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MFM Written/Oral Boards > Preeclampsia > Flashcards

Preeclampsia Flashcards

1
Q

How do you screen for preeclampsia

A

-Biomarkers and uterine artery dopplers have low positive predictive valves and therefore are not used in screening

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2
Q

Do you perform uterine artery Dopplers to assess risk for preeclampsia?

A

No. But there is promise with the uterine doppler in predicting risk for preeclampsia when combined with other risk factors. Thus far the risk factors will already prompt me to start low dose aspirin in patients at risk so I do not use uterine artery dopplers.

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3
Q

What are criteria to diagnose preeclampsia?

A
  • SBP >140
  • DBP >90
  • Pr:Cr >0.3 OR 24 hour urine >300mg
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4
Q

How do you diagnose preeclampsia with severe features?

A
  • SBP >160
  • DBP >110
  • LFT twice the upper limit of normal
  • Creatinine >1.1
  • Platelet <100
  • Pulmonary edema
  • Cerebral disturbance
  • Visual disturbance
  • persistent right upper quadrant pain
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5
Q

Can a patient have preeclampsia without proteinuria? Describe a scenario where this can occur?

A

Yes. HELLP syndrome

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6
Q

How do you define proteinuria?

A

> 0.3 in pr:cr
300 in 24 hour urine
Dipstick - 2+

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7
Q

What options are there for assessing proteinuria?

A
  • 24 hour urine protein
  • Pr:cr
  • UA dipstick
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8
Q

How do you manage a patient with preeclampsia diagnosed in the second trimester?

A

If viable, betamethasone, weekly lab surveillance, twice weekly antenatal testing. inpatient surveillance with severe features.

Deliver if non-viable

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9
Q

How do you manage a patient with preeclampsia diagnosed in the third trimester?

A

Deliver 48 hours after steroid completion if severe and persistent symptoms but with stable BP and labs or at 34 weeks in the setting of severe preeclampsia.

If without severe features and meets criteria for expectant management then manage outpatient and deliver at 37 weeks gestation

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10
Q

What is a therapeutic magnesium level?

A

4.8 - 9.6mg/dl

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11
Q

What is the role of magnesium levels?

A

Obtain magnesium levels in patients with high risk of toxicity due to underlying renal disease or injury (patients with increased serum creatinine >1.0 and oliguria <30ml/hr x 4hrs)

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12
Q

How do you manage magnesium in a patient with renal insufficiency?

A

Loading dose of 4-6 grams with infusion of 1 gram per hour and magnesium check every 4 hours.

If magnesium is over 9.6mg/dl then discontinue and check every 2 hours and restart infusion at lower rate (0.5grams) if magnesium level is less than 8.4mg/dl

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13
Q

What are signs and symptoms of magnesium toxicity?

A
  • Decrease in normal reflexes at 9mg/dl (7mEq/L)
  • Respiratory distress at 12mg/dl (10 mEq/L)
  • Cardiovascular collapse at 30mg/dl (25 mEq/L)
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14
Q

How do you manage magnesium toxicity?

A
  • 1 gram of calcium gluonate 10% IV administer 10ml over 3 minutes (side effect: resp depression if pushed too fast, acute hypertension )
  • Furosemide to promote renal clearance
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15
Q

What do you give for seizures refractory to magnesium?

A
  • Sodium amobarbital 250mg IV over 3 minutes
  • Thopental or phenytoin 1250mg IV at 50mg/min
  • Diazepam 10mg (should use as last resort due to decreased laryngeal reflexes)
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16
Q

Nifedipine dose and side effect

A

10mg-20mg immediate release PO, see effect in 10 minutes
Repeat dose in 20 minutes then every 2-6 hours thereafter

Maximum dose: 180mg

Side effect: headache, reflex tachycardia

17
Q

Hydralazine dose and side effect

A

5-10mg IV or IM, repeat BP in 20 minutes. Can give very 20-40 minutes.
Maximum dose: 20mg

(continuous IV dose of 0.5-10mg/hr)

Side effect: headache, hypotension, abnormal fetal tracings

18
Q

Labetalol dose and side effect

A

20mg->40mg->80mg IV, repeat BP in 20 minutes. onset is 1 minute
max dose: 300mg

Side effect: tachycardia

don’t use in women with asthma, heart block

19
Q

How do you manage the patient who has not responded to IV labetalol and hydralazine therapy?

A
  • ICU transfer
  • IV infusion with nicardipine or esmolol
  • Use sodium nitroprusside for extreme emergencies and use for short periods of time due to cyanide and thiocyanate toxicity of patient and fetus. It can also increase intracranial pressure which an worsen cerebral edema
20
Q

What are the indications for an arterial line?

A
  • For direct continuous intraarterial blood pressure monitoring for patients with:
  • Shock
  • Cardiac arrhythmia
  • Can also be used for frequent blood sampling
21
Q

What would make you suspect that your patient is developing pulmonary edema?

A
  • Decreased saturation
  • Dyspnea
  • Tachypnea
22
Q

What is your differential diagnosis for hypoxemia?

A 
Pulmonary edema
Pleural effusion 
Cardiac failure 
Pneumonia 
Pneumonitis
23
Q

How do you counsel a patient with preeclampsia about her risk of cardiovascular disease?

A
  • Increased risk of cardiovascular disease later in life (4-8 times increased risk)
  • Cardiovascular disease include MI, CHF, Hypertension
  • Cerebrovascular disease
  • Peripheral vascular disease
24
Q

What is the leading cause of maternal mortality in the US?

A

Preeclampsia (occurs in 5-8% of pregnancies)

25
Q

Risk factors for preeclampsia

A
  • majority occur in nulliparous women
  • AMA
  • Obesity
  • History of preeclampsia
  • cHTN
  • Diabetes
  • Multiple gestatation
  • Lupus
  • Sickle cell disease
  • Renal disease
  • Low socioeconomic status
  • long interval between pregnancy (10 years)
  • African American
26
Q

What are the moderate risks for preeclampsia? (requires 2 risks before aspirin recommendation)

A
  • Nulliparity
  • AMA
  • Family history of preeclampsia (mom/sis)
  • Low socioeconomic status
  • BMI >30 pre-gravid
  • Poor personal history (SGA)
27
Q

What are the high risks for preeclampsia? (requires 1 risk before aspirin recommendation)

A
  • DM
  • Multiple gestation
  • History of preeclampsia
  • CHTN
  • SLE
  • APS
  • Sickle cell disease
  • Renal disease
28
Q

Examples of visual disturbance of preeclampsia:

A

Amaurosis fuguax - temporary blindness due to cerebral edema
Retinal detachment- patient reports blindness in one eye
Scintillating scotoma - abnormal electoral impulses related to high blood pressure

29
Q

Pathophysiology of preeclampsia

A
  • Not clear
  • Incomplete trophoblastic invasion into spiral arteries
  • Immune response
30
Q

What are the vascular changes in pregnancy complicated with preeclampsia?

A
  • lack of hypervolemia (hemoconcentration)
  • Intense vasospasm from decrease in prostacyclin
  • Vasoconstrictors increase: Thromboxane A2 and endothelins
  • Vasodilators decrease : Prostacyclin and nitric oxide
  • Decreased oncotic pres. leads to pulm. edema
31
Q

What are the hematologic changes in pregnancy complicated with preeclampsia?

A

Thrombocytopenia results from platelet activation, aggregation, and consumption

32
Q

What are the hepatic changes in pregnancy complicated with preeclampsia?

A
  • ALT (alanine aminotransferase) can help differentiate from other causes of parenchymal liver disease
  • Specifically, liver disease not related to PES will show elevated ALT before AST
  • AST (aspartate aminotransferase) Dominant transaminase due to PES and is related to periportal necrosis
  • Initially will be increased to a greater extent than ALT
  • Bilirubin
  • Increased secondary to significant hemolysis
  • Usually develops only in the late stages of preeclamptic disease
  • Hepatic synthetic function decreases (prothrombin time, partial prothrombin time, and fibrinogen)
  • Evaluation of these parameters probably only useful w/ platelet count less 150x10 9
33
Q

What are the renal changes in pregnancy complicated with preeclampsia?

A
  • Glomerular endotheliosis
  • Proteinuria (non selective) due to increased tubular permeability (albumin, globulin, transferrin, and hemoglobin)
  • Urinary calcium decreases due to increased tubular reabsorption of calcium
  • Contraction of intravascular space from vasospasm incr. retention of sodium + water
  • vasospasm reduces GFR. increases serum creatinine…less filtering
  • ULTIMATELY OLIGURIA. urine output < 100 mL over 4 hours
  • Uric acid concentration in plasma NORMALLY increase late in pregnancy from:
  • Increased rates of fetal or placental production
  • Decreased albumin binding
  • Decreased uric acid clearance
  • IN PES PTs. Increases to a “greater extent” from increased reabsorption
34
Q

Hypertension and Preeclampsia Intervention Trial at Term (HYPITAT Trial) - published in 2009:

A

Population: Singleton pregnancies enrolled at 36 - 41 weeks with GHTN or mild preeclampsia

Intervention: Immediate induction

Control: Delayed induction

  • Primary outcome measure: progression of disease, hemorrhage
  • Conclusion: Induction of labor is associated with improved maternal outcome at 37 weeks
35
Q

What are maternal conditions precluding expectant management in a pregnant woman with preeclampsia?

A
  • Uncontrolled severe HTN
  • Persistent headache
  • Persistent RUQ pain
  • Persistent visual disturbance
  • pulmonary edema
  • eclampsia
  • MI/stroke
  • HELLP
  • creatinine > 1.1
  • acute placental abruption

abnormal fetal testing (reverse end diastolic velocity), fetal death or non-viable period

36
Q

recurrent risk of preeclampsia

A

10%

37
Q

Magnesium for prevention of eclampsia (MAGPIE) trial:

A

Population: Women with preeclampsia

Intervention: Magnesium

Control: Placebo

Outcome: eclampsia

Conclusion: Magnesium sulphate reduces the risk of eclampsia

MFM Written/Oral Boards (127 decks)

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