OBGYN Flashcards

1
Q

Risk factors for aspiration during pregnancy include:

A

Risk factors for aspiration during pregnancy include:
* Weakened lower esophageal sphincter tone; increased progesterone levels can weaken lower esophageal sphincter tone and increase the risk of gastroesophageal reflux in pregnant patients.
* Increased incidence of difficult airway due to swelling, airway mucosal friability, and weight gain
* Gastrointestinal system anatomical alterations due to enlarged uterus resulting in increased abdominal pressure and upward displacement

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2
Q

Justification for general vs. neuraxial anesthesia?

A

The choice of which type of anesthesia is administered for cesarean delivery (CD) depends on the urgency and patient factors, but, ultimately, experience and clinical judgment should always be used. When there is currently an epidural in place (whether it be an epidural alone, combined spinal anesthesia and epidural, or a dural puncture epidural), the epidural can be used for the CD.

If the patient does not have an epidural, the following questions must be answered:
* Does the patient require immediate delivery for maternal and/or fetal health?
* Is massive hemorrhage expected?
* Are there any contraindications to neuraxial anesthesia?

If the answer is “yes” to any of these questions, general anesthesia should be performed.

If the answer is “no” to all of these questions, the following questions must be answered:
* Is the duration of CD > 1.5 hours, or are multiple procedures planned?
* Does the patient have abdominal surgeries or previous CD (uterine scar)?
* Does the patient have risk factors that increase the risk of a poor outcome with general anesthesia (severe obesity, difficult airway, or history of malignant hyperthermia)?

If the answer is “yes” to any of these questions, an epidural can be placed and used for the CD. If the answer is “no” to all of these questions, spinal anesthesia can be performed.

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3
Q

The acid-base status of an otherwise healthy parturient is ________________.

A

The acid-base status of an otherwise healthy parturient is respiratory alkalosis with metabolic compensation.

Due to the effects of progesterone during pregnancy, maternal tidal volume increases by 50%, while respiratory rate remains mostly the same. The increased tidal volume increases minute ventilation with the levels of partial pressure of carbon dioxide in the arterial blood ranging from 27 to 32 mmHg in full-term parturients.

The respiratory alkalosis of pregnancy is compensated for by increased renal excretion of bicarbonate, and these combined physiologic changes result in a pH of approximately 7.44 to 7.46.

The changes in tidal volumes during pregnancy affect ventilation, oxygenation, and anesthesia management. The increased minute ventilation increases maternal oxygenation and causes a high-normal or slightly increased partial pressure of oxygen in the arterial blood. However, the decreased functional residual capacity and residual volume that also occur as the uterus expands during pregnancy render pregnant women more susceptible to hypoxemia in the supine or lithotomy position and during the induction of general anesthesia.

Additionally, the increase in tidal volume with the subsequent decrease in functional residual capacity and residual volume allows quicker equilibration of volatile anesthetics.

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4
Q

Describe the challenges with intubation of pregnant women.

A

The upper airway in pregnant patients becomes friable due to capillary engorgement. Edema of the oropharynx, larynx, and trachea begins to occur in the first trimester. Thus, when the airway is manipulated, there is an increased risk of bleeding. Because of this edema, mask ventilation, laryngoscopy, and intubation are more difficult. In addition, upon extubation, the edema can compromise the airway, leading to obstruction. Repeated attempts at laryngoscopy should be minimized, and a small diameter endotracheal tube (6-7-mm internal diameter) should be used.

The decreased FRC and RV that also occur as the uterus expands during pregnancy render pregnant women more susceptible to hypoxemia in the supine or lithotomy position and during the induction of general anesthesia.

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5
Q

Describe the changes that occur to minute ventilation in a pregnant woman?

A

To meet the increased metabolic demands during pregnancy, a woman’s minute ventilation increases throughout pregnancy to approximately 145% of normal nonpregnant minute ventilation. This effect is primarily due to increased tidal volume (from 450 to 600), with a small contribution from increased respiratory rate by 1-2 breaths/min). It is driven by the respiratory stimulant effects of progesterone, which shifts the carbon dioxide–ventilatory response curve to the left. Respiratory alkalosis occurs as the arterial partial pressure of carbon dioxide (PaCO2) is decreased by ∼ 10 mm Hg (from 40 to 30 mm Hg) by the end of the first trimester.

The respiratory rate then remains relatively constant for the remainder of the pregnancy. Despite respiratory alkalosis, the pH remains normal to only slightly elevated (7.40-7.44) due to compensatory metabolic acidosis. Serum bicarbonate (HCO3-) decreases to 20-21 mEq/L, and the serum base excess falls by 2-3 mEq/L. The increased minute ventilation improves alveolar ventilation, leading to an increase in PaO2. This increase is also due to the decrease in PaCO2 and a lower arteriovenous oxygen difference (which decreases the effect of venous admixture on PaO2).

MORE:
The increased progesterone during pregnancy leads to an increase in minute ventilation (as much as 50% at term), tidal volume (30%-50%), and respiratory rate (0%-15%). One to three weeks after pregnancy, ventilation returns to the nonpregnant levels.

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6
Q

The oxyhemoglobin dissociation curve shifts to the ______ during normal pregnancy.

A

The oxyhemoglobin dissociation curve shifts to the right during normal pregnancy (increased p50), allowing a greater volume of oxygen to be unloaded to the tissues (fetus) at a given arterial oxygen pressure.

TrueLearn Insight: The P50 of maternal hemoglobin during pregnancy increases from 26.8 mm Hg in the prepregnant state, to 30 mm Hg. This results in a rightward shift of the maternal oxyhemoglobin dissociation curve. The fetal oxyhemoglobin dissociation curve sits to the left of the normal adult and maternal dissociation curves. The P50 of fetal hemoglobin is 19-21 mm Hg. The increase in this gradient between P50 values of the mother and fetus facilitates oxygen unloading from maternal hemoglobin to fetal hemoglobin.

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7
Q

The normal FHR range is _____-______ bpm.

A

The normal FHR range is 110-160 bpm.

The normal FHR can vary from beat to beat and is referred to as “short-term variability” or “beat-to-beat variability.” The normal variation from one beat to another is 5-25 bpm. Variability in the FHR is a sign of a healthy autonomic nervous system, chemoreceptors, baroreceptors, and cardiac responsiveness. The FHR becomes nonreassuring if the variability is < 5 or > 25 bpm. A decrease in FHR variability can be due to fetal sleep state, fetal acidosis, or maternal sedation from drugs.
* Minimal variability is an amplitude of 5 bpm or less.
* Moderate variability is normal, with an amplitude range is 6 to 25 bpm.
* Marked variability has an amplitude range > 25 bpm.

Tachycardia may be secondary to fetal hypoxia, maternal fever, chorioamnionitis, anticholinergics, beta-agonists, fetal anemia, or tachyarrhythmias.

Bradycardia could be due to congenital heart block, beta-antagonists, hypoglycemia, hypothermia, or fetal hypoxia.

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8
Q

Variability of FHR is primarily influenced by ____________.

A

Variability of FHR is primarily influenced by the parasympathetic tone, with increasing tone exerting an increased effect on the heart rate, and therefore increasing variability.

This is evidenced by the fact that the maternal administration of atropine, which effectively eliminated the vagal tone in the fetus as it readily crosses the placenta, causes a decrease in FHR variability. Conversely, maternal administration of a beta-blocker which also readily crosses the placenta has minimal effect on the FHR variability.

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9
Q

How is early deceleration differentiated from late deceleration on FHR monitoring?

A

Early deceleration:
Early decelerations occur simultaneously with uterine contractions. The onset, nadir, and offset of each deceleration coincide with the onset, nadir, and offset of the uterine contraction. Head compression can precipitate early decelerations which are believed to result from reflex vagal activity secondary to mild hypoxia. Early decelerations are not ominous/not associated with fetal distress.

Late deceleration:
**Late deceleration starts after the onset of a uterine contraction with a nadir > 30 seconds after the onset of a contraction. **Late deceleration is most likely due to uteroplacental insufficiency/response to hypoxemia. The severity is determined by the magnitude of the deceleration. The delayed onset of the deceleration reflects the time needed for the chemoreceptors to detect decreased oxygen tension and change FHR via the vagus nerve. Late decelerations may also result due to myocardial failure secondary to decreased coronary blood flow.

VEAL CHOP
Variable - Cord compression
Early - Head compression
Accelerations - Okay
Late - Placental insufficiency

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10
Q

How are sustained variable decelerations treated?

A

Amnioinfusion (shown to decrease rate of C-Section)

Variable decelerations, as the name suggests, vary in depth, shape, and duration. They often are abrupt in onset and offset without coinciding with uterine contractions. Variable decelerations result from baroreceptor or chemoreceptor-mediated vagal activity. Umbilical cord occlusion, either partial or complete, results in variable decelerations.

A healthy fetus can typically tolerate mild to moderate variable decelerations without decompensation. With sustained, severe variable decelerations or persistent fetal bradycardia, it is difficult for the fetus to maintain cardiac output and umbilical blood flow.

MORE:
A variable deceleration reflects the fetal autonomic reflex response to transient mechanical compression of the umbilical cord. Umbilical vein and umbilical artery compression both occur. Initially, compression of the umbilical cord occludes the thin-walled and compliant umbilical vein. This results in decreased fetal venous return which triggers a baroreceptor-mediated reflex rise in FHR. Further compression occludes the umbilical arteries, causing an abrupt increase in fetal peripheral resistance and blood pressure. Baroreceptors detect the abrupt rise in blood pressure, triggering an increase in parasympathetic outflow and an abrupt decrease in heart rate. The reverse occurs as cord decompression begins. Prompt attention is required because ongoing hypoxic injury cannot be excluded.

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11
Q

In-utero resuscitation is indicated for fetal distress, with the goal of improving fetal oxygenation. Measures of in-utero fetal resuscitation include:

A

In-utero resuscitation is indicated for fetal distress, with the goal of improving fetal oxygenation. Measures of in-utero fetal resuscitation include:
* Repositioning of the mother to a lateral or “hands and knees” position
* Administration of supplemental oxygen (which is controversial)
* Administration of intravenous fluids
* Administer vasopressors if the patient is hypotensive
* Discontinuation of uterotonic drugs if these have been administered
* Administration of a tocolytic if sustained uterine contraction is suspected.

Fetal hypoxia mnemonic:
SPOILT: Stop oxytocin, Pressure (treat hypotension), Oxygen, Intravenous fluid bolus, Left lateral decubitus (or all fours), Tocolytics

Refractory late decelerations are an indication for emergent cesarean delivery after failure of in-utero resuscitation.

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12
Q

Describe the three stags of labor

A

Labor is divided into 3 stages.

The first stage begins with the maternal perception of regular, painful uterine contractions and ends with complete dilation of the cervix.

The second stage begins with complete dilation of the cervix and ends with the birth of the baby.

The third stage begins with the birth of the baby and ends with the delivery of the placenta.

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13
Q

Epidural analgesia is effective for treating pain in the first and second stages of labor.

What spinal segment coverage is required to relieve the pain of contractions and cervical dilation?

A

Epidural analgesia is effective for treating pain in the first and second stages of labor. T10 to L1 spinal segment coverage is required to relieve the pain of contractions and cervical dilation.

Note, S2-S4 spinal segment coverage is required to relieve the pain of vaginal and perineal distention. Not covered by epidurals.

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14
Q

Although spinal analgesia is effective for treating pain in the first and second stages of labor, it is not commonly employed because…

A

Although spinal analgesia is effective for treating pain in the first and second stages of labor, it is not commonly employed because it may affect the ability of the mother to push during delivery (may be used as a low-dose rescue technique near the time of delivery).

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15
Q

Pudendal nerve block helps relieve pain during the second stage of labor.

The pudendal nerve blocks somatic nerve fibers from what levels?

A

Pudendal nerve block helps relieve pain during the second stage of labor. The pudendal nerve includes somatic nerve fibers from S2-S4.

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16
Q

The lumbar sympathetic block is an effective regional anesthetic technique for first-stage analgesia. A lumbar sympathetic block interrupts the transmission of pain impulses from the cervix and lower uterine segment to the spinal cord.

The lower uterine and cervical visceral afferent sensory fibers join the sympathetic chain at what levels?

A

The lumbar sympathetic block is an effective regional anesthetic technique for first-stage analgesia. A lumbar sympathetic block interrupts the transmission of pain impulses from the cervix and lower uterine segment to the spinal cord.

The lower uterine and cervical visceral afferent sensory fibers join the sympathetic chain at **L2 and L3. **

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17
Q

How does pregnancy affect MAC?

A

The MAC of volatile anesthetics is reduced by about 30% during pregnancy.

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18
Q

Do volatile anesthetics cross the placenta?

A

YES, due to their high lipid solubility, non-ionized nature, and low molecular weight, volatile anesthetics rapidly cross the placenta.

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19
Q

How do volatile anesthetics affect uterine blood flow?

A

Volatile anethetics relax the uterine muscle and thus increase uterine blood flow.

Due to their tendency to cause uterine smooth muscle relaxation (decreased uterine tone), they are associated with increased blood loss during cesarean section. It is therefore recommended to use less than 1 MAC of volatile anesthetic and combine it with other agents such as nitrous oxide for maintenance of general anesthesia during cesarean section.

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20
Q

Pruritus is a side effect of opioids and is particularly prevalent with neuraxial opioids (60-80%). __________ is the drug of choice for the treatment of pruritus induced by neuraxial opioids.

A

Pruritus is a side effect of opioids and is particularly prevalent with neuraxial opioids (60-80%). ** Nalbuphine (mixed opioid agonist/antagonist) **is the drug of choice for the treatment of pruritus induced by neuraxial opioids.

When given in small doses (3 mg) Nalbuphine does not reverse the analgesic effect of neuraxial morphine.

Antihistamines actually have little or no effect on pruritis induced by neuraxial opioids (other than causing sedation).

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21
Q

By definition, amniotic fluid embolism (AFE) symptoms (hypotension in this case) must occur during or within _________ min/hour of labor, during cesarean delivery, during dilation and evacuation, or postpartum.

A

By definition, amniotic fluid embolism (AFE) symptoms (hypotension in this case) must occur during or within 30 minutes of labor, during cesarean delivery, during dilation and evacuation, or postpartum.

Amniotic fluid embolism is a diagnosis of exclusion but describes a syndrome of sudden peripartum shock characterized by pulmonary edema that has a mortality rate (up to 80%).

Amniotic fluid embolism accounts for up to 10% of all deaths for maternal mortality as a whole.

The etiology of AFE is unclear but may be due to the transfer of arachidonic acid metabolites (especially leukotrienes) and other vasoactive substances found in amniotic fluid to the maternal circulation. There may also be an immune-mediated response with massive mast cell activation.

The characteristic cardiac signs and symptoms of AFE may be divided into 2 stages.

Early-stage AFE generally lasts less than 30 minutes and is characterized by transient, often intense, pulmonary vasospasm. The resultant right heart dysfunction can progress to fatal right heart failure. The low cardiac output then leads to ventilation-perfusion mismatch, hypoxemia, and hypotension.

The second phase of AFE is characterized by left ventricular dysfunction or failure and pulmonary edema due to the previous right heart dysfunction. Right heart function may return to close to normal during this phase. Left or biventricular failure is often fatal unless supportive care is initiated.

Maternal coagulopathy occurs in most cases due to disruption of the normal clotting cascade, although the etiology is unclear. This can lead to massive hemorrhage, which then causes consumptive coagulopathy. The onset of maternal symptoms is quickly followed by spontaneous uterine hypertonus, which decreases placental perfusion and leads to profound fetal bradycardia (if the patient is still gravid). Therefore, fetal monitoring should be promptly initiated, and emergent cesarean section should be considered if AFE occurs while the fetus is in utero. Prompt diagnosis and initiation of supportive or resuscitative efforts are critical for maternal and fetal survival. Most mothers will require intubation for mechanical ventilation and oxygen. Cardiopulmonary resuscitation is often required, and cardiogenic shock must be managed. Large quantities of blood products are usually required, and efforts should be made to prevent or reverse coagulopathy via blood product transfusion.

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22
Q

Commonly used uterotonics include:

A

Commonly used uterotonics include:
* Oxytocin (Pitocin)
* Methylergonovine (Methergine)
* Carboprost (Hemabate)
* Misoprostol (Cytotec)

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23
Q

Asthma is a relative contraindication to the use of which uterotonic?

A

Asthma is a relative contraindication to the use of which carboprost.

Carboprost should be carefully administered to patients with a history of reactive airway disease as it can trigger bronchoconstriction. It is safe in patients with mild, asymptomatic cases of reactive airway disease

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24
Q

____________ is a uterotonic that is relatively contraindicated in patients with hypertensive disorders as it can concomitantly increase systemic blood pressure (by increasing systemic vascular resistance).

A

Methylergonovine (Methergine) is a uterotonic that is relatively contraindicated in patients with hypertensive disorders as it can concomitantly increase systemic blood pressure (by increasing systemic vascular resistance).

25
Q

Neonatal Resuscitation Algorithm

A
26
Q

Does neuraxial analgesia prolong labor?

A

YES, neuraxial labor analgesia does cause a slight (~15 min) prolongation of the *second stage *of labor.

It is also believed to cause maternal fever and higher instrumental delivery rate.

27
Q

Describe the mechanism of neuraxial opioid administration.

A

1) During neuraxial opioid administration, the binding of neuraxial opioids at presynaptic and postsynaptic neurons within the substantia gelatinosa of the spinal cord lead to suppression of substance P and glutamate secretion. The transmission of nociceptive information arising from the dorsal horn toward the brain (ie, ascending pathway) is inhibited via this process.

2) Effects in the brain and brainstem also occur through systemic absorption and passage through the cerebrospinal fluid, resulting in projections into the spinal cord that inhibit pain transmission from the dorsal horn as well. Direct effects on the medulla and periaqueductal gray areas that project neurons into the spinal cord cause inhibition of ascending pain transmission from the dorsal horn as well.

28
Q

Steps in managing patients with accidental high spinal include…

A

High/total spinal blockade occurs when the level of anesthesia rises and results in paralysis of the respiratory muscles and diaphragm (C3-5).

High/total spinal blockade can occur after an unintentional injection of local anesthetic into the subarachnoid or subdural space, often occurring around the initial spinal injection or epidural placement (or later with epidural overdose). Although initial aspiration of the epidural and negative test dose limit the possibility of intrathecal injection via the epidural catheter, migration into the intrathecal space can result in delayed high/total spinal blockade.

Patients will often present with symptoms such as agitation, dyspnea, difficulty with phonation, severe hypotension, bradycardia, and loss of consciousness. If high/total spinal blockade is suspected, communication should occur immediately with the patient.

**In pregnant patients, the patient should be placed in the left lateral position to avoid aortocaval compression (increasing blood return to the heart). If it is not already happening, maternal and fetal monitoring should occur (fetal heart rate and maternal heart rate, blood pressure, oxygen saturation, and electrocardiogram). The patient should be given 100% oxygen. If the patient cannot oxygenate or protect the airway, intubation should immediately occur. Cardiovascular stability should be maintained with vasopressors and intravenous fluids.
**
High/total spinal blockade does not equate to brain anesthesia, so, if general anesthesia does not occur, additional anesthetic agents are often required. Moreover, the loss of consciousness results from decreased cerebral perfusion, not brain anesthesia.

Although it is rarely used, CSF lavage is an alternative treatment for high/total spinal blockade.

TrueLearn Insight: As the neuraxial block rises, patients may experience a feeling of dyspnea. If the level increases to C6-8, the patient may feel numbness and weakness of the fingers. If the level rises to C3-5, the diagram may become paralyzed, and the patient may require intubation to protect the airway. When patients do experience the feeling of dyspnea, an assessment of grip strength can be performed rapidly. If the grip strength is strong, the diaphragm is unlikely to be affected; if it is weak, the patient should be continuously assessed to ensure the block does not continue to rise.

29
Q

What happens to platelet count during pregnancy?

A

Due to the increase in plasma volume, there is a dilutional effect on platelets, leading to a slight decrease (a 0%-10% decrease from baseline in most patients).

30
Q

Why is pregnancy considered a hypercoaguable state?

A

Pregnancy is a hypercoagulable state due to significant increases in procoagulant factors I (fibrinogen) and VII and smaller increases in other procoagulation factors. Anticoagulant factors such as antithrombin III and protein S are also decreased tilting the scale toward a hypercoagulable state.

These changes lead to a 20% decrease in prothrombin time (PT) and in partial thromboplastin time (PTT).

31
Q

Which coagulation factors are decreased during pregnancy?

A

XI, XIII

32
Q

Which coagulation factors are increased during pregnancy?

A

I, VII, VIII, IX, X, XII, von Willebrand factor

33
Q

Which anticoagulants are decreased during pregnancy?

A

Antithrombin III and Protein S

No Change in Protein C
(activated protein C resistance occurs but levels do not typically decline.)

34
Q

Drug properties that increase the placental transfer include:

A

Determinants of placental drug transfer include drug charge, lipophilicity, protein binding, tissue binding, pKa, pH, drug size, presence of placental efflux transporter proteins, and blood flow.

Drug properties that increase the placental transfer include small size (< 1000 daltons), uncharged form (pKa), lipophilic, low protein binding, and absence of an efflux transporter for the molecule.

Drugs that don’t cross: “He is going nowhere soon”
Heparin, Insulin, Glycopyrrolate, ND-NMBs, Succ

35
Q

During pregnancy, cardiac output increases up to ____% above the nonpregnant state.

A

During pregnancy, cardiac output increases up to **50% **above the nonpregnant state.

36
Q

Maternal blood volume is increased up to _____% during pregnancy. This effect is mediated by sodium retention via the renin-angiotensin system..

A

Maternal blood volume is increased up to 45% during pregnancy. This effect is mediated by sodium retention via the renin-angiotensin system..

37
Q

APGAR Score

A

The Apgar scoring system is a standardized, easy to perform, and relatively objective way to assess a newborn while performing neonatal care. Apgar scores are traditionally obtained at 1 and 5 minutes after delivery. If scores are low, further scoring can be done in 5- or 10-minute intervals as needed. The Apgar score includes the assessment of five parameters with a score of 0, 1, or 2 for each. See the table below for details.

Apgar scores help determine whether a neonate requires routine post-delivery care or more involved neonatal resuscitation. A score of 8-10 is considered a normal score where only routine post-delivery care is needed. A score of 4-7 suggests the need for close observation and more advanced care. A score of 0-3 suggests the need for immediate resuscitation. The Apgar score is not considered a true predictor of long-term neurologic outcome.

38
Q

Define preeclampsia

A

Preeclampsia is diagnosed by new-onset hypertension during pregnancy (after 20 weeks gestation) with proteinuria OR with severe features.

Diagnostic criteria for preeclampsia:
1) New-onset hypertension of systolic >140 mm Hg, or diastolic >90 mm Hg occurring after 20 weeks of gestation on at least 2 occasions at least 4 hours apart
and
2) Proteinuria of 300 mg >24 hours or a protein:creatinine ratio of ≥0.3

OR

Preeclampsia with severe features is diagnosed with signs and/or symptoms of end-organ ischemia:
1. Systolic >160 mm Hg or diastolic >110 mm Hg
2. Visual or cerebral symptoms (blurry vision, headache, altered mental status)
3. Thrombocytopenia <100,000 μL
4. Creatinine >1.1 or greater than 2 times the baseline creatinine level
5. Aminotransferase and alanine aminotransferase levels >2 times normal or right upper quadrant (RUQ) pain (due to hepatic inflammation and the stretching of the liver capsule)
6. Pulmonary edema

The diagnosis of preeclampsia can be made without the presence of proteinuria with the presence of elevated blood pressure plus any of the severe features listed above for points 2 through 6.

MORE:
Part of the pathophysiology of preeclampsia is thought to involve abnormal implantation of myometrial spiral arteries. Spiral arteries generally remodel during pregnancy to increase blood flow by increasing their diameter. However, during preeclampsia, the arteries are unable to remodel adequately, resulting in high resistance in arterial flow through these arteries causing an overall stress response that leads to the release of vascular mediators that dramatically increase the vascular tone causing an increase in vascular resistance. This increase in overall uterine vascular resistance decreases uterine blood flow. Because uterine blood flow is not autoregulated but rather blood pressure dependent, the maternal systemic vasculature will increase to provide an optimal pressure gradient of blood flow to the uterus. Preeclampsia affects approximately 5% of all pregnancies.

Overall, there are high levels of inflammatory cytokines that lead to a hypervasoconstricted state. Thromboxane increases both vascular tone and platelet aggregation, which increases the risk of thrombosis. Prostacyclin normally decreases both vascular tone and platelet aggregation, which decreases the risk of thrombosis. The high systemic vascular resistance leads to decreased renal blood flow causing renal insufficiency. Pulmonary edema can occur secondary to capillary leakage.

39
Q

Define severe features of preeclampsia

A

Preeclampsia - Severe Features:
- Severe HTN (greater than or equal to 160/110 mm Hg)
- Thrombocytopenia (less than 100,000/microliter)
- Elevated liver enzymes
- Persistent right upper quadrant abdominal pain
- Persistent cerebral symptoms, including visual
- Renal insufficiency (serum creatinine twice normal
- Pulmonary edema

40
Q

Preeclampsia risk factors:

A

A list of risk factors follows, with the most important factors at the top of the list:
- Antiphospholipid antibody syndrome
- Prior preeclampsia
- Chronic hypertension
- Diabetes mellitus (pre-gestational, type 1 or type 2)
- Obesity (pre-gestational or early pregnancy BMI > 30)
- Assisted reproductive technique (postulated to be due to limited preconception exposure to paternal sperm)
- History of placental abruption
- Multifetal pregnancy
- Chronic renal disease
- Prior stillbirth
- Advanced maternal age > 40 years
- Nulliparity
- Systemic lupus erythematosus
- Family history of preeclampsia
- African-American race
- Partner who fathered a preeclamptic pregnancy in another woman (through fetal genes)
- Teenage mother, primipaternity (postulated to be due to limited preconception exposure to paternal sperm)
- Hispanic ethnicity

Identification of risk factors is important because one intervention to prevent preeclampsia is available, namely administration of low-dose aspirin. Aspirin causes a 10% to 20% reduction in the risk of developing preeclampsia, possibly by reducing the thromboxane-to-prostacyclin ratio. Currently, the ACOG suggests daily low-dose aspirin, beginning in the late first trimester, specifically for women with a history of preeclampsia leading to prior preterm delivery before 34 weeks’ gestation, or preeclampsia in more than one prior pregnancy. However, as new studies help better delineate the risk factors for preeclampsia, more women could become candidates for prophylactic therapy in the future.

NOTE:
Smoking, however, is actually a dose-dependent protective factor for the development of preeclampsia. This effect may be due to nicotine inhibition of thromboxane A2 synthesis or stimulation of nitric oxide release.

41
Q

Placental abruption risk factors:

A

Risk factors for placental abruption include
* Maternal hypertension
* Preeclampsia
* Advanced maternal age (age > 35 years at time of delivery)
* Increasing parity
* Maternal and paternal tobacco use
* Cocaine use
* Trauma
* Premature rupture of membranes
* Chorioamnionitis
* Bleeding in early pregnancy
* History of prior abruption
* Increased incidence of placental abruption has been noted in African-American populations and in patients hospitalized for acute and chronic respiratory disease.

Placental abruption is characterized by complete or partial placental separation from the decidua basalis prior to fetal delivery. Placental abruption commonly presents with painful vaginal bleeding, uterine tenderness, increased uterine activity, and possible nonreassuring fetal heart rate patterns (secondary to loss of sufficient placental oxygen and nutrient exchange with the fetus). It can also present as idiopathic preterm labor. Diagnosis is predominantly clinical and while ultrasonography is not very sensitive (24%), it can aid in confirming diagnosis due to high specificity (96%).

42
Q

A blood gas taken from the umbilical artery of a term fetus would have the approximate values:
pH
PaCO2
PaO2
HCO3-

A

A blood gas taken from the umbilical artery of a term fetus would have the approximate values:
pH: 7.27
PaCO2: 50
PaO2: 18
HCO3: -2.7

43
Q

The combination of known placenta previa and ________ puts an obstetric patient at a dramatically increased risk for placenta accreta and peripartum hemorrhage.

A

The combination of known placenta previa and a history of multiple previous cesarean sections put an obstetric patient at a dramatically increased risk for placenta accreta and peripartum hemorrhage.

44
Q

A past history of _________ is the greatest predictor of a successful trial of labor after cesarean (TOLAC).

A

A past history of vaginal birth after cesarean (VBAC) is the greatest predictor of a successful trial of labor after cesarean (TOLAC).

Factors that tend to predict a successful TOLAC include
* Prior VBAC
* Younger maternal age
* TOLAC during spontaneous labor without augmentation or induction
* Advanced cervical dilation on presentation
* Lower prenatal BMI
* White race
* Nonrecurrent indication for the initial cesarean section such as breech positioning or fetal bradycardia

Factors that tend to predict an unsuccessful (failed) TOLAC include
* Prior cesarean section for anatomic issues such as dystocia, cephalopelvic disproportion, or failed induction
* The requirement for augmentation or induction
* Postterm gestational age
* No history of vaginal delivery
* Geriatric mothers (age > 35 years)
* Nonwhite race
* Prenatal maternal obesity
* Fetal macrosomia (> 4,000 g estimated fetal weight)

45
Q

The number one risk factor for placenta accreta is ___________.

A

The number one risk factor for placenta accreta is prior cesarean section with the current placenta overlying the uterine scar.

Other risk factors include
- advanced maternal age
- multiparity
- previous myometrial tissue damage (myomectomy, Asherman syndrome)

In any patient with a previous cesarean section, placenta accreta should be considered prior to subsequent deliveries. Management is planned preterm cesarean section with the placenta left in situ.

46
Q

_____________ is recommended as a fast and efficient tocolytic that resolves quickly.

A

Nitroglycerin is recommended as a fast and efficient tocolytic that resolves quickly.

An appropriate dose and route is 0.4 mg sublingual. If IV dosing is required, then 50 to 200 mcg IV is typical.

47
Q

Postdural puncture headache (PDPH) can present as early as the first time the patient sits up, but the typical presentation timing is ________ to _________ after dural puncture.

A

Postdural puncture headache (PDPH) can present as early as the first time the patient sits up, but the typical presentation timing is **6 to 72 hours **after dural puncture.

The incidence is approximately 50% when the dura is accidentally punctured with the epidural needle, but only in the low single digits if using a spinal needle, particularly when using a small-diameter pencil-tip needle. Therapeutic blood patch is very effective (90%)

Usually after traumatic dural puncture (with large bore Touhy needle) or lumbar puncture / drainage but can also occur with
regular spinal anesthesia using a 25G spinal needle

48
Q

PDPH Presentation

A
  • Positional headache (worse with standing, better with laying flat) often frontal/occipital
  • Associated with neck stiffness, nausea, and photophobia
49
Q

Risk factors for PDPH

A

Risk factors for PDPH
* Female sex
* Pregnancy
* History of headaches
* Extremes of age
* Volume of CSF removed
* Kow BMI

50
Q

Describe the MOA of magnesium as it pertains to treatment of preclampsia/eclampsia

A

Magnesium Sulfate (VAST):
* V: Vasodilator, smooth muscle relaxation
* A: Anticonvulsant
* S: Sedative, skeletal muscle relaxant (decreases release of ACh and decreases sensitivity of
motor endplate to ACh)
* T: Tocolytic, decreases uterine activity which increases uterine blood flow

51
Q

Symptoms of hypermagnesemia

A

Normal serum magnesium levels are between 1.5-2.5 mg/dL. Hypermagnesemia is > 2.5 mg/dL and can result from kidney impairment, overuse of magnesium-based laxatives or enemas, over-infusion of magnesium in preeclampsia treatment, and disorders such as milk-alkali syndrome. Hypermagnesemia results in neurotoxicity by decreasing transmission of the impulse across the neuromuscular junction resulting initially in diminished deep tendon reflexes. As the magnesium levels rise (see table below), the reflexes disappear. Cardiotoxicity results from magnesium acting as a calcium and potassium channel blocker, disrupting cardiac function and leading to complete heart block and cardiac arrest (> 12 mg/dL). Due to its calcium channel blocker effects, elevated magnesium levels can lead to hypotension, bradycardia, and ECG changes including prolonged PR interval and widened QRS. Of note, respiratory failure typically occurs prior to cardiac arrest.

Though magnesium toxicity from preeclampsia treatment is rare in women with good renal function, toxicity can still occur. Despite there being no consensus on the optimal treatment regimen, magnesium sulfate is commonly started at the onset of labor, induction, or prior to and during cesarean delivery. Usually, a loading dose is intravenously administered followed by a maintenance dose. In women with renal insufficiency, the maintenance dose should be lowered or not given. Clinical assessment of magnesium sulfate treatment should occur every one to two hours by assessing the presence of the patellar reflex. The loss of the reflex is the first sign of symptomatic hypermagnesemia. When renal function is normal and there are no signs of magnesium toxicity (see table below), serum magnesium levels are not required. Serum magnesium levels are checked if a seizure occurs during treatment, renal insufficiency is present (creatinine > 1.1 mg/dL), or there are signs of magnesium toxicity. If no toxicity occurs, total treatment should is usually for 24 hours postpartum with the therapeutic range for serum magnesium between 5-9 mg/dL.

52
Q

Physiologic changes during normal pregnancy include:

A
53
Q

The most reliable (sensitive and specific) sign of uterine rupture during labor is _____________________.

A

The most reliable (sensitive and specific) sign of uterine rupture during labor is** non-reassuring fetal heart rate (FHR) patterns.
**
Uterine rupture occurs when the integrity of the entire thickness of the myometrial wall is compromised, usually at the location of a previous uterine wall defect. It can result in fetal compromise or maternal hemorrhage and accordingly, requires timely cesarean delivery or postpartum laparotomy. Uterine rupture typically presents with vaginal bleeding, maternal tachycardia and hypotension, cessation of labor, abdominal pain, and/or fetal compromise. Among these, non-reassuring FHR patterns (e.g. fetal decelerations) are the most sensitive and specific sign of uterine rupture and occur in approximately 75% of cases. Diagnosis is then confirmed by manual exploration of the uterus or with a laparotomy. Risk factors for uterine rupture include a history of prior cesarean section, grand multiparity, fetal malpresentation, bicornuate uterus, prior myomectomy, and labor induction with oxytocin or prostaglandin.

54
Q

Which epidural local anesthetic has the fastest onset and shortest duration of action?

A

Epidural 2-chloroprocaine has an onset time of approximately 6-12 minutes, as a result of the high concentration of local anesthetic that is used.

The ester local anesthetic 2-chloroprocaine is most frequently used in the setting of obstetric epidural analgesia. Compared to other commonly used local anesthetics, is has the fastest onset of action time. 2-chloroprocaine has an onset time of 6-12 minutes, and that may be shortened slightly when high volumes are used. It is available in a 2% and 3% concentration. Duration of action is 45-60 minutes plain and 60-90 minutes when mixed with epinephrine (1:200,000 dilution). Chloroprocaine is hydrolyzed rapidly by plasma cholinesterases (half-life elimination of 21 seconds). However, metabolism is decreased in patients with a pseudocholinesterase deficiency. Chloroprocaine is commonly used to obtain rapid analgesia for an emergency cesarean section, when a working epidural catheter is already in place.

TrueLearn Insight: Administration of 2-chloroprocaine may decrease the efficacy of subsequently administered neuraxial drugs including bupivacaine, morphine, and fentanyl. Chloroaminobenzoic acid (the metabolite of 2-chloroprocaine) may be responsible for decreasing the efficacy of subsequent bupivacaine administration. Chloroaminobenzoic acid may also act as an antagonist of the µ-opioid receptor, leading to reduced efficacy of subsequent opioid neuraxial administration.

55
Q

Maximum allowable dose of the commonly used local anesthetic agents:
Lidocaine (plain): mg/kg
Lidocaine (with epinephrine): mg/kg
Bupivacaine (plain): mg/kg
Bupivacaine (with epinephrine): mg/kg
Ropivacaine (plain only): mg/kg
Chloroprocaine (plain only): mg/kg

A

It is important to know the approximate maximum allowable dose of the commonly used local anesthetic agents. These maximum dosages are irrelevant to the site of injection, and toxicity may occur at lower dosages if inadvertent direct vascular injection is made. Although not all sources agree on the maximum allowable dose, these doses are generally quoted:
Lidocaine (plain): 5 mg/kg
Lidocaine (with epinephrine): 7 mg/kg
Bupivacaine (plain): 2.5 mg/kg
Bupivacaine (with epinephrine): 3 mg/kg
Ropivacaine (plain only): 3 mg/kg
Chloroprocaine (plain only): 12 mg/kg

56
Q

Which epidural opioid lasts the longest? Fentanyl or Morphine

A

Fentanyl
Onset: 5-10 minutes
Duration: 1-2 hr duration

Morphine
Onset: 30-60min
Duration: 12-24 hr

57
Q

Which of the following spinal needles has a cutting tip?
Sprotte
Whitacre
Quincke

A

Quincke

Sprotte and Whitacre are pencil-point needles and are also known as noncutting point needles. Since they are noncutting they reduce the risk of postdural puncture headache.

“Sami Writes Queers are Cute”

NOTE:
The use of smaller guage needles is associated with decreased risk of postdural puncture headaches. On the other hand, higher guage needles provide better tactile sensation and have a lower failure rate than small guage needles.

58
Q

What is the most commonly used epidural needle?

A

Tuohy