145
Q

Alcohol in pregnancy?

A
  • 9% of pregnant women between 15 - 44 report drinking in the past month
  • Associated with liver disease, coagulopathy, cardiomyopathy, and esophageal varices
    • Fetal alcohol syndrome – 33% of heavy drinkers
  • Acute intoxication:
    • GETA w/ RSI and aspiration prophylaxis
  • May also undergo acute alcohol withdrawal during the intrapartum or postpartum period = 6 to 48 hours after cessation
    • Nausea, vomiting, tachycardia, tremors, agitation, hallucinations and seizures
146
Q

Opioids abuse in pregnancy?

A
  • Multiple effects on mother and fetus
  • Increased risk for preeclampsia and bleeding
  • Continue opioids through peripartum course
  • May have increased opioid requirements
  • Monitor neonates for abstinence syndrome
147
Q

Cocaine abuse in pregnancy? consequence?

A
  • Consequences:
    • 1st trimester = congenital anomalies
    • 2nd/ 3rd = premature labor, IUGR, placental insufficiency, or placental abruption
  • Direct vasodilators to avoid CV and CNS complications
    • Tx hypoTN with direct acting agents
      • Ex: phenylephrine
  • General anesthesia may be associated with uncontrolled hypertension/tachycardia and dysrhythmias
  • Chronic a/w thrombocytopenia
  • Abuse Requirement
    • Chronic = decrease MAC
    • Acute use = increase MAC
148
Q

Marijuana use in pregnnacy?

A
  • Frequently used = 4.7%
  • Readily crosses the placenta – however, no know effects
  • Preterm labor and IUGR can occur
  • Long term users = increased secretions, impaired cough & potentially increased airway reactivity
149
Q

Amphetamine use in pregnancy?

A
  • Leads to indirect sympathetic stimulation (serotonin, norepi & dopamine)
    • Vasoconstriction with labile blood pressure and tachycardia
  • Both neuraxial and general anesthesia have been used
  • Acute use may increase risk for urgent cesarean section under general anesthesia
    • Treat like acute cocaine use

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