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5th quarter > OB Exam #3 > Flashcards

OB Exam #3 Flashcards

1
Q

What does the term prematurity mean?

A
  • a birth before 259 days gestation?
  • Defined as regular uterine contractions that occur before 37 weeks gestation and result in dilation and effacement of cervix
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2
Q

What are some common risk factors for prematurity?

A
  • multifetal pregnancy

- preterm rupture of membranes

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3
Q

Define tocolysis:

A
  • stopping labor

- Tocolysis allows corticosteroids for fetal pulmonary maturation and antibiotics to decrease maternal chrioamnionitis.

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4
Q

What pre-existing medical conditions contributes the most to obstetric morbidity/mortality during delivery?

A
  • Pulmonary HTN(98:1000)
  • Malignancy(23:1000)
  • SLE(21:1000)
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5
Q

What are common causes of maternal death?

A
  • Hemorrhage
  • Embolism(amniotic fluid esp.)
  • Preeclampsia
  • Infection
  • CHF
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6
Q

What is the leading cause of preinatal morbidity/mortality?

A
  • Premature delivery

- 50% of all perinatal deaths

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7
Q

Premature labor definition:

A
  • Regular uterine contractions that occur before 37 weeks gestation, or before 259 days from last menstrual cycle
  • Contractions result in dilation or effacement of cervix
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8
Q

Common risk factors of premature labor.

A
  • Multifetal pregnancies

- Preterm rupture of membranes

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9
Q

Late preterm birth definition:

A
  • Those of 34-46 weeks gestation

- Compose 70% of all preterm births

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10
Q

Low birth weights defined:

A
  • Fetal size categories
  • Low birth weight: 500-2500g
  • Very low birth weight: 500-1500g
  • Extremely low birth weight: 500-1000g
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11
Q

T or F: Preterm labor diagnosis is facilitated by measuring fetal fibronectin and maternal cervical u/s.

A

True

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12
Q

What is Tocolysis?

A
  • Stopping labor(especially premature)
  • Often done for 48 hours
  • Critical Goal: allows for corticosteroid administration, which reduces the risks of the neonatal respiratory distress syndrome, IVH, NEC and overall perinatal death
  • Also, allows for latency antibiotic administration, promotes fetal maturation and decreases maternal chorioamniois.
  • As a general rule, if tocolytics are given, they should be given concomitantly with cortiosteriods
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13
Q

T or F: Although preterm labor is not well understood, there are 4 pathways that are well supported causes of preterm labor:

A
  • True
  • Myometrial and fetal membrane overdistention
  • Decidual hemorrhage
  • Precocious fetal endocrine activation
  • Intrauterine infection or inflammation
  • Substance abuse
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14
Q

Fetal Endocrine Signals and preterm labor:

A
  • Increased uterine contractility at term and preterm results from activation and then stimulation of the myometrium
  • Activation can be provoked by: mechanical stretch of uterus and by the endocrine pathway resulting from increased activity of fetal hypothalamic-pituitary-adrenal axis
  • Cortisol provides a crucial link to uterine stimulation: increased fetal production of PGs, corticotropin-releasing hormone output, ect.
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15
Q

When does the initial benefit of corticosteroid therapy occur?

A
  • 18 hours after administration of first dose

- Maximal benefit at about 48 hours

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16
Q

After what gestational age are tocolytics not used?

A
  • At or after 33 weeks

- Bc corticosteroids aren’t used after 33 weeks

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17
Q

Does using tocolytics improve outcome for mom/baby?

A
  • Growing evidence not to
  • Bacterial colonization of fetal membranes and amniotic fluid triggers and inflammatory response in the mom/fetus, leading to preterm labor and long-term neurologic/respiratory complications in the neonate
  • Prolong pregnancy in this state?
  • ?improvement in neonatal outcome with tocolytic use
  • Poor maternal/fetal side-effect profile
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18
Q

Agents used as tocolytics:

A
  • Beta adrenergic receptor agonists
  • Nitric oxide donors
  • Magnesium sulfate
  • Calcium channel blockers
  • Prostaglandin synthesis inhibitors
  • Oxytocin antagonists
  • NSAIDS
  • Labor inhibiting drugs are only marginally effective
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19
Q

What are the primary mechanisms of tocolytic agents?

A
  1. Through generation or alteration of intracellular messengers
  2. Blocking the action of a known myometrial stimulant
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20
Q

Tocolytic agent: Magnesium Sulfate

A
  • Causes relaxation of vascular, bronchial and uterine smooth muscle
  • Alters calcium transport and availability
  • Motor end plate sensitivity and muscle membrane excitability are also depressed
  • Hyperpolarizes the plasma membrane and inhibits myosin light-chain kinase activity by competing with intracellular calcium: reduces myometrial contractility
  • Antagonizes the vasoconstrictive effect of alpha-agonists, so ephedrine and phenylephrine are likely to be less effective to increase maternal BP
  • Eliminated unchanged by the kidneys
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21
Q

What is the normal serum MgSO4 level during pregnancy?

A

1.8 to 3 mg/dL

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22
Q

What serum magnesium level is therapeutic as a tocolytic?

A

4-8 mg/dL

even toxic levels do not eliminate uterine contractility

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23
Q

What does a serum mag level of 5 to 10 cause?

A

P-Q interval prolonged and QRS widening

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24
Q

What does a serum mag level of 10-12 cause?

A

the patellar reflex is eliminated

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25
Q

What does a serum mag level of 12-15 cause?

A

causes respiratory depression

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26
Q

What does a serum mag level of >15 cause?

A

leads to SA and AV node block

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27
Q

What does a serum mag level >18 cause?

A

respiratory distress progresses to apnea

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28
Q

What does a serum mag level of 25 cause?

A

cardiac arrest

women given magnesium must be monitored closely for evidence of hypermagnesemia

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29
Q

What are the side effects of Mag sulfate?

A
  • dose dependent
  • most frequent/serious: pulmonary edema!!
  • skeletal muscle weakness increases
  • CNS depression(sedation)
  • Vascular dilation
  • slight decrease in BP with epidural anesthesia
  • If in therapeutic range, no cardiac muscle effect
  • Ephedrine and phenylephrine are less effective
  • Neonatal SE are rare
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30
Q

T or F: Patients on Mag sulfate therapy have partial, if subclinical NMB.

A
  • True
  • both depolarizing and non-depolarizing NMB are potentiated by mag
  • Admin of priming/defasciculating doses of NMB may cause significant paralysis when combined with mag
  • The NMB effects of mag can be at least partially antagonized by: calcium
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31
Q

Is Magnesium Sulfate overdose treatable?

A
  • yes
  • D/C MgSO4
  • intubate and ventilate
  • IV Calcium Chloride
  • Diuresis to facilitate elimination of mag
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32
Q

Neonatal SE after maternal magnesium administration?

A

-Rare

After prolonged high-dose maternal mag sulfate: hypotonia & respiratory depression

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33
Q

Magnesium for preeclampsia, and other uses:

A
  • Preeclampsia: A vasospastic disease of pregnancy
  • can result in severe HTN, coagulopathy and seizure
  • Mag sulfate causes: relaxation of vascular smooth muscle, a decrease in SVR and a decrease in BP
  • At levels of 7-9.5, it is an anticonvulsant
  • It decreases fibrin deposition, improving circulation to visceral organs that are vulnerable to vasospasm and failure
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34
Q

Beta-agonist:

A

Stimulation of B2-receptors causes:

  • smooth muscle relaxation
  • uterine muscle relaxation

Stimulation of these receptors triggers a cascade of biochemical effects, resulting in:

  • Inhibition of myometrial contractility at the cellular level
  • Increase in progesterone production
  • Progesterone causes histologic changes in myometrial cells that limit spread of contractile impulses

-Myometrial relaxation caused by: B-agonist binding to B2-adrenergic receptors and subsequently increasing levels of intracellular cyclic adenosine monophosphate(cAMP), which activates protein kinase, inactivating myosin light-chain kinase, thus diminishing myometrial contractility

B2 stimulation also:

  • increases glucose and insulin levels
  • When B-agonist infusion is started, blood glucose level increases within a few hours and returns to baseline within 72 hours without treatment
  • Potassium is redistributed from the extracellular to the intracellular compartments: results in decrease serum K level, sometimes less than 3
  • Serum K levels return to baseline, also within 72 hours
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35
Q

T or F: Clinically used B-agonists cross placenta and have fetal and neonatal effects?

A
  • True
  • Fetal tachycardia(FHR > 160 bpm) common
  • Neonatal hypoglycemia, esp. if maternal serum glucose is elevated at delivery

(When maternal and therefore fetal blood glucose levels are elevated, the fetus increases insulin release in response…after delivery, the neonate continues to release insulin at increased rate, leading to hypoglycemia)

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36
Q

Terbutaline(Brethine, Bricancyl, other…):

A
  • Synthetic
  • Relatively B2-receptor-selective, noncatecholamine sympathomimetic amine
  • Due to the high incidence of tachycardia and other significant SE and its lack of efficacy, terbutaline use is currently discouraged
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37
Q

Nitric Oxide Donors

A
  • Vasodilator
  • Essential for the maintenance of normal smooth-muscle tone and is produced in a variety of cells
  • Increase cyclic guanosine monophosphate(cGMP) content in smooth-muscle cells: inactivates myosin light-chain kinases, leading to smooth-muscle relaxation
  • Example:NTG(bolus 1 mcg/kg)
  • Magnesium Sulfate superior to NGT
  • NGT rarely used due to maternal hypotension
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38
Q

Calcium channel Blockers:

A

-Nifedipine most common agent used
-It can be administered orally
-
CCB: inhibit the influx of calcium ions through the cell membrane and the release of intracellular calcium from the sarcoplasmic reticulum. This decreased intracellular free calcium, leading to inhibition of calcium-dependent myosin light-chain kinase-mediated phosphorylation, which results in myometrial relaxation.

Combination of magnesium and nifedipine is potentially dangerous: NMB effects that can interfere with pulmonary and cardiac function

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39
Q

Cyclooxygenase Inhibitors:

A
  • Cyclooxygenas converts arachidonic acid to prostaglandin H2(PGH2)
  • Prostaglandin H2 serves as a substrate for tissue-specific enzymes: critical to parturition(labor). Prostaglandins enhance formation of myometrial gap junctions and increase available intracellular calcium by raising transmembrane influx and sarcolemmal release of calcium.
  • Indomethacin is the most common used cyclooxygenase inhibitor
  • Indomethacin dose: Start 50-100 mg orally, and then maintain at 25-50 mg orally Q4 hours for 48 hours

Ketorolac: Is Not Indicated

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40
Q

Oxytocin Receptor Antagonists:

A
  • Atosiban: oxytocin receptor antagonist that blocks normal effects of oxytocin in the uterus.
  • Normally, oxytocin stimulates contraction by inducing the conversion of phosphatidyl inositol triphosphate to inositol triphosphate, which binds to a protein in the sarcoplasmic reticulum and causes the release of calcium into the cytoplasm
  • Reports of fetal deaths with atosiban administered before 28 weeks gestation have limited this agent
  • NOT FDA approved in the US
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41
Q

Regional Anesthesia and preterm delivery.

Anesthetic Considerations

A
  • When tocolysis fails, preterm deliveries are often done by C-section
  • 1 and 5 min APGAR scoring and maybe a 10 minutes if GETA
  • Patients on Mag Sulfate are often candidates for subarachnoid/epidural blocks as long as careful attention is devoted to volume status
  • Mag causes vasodilation, and maternal hemorrhage is tolerated poorly by parturients on mag
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42
Q

General anesthesia:

A
  • Succinylcholine: muscle relaxant of choice during the RSI of obstetric patient
  • If patient on mag, defasciculation with a small dose of a NDMR is not recommended: significant paralysis may results, increasing risk of aspiration
  • Mag potentiates depolarizing and esp. NDMR
43
Q

S/S of Cocaine Abuse:

A
  • HTN
  • Tachycardia
  • Hyperreflexia
  • Tremors
  • Acidosis
  • Emotional Lability
  • Dilated pupils
44
Q

Anesthetic considerations for the Parturient addicted to Cocaine

A
  • produces life-threatening complications usually associated with accumulation of catecholamines
  • May be present with signs that mimic toxemia(HTN, proteinuria, edema)
  • Most addicts receive little if any prenatal care
  • Urine tests may be positive for 24-72 hours, depending on amount last used
  • Most frequent problem with induction acutely intoxicated patient with GA: SEVERE HTN
  • MAC is increased in those acutely intoxicated
  • MAC is decreased in the chronic abuser(depletion of catecholamines): RISK of HYPOTENSION on induction

-Phenylephrine: more effective in this population than Ephedrine

45
Q

What is the most common potential etiologies of cardiac arrest during the hospitalization for delivery in the US?

A
  • hemorrhage
  • heart failure
  • amniotic fluid embolism
  • sepsis

Approximately 1 in 12000 hospitalizations for delivery is complicated by cardiac arrest.

46
Q

Thromoembolism:

A
  • Pregnant individuals 5 X more often than nonpregnant
  • Likely to occur POSTPARTUM than antepartum

Associated with:

  • Prolonged inactivity
  • C section delivery
  • Obesity
  • Increasing age
  • Increase parity
47
Q

S/S of Pulmonary Embolism:

A
  • Pleuritic chest pain
  • Dyspnea
  • Hyperventilation
  • Hypocapnia
  • Coughing
  • Hemoptysis
  • Distention of neck veins
48
Q

Venous Air Embolism(VAE):

A
  • Can occur during labor, spontaneous vaginal delivery and operative delivery
  • Frequently associated with placenta previa!!
  • During C Section, most VAE are detected between the time of delivery and uterine repair
  • Air is entrained into open maternal venous sinuses in the uterine wall when placenta separates or at the site of surgical incision
  • As air accumulates in pulmonary bed, resultant increase in PVR causes increase in CVP
  • A heavy, nonradiating, retrosternal chest pain may persist for 10 min after even a small VAE, dyspnea common
  • ETCO2 drops b/c CO2 cannot return to the lungs
  • Mill-wheel murmur may be heard over precordium as a frothy air-blood mixture moves through the heart
  • Murmur most pronounced when a large volume of air becomes trapped in the RV
  • If sufficient number of pulmonary arteries are affected, CV collapse can occur
49
Q

Amniotic Fluid Embolism(AFE):

A
  • Rare(1:20,000)
  • May occur during labor, vaginal or operative delivery and is occasionally associated with placental abruption
  • Pathogenesis:almost identical to venous air embolism except thatpatients who develop AFE are prone to develop DIC if they survive the initial insult
  • Amniotic fluid enters maternal circulation through breaks in uteroplacental membranes
  • Classic Triad:Acute hypoxemia, hymodynamic collapse(severe hypotension), and coagulopathy
  • Mortality rate >85%(10% of maternal deaths)
  • 2/3 deaths occur within 5 hours

common procedures high risk: C-section and laparoscopic procedures

50
Q

S/S of Amniotic Fluid Embolism:

A
  • chills
  • anxiety
  • cough
  • dyspnea
  • cyanosis
  • tachypnea
  • pulmonary edema
  • CV collapse
  • O2 sat decreases quickly
51
Q

Which method is the most accurate, sensitive diagnostic device for detecting AFE?

A
  • TEE!!!

- ETCO2 is readily available and can be used to help diagnose and start treatment

52
Q

T/F: Incidence of postpartum thromboembolism can be affected by anesthetic interventions.

A
  • True
  • C sections with GETA: associated with accelerated maternal coagulation c/t regional anesthesia
  • Anesthesia implications: provide adequate analgesia to mom afterwards, will enable activity
  • Epidural opioid analgesia!!!
53
Q

T/F: Air embolism occurs when open veins are above the level of the heart

A
  • True
  • However, head-up tilt of between 5-10 degrees does not appear to decrease the incidence of VAE during C-section and has increased hypotension

-Patrick: do chest compression b/c they have arrested!!! happnes very quickly

54
Q

What can anesthesia do if embolism is suspected during delivery?

A
  • Notify obstetrician immediately
  • OB doc can take steps to stop the entrainment of air/amniotic fluid: Flood surgical field with saline, return uterus to within the abdomen, stimulate uterine contractions
  • 100% O2
  • D/C N2O if in use(will rapidly expand volume of air embolus and prevents 100% O2 delivery)
  • Arterial line: monitor oxygenation and BP
  • If fetus not yet delivered, LUD improves uterine blood flow and facilitates hemodynamic stability
  • Pharmacologic support of CV system
  • Position patient slightly reverse trendelenburg(head up) with left lateral tilt of at least 15 degree: designed to trap air in the RA, from which it can be aspirated via a CVC
  • With amniotic fluid embolism: Treatment of coagulopathy and consult hematologist, support respiration and circulation, prepare for massive transfusion
55
Q

Maternal Diabetes and Pregnancy

A
  • DM is most common disorder associated with pregnancy
  • Type I DM(due to decrease in insulin secretion): occurs in 1 in every 700-1000 gestations
  • Gestational DM occurs in 2-5% of all pregnancies
  • Maternal and fetal mortality are higher in DM parturients
  • Glucose easily crosses placenta
  • Insulin does NOT readily cross the placenta
  • DKA: 8-9% of Type I pregnancies
  • Goal of insulin therapy: AVOID hypo and hyperglycemia!
  • Insulin requirements are increased during pregnancy
  • Preeclampsia and large-for-gestational-age fetuses occur more frequently in parturients with diabetes
  • Due to fetal macrosomia, C/S are more common in diabetics than non diabetics
56
Q

Placenta previa:

A
  • Placenta has implanted on the lower uterine segment and either partially or completely covers the opening of the cervix
  • Incidence: 1%
  • Mortality of those with PP: 1%
  • More common in women who have had it during a prior pregnancy, or experienced prior uterine trauma, multiparity, advanced maternal age, previous C/S

Classic signs:

  • PAINLESS vaginal bleeding before onset of labor that may stop without intervention or hemodynamically significant blood loss
  • No fetal distress during 1st bleed
  • Potential for SUDDEN loss of LARGE amounts of blood
  • Risk of bleeding increases if placenta is disturbed by manual exam of cervix
  • Postpartum bleeding: increased bc lower uterine segment, where PP was implanted, does not contract as well as remainder of uterus
  • Three variations of PP: Total, Partial, Marginal

-Fetus is at risk due to uteroplacental insufficiency 2* placental separation from uterus and preterm labor and its sequelae

-U/S: mainstay for confirming presence of placenta previa


57
Q

Placenta Previa: Vaginal or surgical delivery?

Anesthesia Implications

A
  • Surgical!
  • Prepare for increased blood loss
  • May choose either a general (if actively bleeding) or regional anesthetic (NOT actively bleeding)
  • Assess existing volume status for potential blood loss later
  • T&C minimum 2 Units PRBCs
  • Begin volume resuscitation with LR, NS, or Colloid
  • Consider Ketamine or Etomidate
  • Prepare for postop hysterectomy and large blood loss
58
Q

What conditions is MOST frequently associated with need for transfusion during or after C/S?

A

-Placenta Previa!!

59
Q

Abnormal Placenta implantion

A
  • Normal: endometrium
  • Abnormal: placenta on or in the myometrium, the underlying muscular layer of the uterus
  • Placenta accreta: on the myometrium
  • Placenta increta: Into the myometrium
  • Placenta percreta: completely through the myometrium
  • Abnormal: likely precludes complete separation of placenta from the uterine wall resulting in hemorrhage at delivery
  • Accreta, increta, and percreta: associated with placenta previa, and more common in women who have had previous c-section

-Often not diagnosed until the obstetrician has difficulty separating placenta from uterus during vaginal delivery

60
Q

Placental Abruption

A
  • Placenta begins to separate from the uterus before delivery
  • Allows bleeding behind the placenta and jeopardizes fetal blood supply
  • Results in hemorrhage (#1 cause of maternal death), uterine irritability, abdominal pain, and fetal hypoperfusion
  • Open venous sinuses in the uterine wall may allow amniotic fluid to enter the maternal circulation: increased incidence of DIC
  • Incidence much higher in women with HTN (up to 23% among women with preeclampsia), multiparity, advanced age, PROM, and hx of previous abruption
61
Q

Classic presentation of Placental Abruption

A
  • Vaginal bleeding
  • Uterine tenderness
  • Increased uterine activity
62
Q

Why does fetal distress occur with placental abruption?

A

-Loss of area for maternal-fetal gas exchange

63
Q

T or F: In cases of placental abruption without fetal distress, vaginal delivery may still be possible.

A
  • True
  • However, bc fetal distress can occur without warning, prepare to admin. general anesthesia for an emergency c-section
  • Perform preanesthetic eval ASAP, when 1st diagnosis of placental abruption becomes known
  • Confirm adequate IV access (large bore)
  • Aggressive volume resuscitation is critical
  • Operate if: mom or fetal distress
  • Consider Ketamine (
64
Q

What is the incidence of postpartum hemorrhage (PPH)?

A
  • About 4% of all parturients who deliver vaginally
  • Clinicians typically underestimate true blood loss
  • Aggressive treatment has potential to prevent the development of serious PPH
65
Q

Postpartum Hemorrhage (PPH).

A

May occur bc of:

  • Uterine atony (80% of all PP bleeding)
  • Placental retention
  • Abnormalities of uterus
  • Lacerations of cervix/vaginal wall
  • Uterine inversion
  • Coagulopathy
66
Q

Uterine atony

A

Associated with:

  • Multiparity
  • Prolonged infusions of oxytocin before delivery
  • Polyhydramnios
  • Multiple gestation
67
Q

T or F: A retained placenta or placental fragments must be removed manually.

A
  • True
  • NTG, a potent uterine relaxant with short duration, can be used to provide uterine relaxation adequate for placental extraction
  • SL NTG spray effective
  • Caution: NTG is potent smooth muscle relaxant/vasodilator…Ensure adequate intravascular volume present prior to administration
68
Q

When is an intrauterine balloon used?

A
  • When hemeostasis not achieved, despite vigorous fundal massage, pharmacologic adjuncts (oxytocin, ergot alkaloids, prostaglandins)
  • Balloon specifically designed for uncontrollable uterine hemorrhage
  • Placed in the uterine cavity
  • Filled with saline
  • Provides a tamponade effect
  • Balloon tamponade: minimally invasive, rapidly applied approach that can be used as a temporizing measure while other resources are being mobilized
69
Q

T or F: An atonic uterus, especially an incised uterus, can lose several liters of blood within a few minutes, outpacing the ability of even the most prepared anesthetist to replace intravascular volume.

A
  • True
  • Trauma mode!
  • Primary goal: Maintenance of vital organ perfusion and oxygenation
  • Maternal analgesia and amnesia are important, but is SECONDARY!
  • Safe trauma drugs: Etomidate, ketamine, benzodiazepines, opioids (result in minimal hemodynamic depression)
  • If rapid blood loss occurs during c-section with regional anesthesia, consider RSI and GETA
  • It’s difficult to manage volume resuscitation and keep an awake patient both mentally and physically comfortable
70
Q

When is the continuous epidural infusion routinely discontinued?

A
  • At completion of delivery and repair

- However, keep epidural catheter until maternal condition has stabilized

71
Q

Complete Uterine Rupture.

A
  • Nonsurgical disruption of all uterine layers
  • Involves entire thickness of the uterine wall and fetal membranes
  • Results in communication between the uterine and peritoneal cavities
  • “Sudden, sever, tearing abdominal pain in a multiparous woman in active labor”
  • Pain may suddenly break through a previously adequate labor epidural
  • Fetal distress often rapidly develops
  • Some ruptures occur during periods of mild labor
  • Bleeding often severe: uterus receives about 800 ml of blood per min (CO = 10%)
  • Mortality from uterine rupture accounts for half of the maternal deaths attributed to blood loss each year
  • Fetal mortality after uterine rupture: nearly 80%

**Clinical finding most commonly associated with uterine rupture: ABNORMAL FHR tracing!!

72
Q

Incomplete Uterine dehiscence

A
  • Does not include the entire thickness

- Maternal peritoneum remains intact

73
Q

Uterine rupture and dehiscence are most commonly associated with…?

A
  • Labor in the presence of a previous uterine incision (trial of labor after cesarean or TOLAC)
  • Also may occur in an unscarred uterus
74
Q

TOLAC

A
  • Most often successful if prior low-transverse uterine incision
  • Also success after previous vaginal delivery
  • Labor dystocia, maternal obesity, and the need for induction reduce likelihood of successful vaginal birth after c-section (VBAC)
  • Anesthesia providers MUST be immediately available!!
  • Neuraxial analgesia will enhance safety by affording the ability to rapidly provide surgical anesthesia if necessary
75
Q

Disseminated Intravascular Coagulation (DIC)

A
  • Generalized activation of the clotting system
  • Can occur when a large portion of the vascular system suffers damage or when thromboplastic material enters the general circulation

Frequently associated with 3 obstetric problems:

  • Intrauterine fetal demise
  • Placental abruption
  • Amniotic fluid embolism
  • Circulatory shock, which often accompanies DIC, worsens the problem: decreasing peripheral and hepatic blood flow and causing further cell damage
  • Renal failure may result: deposit of fibrin and cellular debris in the microvasculature
  • Consumption of clotting factors results in uncontrolled bleeding
  • Labs: Decreased levels of fibrinogen and platelets, increased prothrombin and partial thromboplastin times, excessive amounts of fibrin degradation products
76
Q

DIC definitive treatment.

A
  • Elimination of the cause
  • In the parturient, often requires evacuating the uterus
  • General anesthesia: due to clotting disorder…surgically remove uterus
  • Replace specifically depleted clotting factors and intensive support of accompanying multiple organ system involvement
  • No universally accepted treatment
  • Platelets, cryo, FFP should be administered to support platelet count and fibrinogen level
  • Fluid resuscitation due to hemorrhage
  • Increased peripheral and hepatic perfusion limits cellular damage and improves clearance of activated clotting factors
77
Q

Breech Presentation

A
  • Usually elective C-section
  • Either regional or general can be used
  • If vaginal delivery, strong recommendation of neuraxial anesthesia!
  • Increased incidence of umbilical cord prolapse
  • The pelvic muscle relaxation that is provided may aid in the delivery of fetal head
78
Q

Multiple Gestation

A
  • Associated with complications requiring emergent surgical intervention (esp. monoamniotic pregnancies)
  • Fetuses are often small and premature
  • Large uterus: aortocaval compression
  • LUD: maintained at all times
  • Epidural indicated if vaginal delivery
79
Q

Prolapsed Umbilical Cord

A

Prolapsed Umbilical Cord -Cord protrudes through the cervix ahead of the presenting part
-Cord may then be compressed against cervix: impaired flow to fetus

Maneuvers to restore blood flow:

  • Manual pressure against the presenting part to restore flow
  • Uterine relaxation
  • Emergency C-section
  • Choice of anesthetic: directed by urgency of the fetal condition
80
Q

Preeclampsia

A

Preeclampsia -Pregnancy specific multisystem disorder of unknown etiology

-Probable Cause: Imbalance between Prostacyclin and Thromboxane!!

  • Disorder affects about 5-9% of pregnancies
  • Significant cause of maternal and fetal morbidity and mortality
  • Highest incidence in primigravidas younger than 20 years or older than 35, women who have had preeclampsia during a previous pregnancy, as well as those with multiple gestation, DM type I, and Obesity (BMI >35)
  • Imbalance of prostacyclins and thromboxanes, both of which are produced by the placenta, has been demonstrated in preeclampsia

Defined:
-New-onset HTN and proteinuria after 20 weeks’ gestation

  • Mild: BP is higher than 140/90 and proteinuria is at least 300 mg/24 hr.
  • Severe: BP higher than 160/110 and proteinuria greater than 5 g/24 hr. Also, if BP and proteinuria increased substantially or symptoms of end-organ damage (including fetal growth restriction) occur

Additional symptoms Severe Preeclampsia:

  • Oliguria (less than 500 ml/24 hr)
  • Cerebral or visual disturbances
  • Pulmonary edema or cyanosis
  • Epigastric or RUQ pain
  • Impaired liver function
  • Thrombocytopenia
  • Intrauterine growth restriction
81
Q

Management of Preeclampsia before onset of labor

A
  • Close monitoring of maternal and fetal status
  • Management during delivery: seizure prophylaxis with mag sulfate, medical management of HTN
  • Delivery of fetus: ultimate treatment!!
82
Q

What is the chief cause of maternal mortality due to preeclampsia?

A
  • Cerebral hemorrhage caused by HTN

- Pulmonary edema, renal failure, hepatic rupture, cerebral edema, and DIC also associated with death

83
Q

Eclampsia

A

-Onset of seizures in a patient with S/S of preeclampsia

84
Q

Pathophysiology of Preeclampsia

A
  • Complex
  • Likely involves failure in normal placental angiogenesis resulting in decreased placental perfusion and placental infarcts
  • Placental ischemia worsens as pregnancy progresses, often causing intrauterine growth restriction
  • Hypoperfused placenta releases factors into the maternal circulation that damage the maternal endothelium: system-wide manifestations
  • Upper airway edema (already common in pregnancy) more pronounced
  • Decreased colloid osmotic pressure associated with urinary protein loss combined with increased vascular permeability predisposes parturient to pulmonary edema and resp. distress
  • CNS effects: h/a, hyper-excitability, hyperreflexia
  • Thrombocytopenia: occurs in up to 20% of women, r/t severity of the disease process
  • Increased vascular tone: hypersensitivity to endogenous catecholamines
  • SVR: increased, resulting in end organ ischemia
  • Plasma volume: normal in mild disease, but may be reduced by up to 40% in severe disease
  • Hepatocellular necrosis results in hepatic enlargement: lead to hepatic capsule rupture

***Hallmark diagnostic sign of proteinuria: occurs as a result of glomerular capillary endothelial destruction

85
Q

Additional Factors associated with Preeclampsia

A

-Immunologic Factors: imbalance of prostacyclin (PGI2), NO, Thromboxane

Genetic Factors:

  • Angiotensinogen
  • Angiotensin II Type I Receptor
  • Factor V Leiden: increased resistance to activated Protein C (predisposes parturients to thrombosis)

Endothelial Factors: Vascular endothelial damage and dysfunction is a common pathologic feature

Platelet Factors: Hypercoaguable

  • Calcium
  • Coagulation Factors
  • Fatty Acid Metabolism
86
Q

T or F: Delivery is presently the only definitive way of ending preeclampsia.

A
  • True
  • If gestational age > 37 weeks: deliver baby
  • If gestational age
87
Q

Obstetric Management of Preeclampsia

A
  • True
  • If gestational age > 37 weeks: deliver baby
  • If gestational age
88
Q

Regional Anesthesia and Preeclampsia

A
  • Regional analgesia and anesthesia preferred unless contraindicated
  • Epidural infusion: helps control HTN and may improve organ blood flow
  • During C-section: avoids stimulation of airway, which can aggravate HTN and possibly cause cerebral bleeding
  • During premature vaginal delivery: epidural analgesia allows a slower, more controlled delivery of infant and decreases likelihood of fetal head trauma
89
Q

Regional Anesthesia for Preeclampsia Considerations.

A
  • Thrombocytopenia and other coagulation problems associated with severe preeclampsia
  • Check coag and bleeding hx status prior to neuraxial block
  • A bleeding tim is NO LONGER considered an adequate method of assessing the risk of bleeding
  • Regional anesthesia generally not contraindicated in mild preeclampsia with platelet counts greater than 100,000, and considered betw 80,000-100,000 if PT/PTT/fibrinogen/INR are ok
90
Q

General Anesthesia and Preeclampsia

A
  • Most common indication: Coagulopathy, or serious deterioration in the maternal or fetal condition
  • Laryngoscopy results in exaggerated HTN response
  • Concomitant upper airway edema may make intubation more difficult
  • Difficulty in intubation increases the duration of airway stimulation and potentially worsens HTN
  • Challenge with induction: prevent further increase in BP, which may lead to intracranial hemorrhage
91
Q

What is the 1st line treatment of treating HTN during anesthesia of preeclampsia pt.?

A
  • Labetalol
  • Treat BP > 160 should be a guide in order to avoid intracranial bleeding
  • Esmolol: also can be safely given without significant neonatal effects
  • Opioids administered prior to delivery: Normally avoided as they can result in undesirable neonatal and maternal respiratory depression
  • Maternal resp depression: significant issue if failed intubation
  • Remifentanil: shown to blunt HTN response to laryngoscopy, but resulted in significant fetal resp. depression
92
Q

Beneficial Effects of Magnesium for Preeclampsia/Eclampsia

A
  • Anticonvulsant
  • Vasodilaton
  • Increased Uterine Blood flow
  • Antihypertensive
  • Increased prostacyclin release by endothelial cells
  • Decreased plasma renin activity
  • Decreased angiotensin-converting enzyme
  • Attenuation of vascular response to pressor substances
  • Reduced platelet aggregation
  • Bronchodilation
  • Tocolysis: improves uterine blood flow and antagonizes uterine hyperactivity
93
Q

Detrimental Effects of Magnesium

A
  • Tocolysis with prolonged labor and increased postpartum hemorrhage
  • Decreased FHR variability
  • Myoneural blocking effects
  • Generalized muscle weakness
  • Increased sensitivity to muscle relaxants, esp. NDMR
  • Neonatal effects: lower APGAR scores and decreased muscle tone (only with maternal overdose)
94
Q

Mg Therapy

A
  • Loading dose: 4-6 g
  • This raises Mg level to the high range of therapeutic almost immediately
  • This high-norm lasts about 1 hour, then returns to low level of therapeutic

-Maintenance infusion after loading dose: 2 g/hr

Magnesium Toxicity:

  • Controlled PPV (ETT)
  • IV Calcium Gluconate: 1 gm over 3 min
  • Subcut. Physostigmine: 0.5-1 mg
95
Q

NDMR

A
  • Markedly potentiated in preeclampsia women who have therapeutic levels of magnesium
  • Mag sulfate reduces the onset time of rocuronium and prolongs total recovery time by about 25%
  • If must use: small doses, and monitor with peripheral nerve stimulator
96
Q

HELLP Syndrome

A 
H = Hemolysis
E = Elevated 
L= Liver enzymes
L = Low
P = Platelet count

-From 5-10% of preeclampsia women develop HELLP syndrome

Clinical signs:

  • Epigastric pain
  • Upper abdominal tenderness
  • Proteinuria
  • HTN
  • Jaundice
  • N&V
  • Liver rupture (RARE)
  • Some believe that a degree of compensated DIC is present in all patients with HELLP
97
Q

What maternal catastrophes pose the greatest acute risk to fetus?

A
  • Hypoxia
  • Hypotension
  • Acidosis

-Also avoid Hyperventilation

98
Q

Anesthesia for the Pregnant Patient undergoing a Nonobstetric Procedure.

A
  • Happens often
  • Organogenesis: 15-56 days (3-8 wks). Most susceptible to teratogenic agents
  • Maternal risks associated with anatomical and physiological changes
  • Dx of abdominal conditions is usu. delayed in pregnancy leading to increased risk of maternal and fetal morbidity
  • BAD: hypoxia, Hypotension, and Acidosis
99
Q

Fetal risks associated with maternal surgery

A
  • Fetal loss
  • Increased incidence of preterm labor
  • Growth restriction
  • Low birth weight

**Clinical studies: suggest that anesthesia and surgery during pregnancy do not increase risk of congenital anomalies

100
Q

T or F: No anesthetic agent is a proven teratogen in humans.

A
  • True

- N2O in animals is known to be teratogen

101
Q

T or F: When performing a maternal laparoscopy, use an open technique to ender the abdomen when possible

A
  • True

- Maintain low pneumoperitoneum pressures or use a gasless technique

102
Q

T or F: Limit the extent of Trendelenburg or reverse-T positions and initiate any position slowly.

A

-True

103
Q

If you are a lone anesthetist, who is priority: mom or fetus?

A

-Care of the MOTHER

104
Q

Apgar Score

A

Derived from 5 parameters:

  • HR
  • RR
  • Muscle tone
  • Reflex irritability
  • Color
or backronym:
A = Appearance
P = Pulse
G = Grimace
A = Activity
R = Respiration
  • Assessment performed at 1 min and again at 5 min
  • Score is used to guide resuscitation
  • Score of 7-10: normal
  • 4-6: indicates moderate distress or impairment
  • 0-3: Need for immediate resuscitation

**Created by Dr. Virginia Apgar in 1952

5th quarter (11 decks)

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