Week 13 - OB Complications Flashcards

1
Q

What are the risk factors for preeclampsia and eclampsia?

A
  • Primigravida
  • Chronic HTN
  • Diabetes (pre-existing or gestational)
  • Obesity
  • Family history of preeclampsia
  • Multiple gestation
  • Use of assisted reproductive technology
  • Homozygous angiotensin T-235
  • Chronic renal disease
  • Antiphospholipid syndrome
  • > 40 years old
  • African American race
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2
Q

What is preeclampsia?

A
  • Starts with an issue related to the utero-placental interface
  • The uterine spiral arteries don’t form correctly which leads to placental hypoxia
  • This leads to an increase in cytokines and inflammatory factors
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3
Q

What are the signs and symptoms of preeclampsia?

A

Hypertension: SBP >140 or DBP >90 occurring after 20 weeks gestation or in early postpartum (returns to normal within 3 months of delivery)

Proteinuria: >300 mg/24 hrs confirms but is not necessary to diagnose preeclampsia

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4
Q

In the absence of proteinuria, what is needed for preeclampsia to be diagnosed?

A

One of the Following:

  • Thrombocytopenia (platelet count <100,000)
  • Renal insufficiency (Cr >1.1 or doubling of Cr absent other renal disease)
  • Impaired liver function (elevated labs, LFT 2x normal)
  • Cerebral disturbances (headaches w/ hyperreflexia or visual disturbances)
  • Pulmonary edema or cyanosis
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5
Q

The imbalance of what two mediators is associated with preclampsia?

A

Prostacyclin and Thromboxane

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6
Q

What are the airway clinical features of preeclampsia?

A

Possibly upper airway edema

Pulmonary edema in 3% of pts due to:

  • high LAP and PCWP
  • low plasma colloid and osmotic pressure
  • increased capillary permeability
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7
Q

What are the cardiovascular clinical features of preeclampsia?

A

Clinical features are varied:

  • Hyperdynamic circulation – high CO, normal to increased SVR, normal or slightly decreased blood volume and preload
  • Normal CO, lower preload, increased SVR
  • Highly increased SVR, decreased blood volume and preload
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8
Q

What are the renal clinical features of preeclampsia?

A
  • Increased uric acid due to decreased excretion
  • Acute renal failure rare but possible
  • Beware of HELLP syndrome (increased renal and hepatic failure)
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9
Q

What is HELLP Syndrome?

A

Hemolysis, Elevated Liver enzymes, and Low Platelets

-mild self limiting to fulminant causing multiple organ failure

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10
Q

What are the lab values to diagnose HELLP syndrome?

A

Hemolysis: abnormal peripheral blood smear and increased bilirubin level

Elevated Liver Enzymes: AST >70, LDH >600

Low Platelet Count: <100,000 (assuming no other coagulation issues)

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11
Q

How do you treat preeclampsia?

A

Definitive Treatment = Delivery of fetus

  • Control HTN: hydralazine vs labetalol; NTG, Nifedipine, Esmolol
  • Prevent seizures: magnesium is drug of choice to prevent eclampsia and seizures
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12
Q

What is the anesthetic management for preeclampsia?

A
  • Detailed pre-op focused on severity of case: airway, fluid status, BP control, CBC, renal profile, LFTs, Coags IF abnormality suspected, platelet count needed before neuraxial block
  • Epidurals preferred for preeclampsia: gradual onset of blockade, CV stability and avoidance of fetal distress, reduce airway challenges
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13
Q

What are the comorbidities for obesity and pregnancy?

A
  • Gestational DM
  • Preeclampsia
  • Thromboembolic disease
  • Wound infections
  • C section
  • Adverse neonatal outcome
  • Increased surgical and anesthesia risk
  • Increased risk for postpartum hemorrhage
  • Magnifies pregnancy induced physiologic changes (FRC, GERD, Aortocaval compression, etc)
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14
Q

What are regional anesthetic considerations for obesity and pregnancy?

A
  • Increased difficulty
  • Recommend early epidural placement to ensure functioning catheter in case of C-section
  • Greater use of continuous SAB catheters (decreased incidence of PDPH – decreased amount of dural punctures)
  • Reduced dose of LA – avoid high spinal (decreased CSF volume w/ increased abdominal pressure pushes drug higher)
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15
Q

Why is there increased mortality with general anesthesia in obesity and pregnancy?

A
  • Rapid desaturation
  • Increased risk of regurgitation and aspiration
  • Difficult mask ventilation
  • Difficult OET
  • Difficult ventilation
  • Difficult positioning
  • Prolonged operation

*why we try to do regional anesthesia when we can

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16
Q

What are the causes of obstetrical bleeding during the peripartum period?

A
  • Placenta Previa (22% incidence of 3rd trimester bleeding) – occurs when placenta lies near the base of the uterus or across the cervix
  • Abruptio Placenta (31% incidence of 3rd trimester bleeding) – premature separation of normally implanted placenta after 20 weeks and before delivery
  • Placenta Accreta – accreta = onto myometrium, increta = into myometrium, precreta = through myometrium
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17
Q

What are the causes of obstetrical bleeding during the postpartum period?

A
– Uterine atony
– Retained placenta
– Vaginal Laceration
– Uterine rupture
– Uterine Inversion
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18
Q

What are the differential diagnoses of 3rd trimester bleeding?

A
  • Placenta Previa = painless vaginal bleeding, maybe or may not fetal distress
  • Abruptio Placenta = painful concealed bleeding, possible S&S of shock, probable fetal distress, possible coagulopathy
  • Uterine Rupture = SEVERE abdominal pain, likely S&S of shock, absent fetal heart tones
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19
Q

What is placenta previa and its hallmark sign?

A

Placenta is lateral, near, or across the os (normal placenta is at the top of the uterus)

  • With contraction, the placenta can be torn from the wall of the uterus
  • Hallmark is PAINLESS vaginal bleeding during 2nd or 3rd trimester
  • 5% of pregnancies at 4 months
  • Diagnosed with ultrasound
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20
Q

What are the risk factors of placenta previa?

A

Prior c-section or uterine surgery
Smoking
Multiparous
DM (large placentas)

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21
Q

How common are each type of placenta previa?

A

Total Previa = 40%
Partial Previa = 30%
Marginal and Low Lying = 30%

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22
Q

What is the anesthetic management for placenta previa?

A
  • Early eval and discuss options with mother – regional anesthesia is preferred (typically epidural)
  • OR set up in case of emergent c-section if bleeding becomes uncontrollable during vaginal delivery

*Depends on location of previa, amount of bleeding, and delivery expectation

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23
Q

What is Abruptio Placenta? What are the signs and symptoms

A

Placenta separates from decidua before delivery of the fetus
-fetal distress occurs due to loss of area for maternal-fetal gas exchange

Usually presents with PAINFUL vaginal bleeding (beware, uterus can hold 2500+ cc of blood with minimal external bleeding)
-shock, DIC, ARF, fetal demise due to hypoxia

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24
Q

What are the risk factors of abruptio placenta?

A
HTN
Increased age
Multiparity
Smoking
Cocaine
Trauma
Premature rupture of membranes
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25
Q

What is the anesthetic management for abruptio placenta?

A

Frequently requires emergent GA, RSI, C-section, aggressive volume resuscitation, and ICU stay

  • GETA, A-line, +/- CVC
  • 2 large bore IVs
  • Baseline Hct, coags, type & screen
  • Monitor for DIC (occurs in 30% of cases when fetal demise)
  • Deliver fetus and placenta
  • Replace maternal intravascular volume, correct coagulopathy
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26
Q

What is Placenta Accreta?

A

Abnormally adherent placenta:

  • accreta = adherence to myometrium (76%)
  • increta = invasion into myometrium (18%)
  • percreta = through myometrium into serosa and other pelvic structures (6%)
  • prior uterine trauma, prior c-section, and current previa are suspicious for accreta
  • can be diagnosed with ultrasound prior to delivery
  • may perform arterial embolization of some vessels to reduce blood loss
  • potential massive EBL indicates possible use of cell saver
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27
Q

What is the anesthetic management for placenta accreta?

A

GETA preferred as hysterectomy is likely as soon as the fetus is delivered (most common indication for postpartum hysterectomy in the US)

Regional technique is possible but not popular (pt discomfort, operating conditions, timing of removal of catheter, potential for DIC)

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28
Q

What is the most common cause of postpartum hemorrhage?

A

Uterine Atony

-can occur immediately or late postpartum

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29
Q

What are the risk factors of uterine atony?

A
Multiparity
High parity
Prolonged labor
Precipitous labor
Augmented labor
Tocolytics
High concentration of halogenated agents
30
Q

How is uterine atony treated?

A

Usually treated with uterine massage or meds

-may require hysterectomy if hemorrhaging

31
Q

What medications increase and which decrease uterine tone?

A

Increase: oxytocin, ergot akyloids (methergine), PGE2, hemabate (15-methyl PGF2a)

Decrease: magnesium, beta agonists, ethanol, methylxanthines, volatile anesthetics

32
Q

What is the treatment for retained placenta?

A

Retained placental fragments = leading cause of both early and late postpartum hemorrhage – possibly due to early oxytocin admin

Treatment involves:

  • manual removal of retained fragments
  • enhanced uterine tone via oxytocin
  • observation

*epidural anesthesia frequently adequate – SAB for pts w/o epidural

33
Q

What are the risk factors for uterine rupture?

A
  • Previously scarred uterus
  • Uterine manipulation
  • Trauma
  • Over aggressive labor augmentation (Pitocin)

*about 1% incidence in vaginal birth after c-section

34
Q

What are the ACOG recommendations for a vaginal birth after c-section (VBAC) trial?

A

OB capable of C-section be present and available for all VBAC trials of labor

Anesthesia be present for all VBAC trials

35
Q

What are signs and symptoms of uterine rupture?

A

Maternal hypotension with loss of uterine pressure monitor

Fetal bradycardia

*GETA for emergent laparotomy and c-section

36
Q

What is uterine inversion? How do you treat it?

A

Uterine fundus inverts through the vagina

  • usually results in hypotension
  • fluid restoration and replace the uterus
  • may need uterine relaxation to achieve (Mg Sulfate, Beta sympathomimetics, NTG)

*GETA via ETT w/ RSI w/ cricoid and inhaled anesthetics if conservative measures unsuccessful

37
Q

What are the classes of hypovolemic shock? What are the S&S of each?

A

Class I: 15% blood volume lost - minimal symptoms

Class II: 20-25% lost - orthostatic HoTN, narrowed pulse pressure, decreased peripheral perfusion, prolonged cap refill, peripheral vasoconstriction

Class III: 30-35% lost - overt HoTN, tachycardia, tachypnea, cold, clammy skin

Class IV: 40% lost - profound shock, unable to palpate BP or pulses, circulatory arrest, death

38
Q

What is Vasa Previa?

A

Umbilical vessels run through the amniotic membranes traversing between the presenting fetal part and the cervical os

  • suspected when vaginal bleeding is noticed upon rupture of membranes and fetal heart rate abnormalities – the bleeding is fetal because vessels torn, high fetal mortality
  • GETA is preferred because of true fetal emergency requiring emergent delivery to avoid fetal mortality
39
Q

How is prolapsed umbilical cord diagnosed?

A

With sudden fall in fetal heart rate with ROM in a pt with known abnormal presentation

  • confirmed with umbilical palpation on vaginal exam
  • must hold head off cord until delivery by C-section

Regional anesthesia is possible if indwelling epidural or very rapid SAB can be placed
*if any fetus distress at all –> GETA

40
Q

What does multiple birth pregnancy increases the incidence of?

A
  • Perinatal and maternal mortality
  • Premature labor and delivery
  • Abnormal presentation
  • Preeclampsia
  • Cord prolapse
  • C section
  • Uterine atony
  • Postpartum hemorrhage
41
Q

What is the anesthetic management considerations for multiple births?

A
  • Physiologic changes are amplified (FRC greatly decreased = increased hypoxemia, worsened aortocaval compression, increased risk of hemorrhage and atony)
  • Delivery – OB likes vertex presentation of presenting twin, if twin B has nonvertex presentation may be turned or c-section
  • Epidural is good
42
Q

What is a cervical cerclage? What are its complications?

A

A stitch placed in the cervix to keep it closed to prevent premature delivery

  • non emergent: 13-15 weeks gestation
  • usually removed around 37 weeks

Complications: rupture of membranes with placement, precipitation of labor, infection, damage to uterus

*MUST be removed prior to L&D

43
Q

What is DIC a response to?

A

DIC is a response to tissue factor VIIa complex exposure and activation of the extrinsic coagulation pathway

-trauma, AFE, malignancy, sepsis, incompatible transfusion may precipitate DIC

44
Q

What is the clinical presentation of DIC?

A

– Diffuse bleeding assoc with consumption of clotting factors and platelets
– Widespread microvascular thrombosis
– Underlying fibrinolysis

*About 50% of DIC cases result from pregnancy complications

45
Q

What is the progression of DIC?

A
  • Injury
  • TF release and activation of Extrinsic and Intrinsic pathways
  • Excess circulating thrombin – cleaves fibrinogen which causes multiple fibrin clots in the circulation, clots trap platelets, become larger clots, lodge in microcirculation, larger vessels, and organs – ischemia, organ damage
  • Inhibitors of coagulation also consumed – leads to more clotting, thrombocytopenia, lots of clots in the wrong places
  • Circulating thrombin converts plasminogen to plasmin – fibrinolysis, production of FDPs which are clot-busters which leads to more hemorrhage
46
Q

How do you treat DIC?

A

If low grade, chronic, subacute DIC = remove triggering mechanism (deliver the fetus and placenta)

If fulminant (hemorrhaging) DIC =

  • resuscitate mother for dual survival
  • large bore IV
  • transfuse blood products, crystalloids (Dextran containing colloids can worsen bleeding)
  • vasopressors frequently needed
  • if compromised airway GETA and ETT
  • monitor PT, PTT, FDP, Platelet counts
  • institute massive transfusion protocol
  • contact pathologist on call
  • maintain mothers temperature or you’re in trouble
47
Q

What is the headache in post dural puncture headache due to?

A

Traction on the meninges

Cerebral vasodilation to compensate for loss of intracranial volume

48
Q

What are the S&S of PDPH?

A
  • CSF when placing epidural (aspiration of CSF from epidural catheter - can occur in absence of noted CSF leak)
  • Headache (postural, neck tension, tinnitus, photophobia, N&V, severity of HA doesn’t correlate directly w/ volume of CSF lost)
  • Onset: typically 12-72 hrs
  • Duration: few days to six weeks
49
Q

How do you treat PDPH?

A

Non-Invasive: Analgesics, NSAIDs, Opioids, Hydration, Caffeine

Invasive:

  • Epidural blood patch (75-90% success, 10-20 mL autologous blood, sometimes need two patches)
  • Saline patch (less effective, high incidence of recurrence)
50
Q

What are the neurologic complications in OB?

A
  • Post dural puncture headache
  • Back pain
  • Nerve trauma
  • Hematoma
  • Abscess
  • Meningitis
  • Anterior spinal artery syndrome
  • Cauda equina syndrome (LA neurotoxicity r/t hyperbaric 5% lidocaine)
  • Lumbar plexus neuropathies (compression of lumbosacral plexus by fetal head or forceps)
  • Headache = most common, usually not emergent, rule out subdural, tumor, ASH, cortical vein thrombosis, and sinusitis
  • Spinal cord compression and ischemia (mass effect - abscess, hematoma, disc protrusion; loss of circulation, hypoperfusion)
  • 8% of ALL OB claims were for nerve damage
  • 90% of claims for nerves outside CNS (ulnar nerve, brachial plexus, lumbosacral nerve roots)
51
Q

What are possible central neurologic complications in OB?

A
  • Cortical vein thrombosis
  • Epidural needle trauma
  • Abscess unrelated to anesthesia
  • Backache with epidural
  • SAH during pregnancy
  • Epidural vein damage during -placement
  • Spinal hemorrhage after LP in anticoagulated
52
Q

What are possible peripheral neurologic complications in OB?

A
  • Paresthesia and motor dysfunction
  • Femoral nerve palsies
  • Lateral femoral cutaneous nerve
  • Lumbosacral cord
53
Q

When do the following sensory pathways cross the spinal cord?

  • pain and temp
  • proprioception and stereognosis
  • fine touch
A
  • Pain & Temp pathways cross almost immediately and ascend on the opposite side of the cord
  • Proprioception & Stereognosis remain on the same side of the cord until they reach the brain then cross over
  • Fine touch is crossed AND uncrossed - is preserved in unilateral lesions
54
Q

What is the most common cause of back pain in neurologic complications in OB?

A

Sacroiliac joint dysfunction – may persist up to one year post delivery

55
Q

What spinal level is disc herniation most common in OB?

A

Lumbar Disc Protrusion at L4-5 and L5-S1

  • straining, coughing, sneezing aggravates pain
  • straight leg raises reproduces pain
56
Q

What are the characteristics of a spinal/epidural hemotoma?

A
  • Acute hemorrhage usually presents with pain localized to the adjacent segments
  • Pain may be radicular and mimic a herniated disc
  • Location determines plegia (cervical = quad; thoracic/lumbar = para)
  • Majority occur in coagulopathic pts with difficult or traumatic placement

*requires surgical removal to prevent cord compression and paralysis

57
Q

What are the 4 stages of an epidural abscess?

A

Spinal Ache, Nerve Root Pain, Weakness (bowel and bladder dysfunction), Paralysis

S&S appear 3 days to months after injection
Early intervention results in complete recovery in 50-70% of pts

*very rare

58
Q

What is Anterior Spinal Artery Syndrome?

A

ASA provides blood to anterior 2/3 of spinal cord – ASA syndrome d/t decreased blood flow or thrombosis

  • motor weakness or paralysis; loss of pain and temperature sensation
  • 85% of women, Artery of Adamkiewicz supplies the conus medularis and originates T9-L2
  • 15% of women, the artery originate higher and the internal iliac artery supplies this area – susceptible to compression of this blood supply by the fetal head during delivery d/t location in the posterior wall of the pelvis
59
Q

What is adhesive arachnoiditis?

A

Inflammatory condition that results in the obliteration of the SAB space with adhesions

60
Q

What are the S&S of lumbosacral neuropathy in OB?

A
  • Numbness; dead feeling; asleep foot; pins & needles; thermal changes
  • Foot drop unilateral on side of brow descent
  • Postpartum c/o pain, numbness or tingling, heaviness or weakness
  • May limp or have diminished touch and pain sensations
  • May have loss of control over extensors of toes and dorsiflexors of ankle; foot drop
61
Q

What peripheral nerves are common for potential nerve damage in OB?

A
  • Peroneal nerve
  • Femoral (anterior crural)
  • Lateral femoral cutaneous (meralgia paresthetica)
62
Q

What is the etiology of fetal distress?

A

Insufficient O2 available to the fetus

  • initially shunts O2 from nonvital organs
  • eventually results in anaerobic metabolism and fetal acidosis
63
Q

What are the causes of decreased O2 supply to the fetus?

A
  • Maternal hypoxia
  • Maternal hypotension (decreased UBF)
  • Increased uterine pressure = contractions
  • Placental problems (abruption, gestational DM, toxemia of pregnancy)
64
Q

How is fetal distress diagnosed?

A

-Monitors have low positive predictive value so tendency is to “treat” all pts to avoid poor fetal outcomes

Fetal HR Monitor:

  • late decellerations
  • decreased variability
  • fetal tachycardia

Fetal Scalp pH testing: >7.25 WNL – 7.2-7.25 repeat – <7.2 prepare for delivery

65
Q

What are reversible causes of fetal distress? How are they treated?

A
  • Maternal Hypoxia: supplemental O2
  • Maternal Hypotension: IV fluids, ephedrine
  • Uterine Vasoconstriction: LUD, Reassure, relieve pain
  • Umbilical Cord Compression: change maternal position, amniotic fluid infusion
  • Uterine Hyperstimulation: Tocolytics
66
Q

What are causes of stable fetal distress? What is the anesthetic management?

A
  • Chronic uteroplacental insufficiency
  • Malpresentation
  • Previous lower segment C-section
  • Preeclampsia

Management: similar to elective c-section, RA preferred over GA, time is not really an issue

67
Q

What are causes of urgent fetal distress? What is the anesthetic management?

A
  • Failure to progress
  • Active herpes with rupture of membranes
  • Nonbleeding previa
  • Abruption without distress
  • Severe preclampsia or HEELP
  • Chorioamnionitis
  • Prolapsed cord without distress

Management: RA preferred to GA, indwelling epidural, SAB? preferred to epidural

68
Q

What are causes of emergent (STAT) fetal distress? What is the anesthetic management?

A
  • Agonal fetal distress
  • Prolapsed cord with distress
  • Placental abruption with distress
  • Massive hemorrhage
  • Uterine rupture

Management: if high indwelling epidural T10 or higher – augment and use it; GETA preferred over RA for true fetal distress

69
Q

What are the 4 primary causes of DKA in OB?

A
  • Relative insulin deficiency
  • Excess stress hormones
  • Lack of food
  • Dehydration
  • 90% fetal death rate with DKA
  • despite dehydration and hyperosmolarity, most are hyponatremic (insulin deficiency and glucagon excess exacerbate sodium loss in the urine, intracellular H2O shifts extracellular)
70
Q

What are OB anesthesia considerations for the diabetic patient?

A
  • Incidence of HTN and preeclampsia increased
  • Pts with nephropathy and DM more prone to pulmonary edema
  • Stiff joint syndrome
  • Higher morbidity
71
Q

How do you manage DM in an OB patient?

A
  • Diet control
  • Avoid hyperglycemia & hypoglycemia
  • Tight control during L&D period
  • Beware placental abnormalities
  • O2 release at the tissue level may be impaired due to maternal Hbg A1c levels
  • Altered buffering capacity in the fetus
72
Q

What are anesthetic considerations for DM in OB patient?

A
  • Acute hydration w/ dextrose free solutions
  • LUD is mandatory
  • Treat hypotension with ephedrine
  • Ester-type local anesthetics may be preferred
  • Long acting amides should be avoided
  • GA is fine if necessary