Mod VIII: Hypertensive Disorders during Pregnancy - Pre-eclampsia Flashcards
Definition of High-Risk Pregnancies
“High-risk obstetric patients include women with pre-existing medical problems as well as pregnant women experiencing complications of the pregnancy itself.”
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Anesthesia and the High Risk Parturient
Physiologic abnormalities that make a parturient a “high risk parturient” include:
Cardiac disease
Pre-eclampsia/HTN
Obstetric hemorrhage
Abnormal fetal presentation
Multiple gestation
Preterm labor
DM
Morbid obesity
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Anesthesia and the High Risk Parturient
Hypertensive Disorders during Pregnancy include:
Chronic HTN
Onset prior to 20th week gestation
No resolution PP
No proteinuria end-organ damage
Gestational HTN
Onset after mid pregnancy to 24 hrs. PP
Resolves within 10 days PP
No proteinuria/end-organ damage
Chronic HTN with superimposed Preeclampsia
Onset prior to 20th week gestation
Sudden increase HTN during pregnancy
Proteinuria present
Preeclampsia (PIH)
Mild
Severe
Eclampsia
Hypertensive Disorders during Pregnancy - Chronic HTN
When does Chronic hypertension start?
Chronic hypertension may precede pregnancy and
may or may not be complicated by superimposed preeclampsia
Onset is usually prior to 20th week gestation
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Hypertensive Disorders during Pregnancy - Chronic HTN
T/F: Chronic hypertension resolves PP
False
No resolution PP
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Hypertensive Disorders during Pregnancy - Chronic HTN
T/F: Chronic hypertension is associated with proteinuria end-organ damage
False
No proteinuria, No end-organ damage w/ chronic HTN
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Hypertensive Disorders during Pregnancy - Gestational HTN
When is the onset of Gestational HTN? When does it resolve?
Onset after mid pregnancy to 24 hrs. PP
Resolves within 10 days PP (this is why it’s called gestational)
Hypertensive Disorders during Pregnancy - Gestational HTN
T/F: Gestational HTN is associated w/ proteinuria and end-organ damage
False
No proteinuria/end-organ damage
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Hypertensive Disorders during Pregnancy
T/F: Proteinuria and End-organ damge are absent in both chronic HTN and Gestational HTN
True
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Hypertensive Disorders during Pregnancy - Chronic HTN with superimposed Preeclampsia
When is the Onset of Chronic HTN with superimposed Preeclampsia? How does it manifest?
Onset prior to 20th week gestation
Manifest as Sudden increase HTN during pregnancy
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Hypertensive Disorders during Pregnancy - Chronic HTN with superimposed Preeclampsia
T/F: Proteinuria is present in Chronic HTN with superimposed Preeclampsia
True
Proteinuria present
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Hypertensive Disorders during Pregnancy - Preeclampsia (PIH)
What are the different forms of Preeclampsia aka [Pregnancy-Induced Hypertension (PIH)]?
Mild Preeclampsia
Severe Preeclampsia
Can evolve into Eclampsia
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Hypertensive Disorders during Pregnancy
Development of HTN and proteinuria after 20 weeks gestation resolving within 48 hrs after delivery is also known as:
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Preeclampsia
Complicates 7% of all pregnancies
Major cause of maternal morbidity/mortality
20% of perinatal deaths
Multisystem disorder unique pregnancy
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Hypertensive Disorders during Pregnancy
Why is Preeclampsia a multisystem disorder unique to pregnancy?
A placenta is required for Preeclampsia
Mild Preeclampsia
How are SBP & DBP values in Mild Preeclampsia?
Mild Preeclampsia
SBP ≥ 140 mmHg or ≥ 30 mmHg above baseline
or
DBP ≥ 90 mmHg or ≥ 15 mmHg above baseline
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Mild Preeclampsia
How is Proteinuria w/ Mild Preeclampsia?
Proteinuria
UOP ≥ 500 mg/24hr
Urine protein < 5g/24hr
Urine protein ≥ 1+ dipstick
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Mild Preeclampsia
T/F: Edema can be a physiologic or pathologic occurrence w/ Mild Preeclampsia, but should not be used in the diagnosis
True
Edema can be a physiologic or pathologic occurrence w/ Mild Preeclampsia, therefore should not be used in the diagnosis of Mild pre-eclampsia
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Mild Preeclampsia
T/F: Evidence of other organ dysfunction is present in Mild Preeclampsia
False
Evidence of other organ dysfunction is NOT present in Mild Preeclampsia
Hypertensive Disorders during Pregnancy
T/F: Organ dysfunction is absent in Chronic HTN, Gestational HTN and Mild pre-eclampsia
True
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Severe Preeclampsia
What physiologic changes accompany Severe Preeclampsia?
Hypertension
SBP ≥ 160 mmHg or DBP ≥ 110 mmHg
Severe proteinuria
3-4+ dipstick / ≥ 5 gm/24hr
Oliguria
< 400 ml/24hr
Pulmonary edema
Thrombocytopenia
PLT < 150K
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Severe Preeclampsia
How are BP values w/ Severe Preeclampsia?
Severe Preeclampsia
SBP ≥ 160 mmHg or DBP ≥ 110 mmHg
Severe Preeclampsia
How is proteinuria w/ Severe Preeclampsia?
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Severe proteinuria
Urine protein ≥ 5 gm/24hr
Urine dipstick 3-4+
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Severe Preeclampsia
What’s the characteristic of oliguria in Severe Preeclampsia
Severe Preeclampsia
UOP < 400 ml/24hr
Severe Preeclampsia
What’s the characteristic of Thrombocytopenia in Severe Preeclampsia?
Severe Preeclampsia
PLT < 150K
Preeclampsia
Most of the significant morbidity and mortality related to Preeclampsia is found in which subset of the condition?
Severe Preeclampsia
Severe Preeclampsia
To meet the diagnosis criteria of severe pre-eclampsia, the pt must
Meet the mild pre-eclamptic criteria and
one or more of the Severe Preeclampsia criteria
(Hypertension*, Severe proteinuria, Oliguria, Pulmonary edema, Thrombocytopenia)
Severe Preeclampsia
Under which conditions could BP elevation be included in the diagnosis of severe pre-eclampsia?
BP elevation should occur on two occasions
6 or more hours apart in a pregnant woman on bedrest
before it can be said that they are serverely pre-eclamptic
Severe Preeclampsia
Organ system involvement in Severe Preeclampsia include:
Hepatocellular dysfunction
↑ Liver enzymes, Epigastric/RUQ pain
HELLP Syndrome
Hemolysis, Elevated Liver enzymes, Low PLT
Cerebral edema with visual disturbances
Headache, Blurred vision, LOC, Seizure (Eclampsia)
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Severe Preeclampsia
Hepatocellular dysfunction in Severe Preeclampsia is a/w:
↑ Liver enzymes
Epigastric/RUQ pain
(usually d/t liver edema or subcapsular hematomas)
Severe Preeclampsia
Epigastric/RUQ pain in Hepatocellular dysfunction due to Severe Preeclampsia is usually the result of:
Liver edema. or
Subcapsular hematomas
Severe Preeclampsia
Cerebral edema with visual disturbances in Severe Preeclampsia is a/w:
Headache
Blurred vision
LOC
Seizure (Eclampsia)
Severe Preeclampsia
HELLP Syndrome in Severe Preeclampsia is a/w:
Hemolysis
Elevated Liver enzymes
Low PLT
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Severe pre-eclampsia
Seizure is only present in which eclamptic subset?
Eclampsia
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Preeclampsia
Risk Factors of Preeclampsia:
Chronic HTN
Family Hx
Obesity
Prior pre-eclampsia
Nulliparity and young age
(never given birth or 1st pregnancy)
Advanced maternal age (>40yo)
African-Americans
Multiple gestations
DM
Chronic Renal Failure
Pathophysiology of Preeclampsia
OBSCURE & COMPLEX!!!
Uncertain etiology
Immunological - Genetic - Environmental
Exact mechanism unclear
Abnormal prostaglandin metabolism - Endothelial dysfunction
Vascular hyperactivity
Presence of placental tissue is necessary
Systemic disorder
Pathophysiology of Preeclampsia
Possible etiologies of Preeclampsia include:
Immunological
Genetic
Environmental
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Pathophysiology of Preeclampsia
Possible Pathophysiologic mechanisms of Preeclampsia include:
Abnormal prostaglandin metabolism
Endothelial dysfunction
Vascular hyperactivity
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Pathophysiology of Preeclampsia
T/F: Presence of placental tissue is necessary for Preeclampsia and the condition is a/w Systemic disorder
True
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CNS Manifestations of Preeclampsia:
Headache
Visual disturbances
Hyperreflexia
Focal hypoperfusion => Cerebral ischemia/infarction
Seizures (Eclampsia)
Edema
Intracranial hemorrhage => Leading cause maternal death in preeclamptic parturient
CNS Manifestations of Preeclampsia
What’s the Leading cause maternal death in preeclamptic parturient?
Intracranial hemorrhage
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CV Manifestations of Preeclampsia
Systemic vasoconstriction
↑ vascular response to SNS stimulation
LV hypertrophy → CHF & Pulmonary edema
Hemodynamic changes variable!!!*
CV Manifestations of Preeclampsia
Changes in Hemodynamic variable include:
↑ SVR
↓ CVP
PCWP can be unchanged or increased
CO can be Hyperdynamic or low
Most: Low C.O with normal filling pressures & ↑ SVR
CV Manifestations of Preeclampsia
For the most part, how does Preeclampsia affect CO?
Lowers C.O with normal filling pressures & ↑ SVR
CV Manifestations of Preeclampsia
What causes Contracted vasculature in Preeclampsia?
Fluid/protein shift from intravascular to interstitial
(this is d/t ↓ colloid oncotic pressure/↑ capillary leakage)
CV Manifestations of Preeclampsia
What are the net volume, hemoconcentration, and electrolyte changes caused by a contracted vasculature in Preeclampsia? What aggravates these effects?
Hypovolemia - Hypoproteinemia
Hemoconcentration → ↑ blood viscosity
Pulmonary edema
(Non-cardiogenic vs. cardiogenic)
Aggravated by proteinuria!!!!
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Hepatic Manifestations of Preeclampsia
Periportal necrosis
d/t ↓ blood supply to liver
Subscapular hemorrhage
evidenced by Epigastric/RUQ pain
Rupture of overstretched liver capsule
Leads to Massive hemorrhage into abdominal cavity
Elevated liver enzymes
HELLP syndrome
Stands for Hemolytic, Elevated Liver enzymes, Low Platelets
Hepatic Manifestations of Preeclampsia
Decreased blood supply to liver in Preeclampsia could result in:
Periportal necrosis
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Hepatic Manifestations of Preeclampsia
The Epigastric/RUQ pain seen in Preeclampsia is often the result of:
Subcaspular hemorrhage
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Hepatic Manifestations of Preeclampsia
Massive hemorrhage into abdominal cavity in preeclampsia is often the result of:
Rupture of overstretched liver capsule
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Renal Manifestations of Preeclampsia:
How could swelling of glomerular endothelial cells and deposition of fibrin affect renal capillaries?
Renal capillary constriction
Renal Manifestations of Preeclampsia:
What are the consequences of Renal capillary constriction from Swelling of glomerular endothelial cells and deposition of fibrin?
↓ Renal blood flow
↓ GFR
Oliguria
Proteinuria
Na+ & H20 retention (edema)
↓ urea & creatinine clearance
Acute tubular necrosis
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Pulmonary Manifestations of Preeclampsia:
Upper airway narrowing from pharyngolaryngeal edema
(Leading to Respiratory compromise and Difficult intubation)
Pulmonary edema
(D/t ↑ capillary permeability, ↓ colloid oncotic pressure, Heart failure and Circulatory overload)
Pulmonary Manifestations of Preeclampsia
What’s responsible for Respiratory compromise and Difficult intubation a/w Preeclampsia?
Upper airway narrowing from Pharyngolaryngeal edema
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Pulmonary Manifestations of Preeclampsia
What’s responsible for Pulmonary edema a/w Preeclampsia?
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↑ capillary permeability
↓ colloid oncotic pressure
Heart failure
Circulatory overload
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Pulmonary Manifestations of Preeclampsia
Upper airway narrowing from pharyngolaryngeal edema can cause:
Respiratory compromise
Difficult intubation
(especially if the pt is already experiencing edema and swelling b/c of the increased blood volume and airway changes that occur normally w/ pregnancy)
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Pulmonary Manifestations of Preeclampsia
What are cause of Pulmonary edema a/w Preeclampsia?
↑ capillary permeability
↓ colloid oncotic pressure
Heart failure
Circulatory overload
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Uteroplacental Manifestations of Preeclampsia:
Vasoconstriction/occlusive lesions
Hyperactive/Hypertonic Uterus
(could lead to premature labor)
Uteroplacental Manifestations of Preeclampsia
Vasoconstriction/occlusive lesions from Preeclampsia cause decreased intervillous blood flow (despite ↑ maternal BP). What are the possible negative consequences of decreased intervillous blood flow?
Uteroplacental hypoperfusion
Placental Abruption
Ischemia/infarction → necrosis of supporting placental structure => Placental Abruption
Chronic fetal hypoxia
Fetal malnutrition (IUGR)
Preterm L/D
Perinatal death
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Uteroplacental Manifestations of Preeclampsia
How could Hyperactive/Hypertonic Uterus from preeclampsia affect the process of labor?
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Could lead to premature labor
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Uteroplacental Manifestations of Preeclampsia
T/F: Vasoconstriction/occlusive lesions from preeclampsia could lead to decreased intervillous blood flow despite increasedd in maternal BP
True
Decreased intervillous blood flow occurs despite increase in maternal BP
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Uteroplacental Manifestations of Preeclampsia
Vasoconstriction/occlusive lesions → ↓ intervillous blood flow despite ↑ maternal BP - What are the consequences of this?
Uteroplacental hypoperfusion
Ischemia/infarction → necrosis of supporting placental structure
=> Placental Abruption
Chronic fetal hypoxia
Fetal malnutrition (IUGR)
Preterm L/D
Perinatal death
Coagulation Manifestations of Preeclampsia:
Consumption coagulopathy
PLT adherence at sites of endothelial damage
Activation of fibrinolytic system
DIC
Thrombocytopenia
PLT <100K correlates with severe disease
Prolonged PTT
↓ fibrinogen
↑ D-dimer (DIC specific)
↑ incidence of placental abruption => DIC
Coagulation Manifestations of Preeclampsia
How does Consumption coagulopathy a/w Preeclampsia manifest?
PLT adherence at sites of endothelial damage
Activation of fibrinolytic system
DIC
Coagulation Manifestations of Preeclampsia
Thrombocytopenia in severe preeclampsia manifest as a plt count of which values
PLT <100K
correlates with severe disease
Coagulation Manifestations of Preeclampsia:
How is PTT in preeclampsia?
Prolonged PTT
Coagulation Manifestations of Preeclampsia
How is fibrinogen in preeclampsia?
Fibrinogen is decreased
Coagulation Manifestations of Preeclampsia
How are D-dimer in Preeclampsia?
Increased D-dimer (DIC specific)
Increased incidence of placental abruption => DIC
Obstetrical Management of Preeclampsia
What’s the Definitive treatment of Preeclampsia?
Delivery of fetus & placenta
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Obstetrical Management of Preeclampsia
After Delivery of fetus & placenta, how soon do symptoms of preeclampsia begin to resolve?
Symptoms begin to resolve within 48 hrs
Obstetrical Management of Preeclampsia
Until definitive treatment is possible, what are the Goals and Priorities of Obstetrical Management of Preeclampsia?
Control HTN
Prevent seizures (eclampsia)
Correct coagulopathies
Improve organ perfusion
Antihypertensive Therapy in the Management of Preeclampsia
What are the benefits of Antihypertensive Therapy in the Management of Preeclampsia?
Decrease risk of intracranial bleeding, placental abruption, seizures
Improves organ perfusion
Antihypertensive Therapy in the Management of Preeclampsia
When should Antihypertensive Therapy in the Management of Preeclampsia be initiated?
Initiate when DBP rises above 110 mmHg
Antihypertensive Therapy in the Management of Preeclampsia
Which specific antipypertensive modalities are used for the Therapeutic Management of Preeclampsia?
Vasodilators + plasma volume expansion
Antihypertensive Therapy in the Management of Preeclampsia
In the Antihypertensive management of Preeclampsia, BP is NO to “normalize” BP. Rather the goal of therapy is DBP of 90 – 100 mmHg. Why is that?
Decreasing maternal BP will lead to decrease uterine perfusion pressure
This could cause Fetal distress!!!
Antihypertensive Therapy in the Management of Preeclampsia
Common drugs used in the Antihypertensive Therapy in the Management of Preeclampsia include:
Hydralazine (IV)
Direct arterial vasodilator
Improves both renal & uteroplacental blood flow
Good first-line drug
Labetalol (p.o./IV)
β & α- adrenergic antagonist - Acute/long term treatment
Useful for treatment reflexive tachycardia
Methyldopa (p.o.)
Selective α2- adrenergic agonist
Long-term only
NTP
Potent, immediate acting vasodilator of both capacitance & resistance vessels
<u>Use</u>: Acute ↑ in BP (DL/extubation), Malignant HTN crisis
<u>Cautions</u>: Prolonged use → cyanide toxicity
Cyanide crosses placenta resulting in accumulation in fetus → detrimental to fetus
Antihypertensive Therapy in the Management of Preeclampsia
Benfits of Hydralazine (IV) when used in Antihypertensive Therapeutic Management of Preeclampsia:
Direct arterial vasodilator
Improves both renal & uteroplacental blood flow
Good first-line drug
Antihypertensive Therapeutic Management of Preeclampsia
Which characteristics of Labetalol (p.o./IV) make it useful in the Antihypertensive Therapeutic Management of Preeclampsia? when is its use indicated?
β & α- adrenergic antagonist
Indicated for Acute/long term treatment
Useful for the treatment of reflexive tachycardia
Antihypertensive Therapeutic Management of Preeclampsia
Which characteristics of Methyldopa (p.o.) make it useful in the Antihypertensive Therapeutic Management of Preeclampsia? when is its use indicated?
Selective α2- adrenergic agonist
Indicated for Long-term only
Antihypertensive Therapeutic Management of Preeclampsia
Which characteristics of NTP make it useful in the Antihypertensive Therapeutic Management of Preeclampsia? when is its use indicated?
Potent, immediate acting vasodilator of both capacitance & resistance vessels
Indicted for Acute increase in BP (DL/extubation), Malignant HTN crisis
Antihypertensive Therapeutic Management of Preeclampsia
Why must caution be used w/ prolonged use of NTP in the Antihypertensive Therapeutic Management of Preeclampsia
Cyanide toxicity
Cyanide crosses placenta resulting in accumulation in fetus → detrimental to fetus
Seizure Prophylaxis in Preeclampsia
Which drug 1st line agent in Seizure Prophylaxis during Preeclampsia?
MgSO4
This is the Gold standard for Seizure Prophylaxis
Seizure Prophylaxis in Preeclampsia
How does MgSO4 work in Seizure Prophylaxis during Preeclampsia?
Decreases CNS irritability
Relaxes uterine & vascular smooth muscle tone
=> (↑ UBF & ↑ RBF)
Seizure Prophylaxis in Preeclampsia
What are MgSO4 loading and maintenance doses for Seizure Prophylaxis during Preeclampsia?
Loading: 4-6 gm IV over 20”
Maintenance: 1-2 gm/hr
This is the Gold standard for Seizure Prophylaxis
MgSO4 Toxicity
What’s the Therapeutic level of MgSO4?
4-8 mEq/L of MgSO4
MgSO4 Toxicity
Which MgSO4 levels are associated with Prolonged QT and/or Widened QRS?
5-10 mEq/L of MgSO4
Prolonged QT and/or Widened QRS
MgSO4 Toxicity
Which MgSO4 levels are associated with Loss DTR?
10-12 mEq/L of MgSO4
Loss DTR
MgSO4 Toxicity
Which MgSO4 levels are associated with Respiratory depression?
12-15 mEq/L of MgSO4
Respiratory depression
MgSO4 Toxicity
Which MgSO4 levels are associated with Respiratory arrest?
15-20 mEq/L of MgSO4
Respiratory arrest
MgSO4 Toxicity
Which MgSO4 levels are associated with Cadiac arrest?
> 20 mEq/L of MgSO4
Cadiac arrest
MgSO4 Toxicity
What’s the treatment for MgSO4 Toxicity?
Stop infusion if in toxic levels
Calcium gluconate 10 ml of 10% solutions over 2”
Oxygen
Airway support/mechanical ventilation
Seizure Prophylaxis in Preeclampsia
What are some notable undesirable effects of MgSO4?
Enhances neuromuscular blockade of both depolarizing & NDMR’s
↓ presynaptic release of ACH
↓ sensitivity of end-plate to ACH
↓ uterine tone → uterine atony
=> ↑ PostPartum bleeding d/t boggy ueterus
Enhances effects of sedative/opioids
Readily crosses placenta
→ ↓ neonatal muscle tone
Seizure Prophylaxis in Preeclampsia
How does MgSO4 Enhances neuromuscular blockade of both depolarizing & NDMR’s?
Decreases presynaptic release of ACH
Decreases sensitivity of end-plate to ACH
Seizure Prophylaxis in Preeclampsia
Via which mechanism can MgSO4 cause increased PP bleeding?
Decrease uterine tone → uterine atony → boggy ueterus
Seizure Prophylaxis in Preeclampsia
T/F: MgSO4 Enhances effects of sedative/opioids
True
Seizure Prophylaxis in Preeclampsia
MgSO4 readily crosses placenta. What effect could this have on the neonate?
Decreased neonatal muscle tone
Obstetrical Management in Preeclampsia
What are the goals of Obstetrical Fluid management in Preeclampsia?
Correct intravascular depletion with crystalloid
Monitor U/O for effectiveness
If remains oliguric or aggressive resuscitation necessary, guide by CVP measurements
Obstetrical Management in Preeclampsia
Obstetrical correction of coagulopathies involves:
PLT replacement
< 20K during <u>vaginal delivery</u>
< 50K if <u>C/S </u>required
FFP/Cryoprecipitate
if <u>DIC</u> evident
Obstetrical Management in Preeclampsia
Which plt count values warrant replacement if vaginal delivery?
Plt < 20K
Obstetrical Management in Preeclampsia
Which plt count values warrant replacement if C-S required?
Plt < 50K
Obstetrical Management in Preeclampsia
When is coagulopathy treated w/ FFP/Cryoprecipitate
if DIC evident
Obstetrical Management in Preeclampsia
T/F: Invasive Monitoring is beneficial for Obstetrical Management of Preeclampsia
False
Invasive Monitoring has Not proven beneficial for Obstetrical Management of Preeclampsia
Standard monitoring of BP & U/O acceptable
There are some acceptable indications to switch over to Invasive Monitoring
Obstetrical Management of Preeclampsia
What are accepted indications to switch over to Invasive Monitoring in Obstetrical Management of Preeclampsia?
Refractory HTN
Pulmonary edema
Refractory oliguria unresponsive to fluid challenges
Severe cardiopulmonary disease
Obese
Obstetrical Management of Preeclampsia
What are the benefits of High dose corticosteroid therapy in the Obstetrical Management of Preeclampsia?
Improves fetal lung maturity
Prevents further decline in PLT
(actually increases PLT in HELLP syndrome)
Obstetrical Management of Preeclampsia
T/F: High dose corticosteroid therapy in the Obstetrical Management of Preeclampsia is Effective only during antepartum period, not PP
True
High dose corticosteroid therapy is Effective only during antepartum period, not PP
Obstetrical Management of Preeclampsia
When should High dose corticosteroid therapy for the Obstetrical Management of Preeclampsia be initiated? How long should it be continued?
Initiated with PLT < 100K
Continue until LFT’s improve or PLT > 100K
Obstetrical Management of Preeclampsia
When High dose corticosteroid therapy is used for the Obstetrical Management of Preeclampsia, which drug is administered? at what dose?
Dexamethasone (Decadron) 10 mg IV every 12 hrs.
Obstetrical Management of Preeclampsia
In the Obstetrical Management of Preeclampsia, what are indications for Labor Induction & Delivery?
> 36 weeks gestation
Fetal lung maturity
Favorable cervix
Refractory HTN despite conservative measures
Evidence of maternal or fetal deterioration regardless of gestational age
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Obstetrical Management of Preeclampsia
Which anesthetic technique are appropriate when Labor Induction & Delivery are indicated in the Obstetrical Management of Preeclampsia?
Epidural vs. Spinal
GETA
Refer to the Anesthesia & Analgesia for Obstetrics lecture