severe pre-eclampsia. tom archer, md, mba director, ob anesthesia ucsd hillcrest march 28, 2012
TRANSCRIPT
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Severe pre-eclampsia.
Tom Archer, MD, MBADirector, OB Anesthesia
UCSD HillcrestMarch 28, 2012
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Hypertension in pregnancy
• Pre-eclampsia (HBP, proteinuria, edema, after 20 weeks ega)
• Gestational hypertension (HBP after 20 weeks ega, no proteinuria). Old term: “pregnancy-induced hypertension”.
• Chronic hypertension (HBP antedating pregnancy).
• “Superimposed” pre-eclampsia– pre-eclampsia on top of chronic hypertension
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Three causes of death in pregnancy:
#1 Pulmonary thromboembolism
#2 Hemorrhage
#3 Hypertensive disorders / pre-EStrokeSeizuresDIC
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Pre-eclampsia variants
• Eclampsia– pre-eclampsia with seizures
• HELLP syndrome (hemolysis, elevated liver enzymes and low platelets)
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Severe pre-eclampsia
• SBP > 160 or DBP > 110, X2, 6 hours apart.
• Proteinuria > 5 gm / 24 hours (Hence 24-hour urine collection)
• Oliguria < 500 mL / 24 hours
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Severe pre-eclampsia
• Cerebral or visual disturbances: HA, blurred vision or altered consciousness.
• Pulmonary edema (or low Sp02).
• Epigastric or RUQ pain (liver edema or rupture)
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Severe pre-eclampsia
• Increased liver enzymes-- common.
• Prolonged PT or PTT or decreased fibrinogen implies DIC– fortunately rare.
• Thrombocytopenia
• Fetal growth restriction
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Traditional pre-eclampsia triad:
• Hypertension
• Proteinuria
• Edema
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New understanding of traditional pre-eclampsia triad:
• Hypertension arteriolar constriction (endothelial dysfunction).
• Proteinuria leaky glomerulus (capillary) (endothelial dysfunction).
• Edema leaky capillaries in skin, muscle, liver, brain, airway, nose. (endothelial dysfunction).
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“4th component” of endothelial dysfunction in pre-eclampsia
• Muscular artery spasm increased arterial wave reflection back to heart
• Increased “augmentation index” (AIx)
• Increased AIx extra work for heart muscle
• LVH, increased BNP release CHF.
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Modern concept of pre-eclampsia: symptoms are due to arterial,
arteriolar and capillary endothelial damage.
Q: Damage by what?A: Chemical mediators from
placenta
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“Toxemia of pregnancy”
• The old-fashioned term is actually very descriptive!
• The ischemic placenta gives off toxins which damage the mother’s vascular endothelium throughout her body.
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www.siumed.edu/~dking2/erg/images/placenta.jpg
Say “OUCH!”
Pre-E
mediators
Poor placentation
Pre-eclampsia: ischemic chorionic villi release pre-E mediators into maternal blood.
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Pre-E: endothelial damage
• Deranged smooth muscle function, due to damaged endothelium overlying smooth muscle.
• Leaky capillary endothelium (no smooth muscle).
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vasodilatory signals (NO, prostacyclin)
vasoconstrictive signals (thromboxane, endothelin)
Endothelial cells send molecular signals to surrounding smooth muscle
Vessel lumen
Insulin makes endothelium produce
Pre-eclampsia mediators (and glucose) make endothelium produce
Archer TL 2006 unpublished, Idea from Dandona P 2004
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Endothelial factors in pre-E:
• In health, there is a balance between– vasodilatory factors: NO, PGI2 (Prostacyclin) and
– vasoconstrictive factors: thromboxane, endothelin.
• This normal balance is messed up in pre-E.
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Obesity, hyperglycemia, sepsis and pre-eclampsia all “activate” (damage) endothelium, white cells and platelets, leading to white cell adhesion and infiltration, thrombosis and edema (inflammation).
Obesity, hyperglycemia, sepsis or pre-eclampsia
WBC
Platelet
Protein (edema)
WBC
Platelets
Archer TL 2006 unpublished
Capillary endothelium (no underlying smooth muscle)
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Endothelial damage causes problems in 3 sizes of blood vessels:
• Muscular arteries increased wave reflection (heart work, augmentation index).
• Arterioles increased SVR
• Capillaries proteinuria and tissue edema (glomerulus, liver, skin, muscle, brain)
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Figure 1. Pt HB, PreE for CS, superimposed on CHTN and CRF, 33 weeks. Hemodynamic parameters before and after treatment with antihypertensive medication A. Labetalol 25 mg and hydralazine 5 mg, B. Nicardipine 250 μ total in divided doses
8
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2000
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0 10 20 30 40
A minutes B
Nominal cardiac output L/min
Nominal systemic vascular resistance dyn.sec.cm-5
Blood pressure mm Hg
Heart rate beats/min and nominal stroke volume mL
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Posterior reversible encephalopathy syndrome (PRES):
Occipital-parietal cortical and white matter changes in pre-eclampsia.
Is this due to capillary damage in the brain?
Port JD, BeauchampRadioGraphics 1998; 18:353-36ı‘
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Figure 1b
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Figure 1c
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Edema– imagine same process in liver and brain!
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Pre-eclampsia:
Probably a
disorder of placentation.
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http://pharyngula.org/images/preeclampsia_model.jpg
Poor-placentation theory of pre-E:
Synciotrophoblast invades myometrium but does not denervate spiral arteries of mother properly.
Hence, intervillous flow is sub-optimal.
Chorionic villi are ischemic and release mediators (VEGF, etc) which damage maternal endothelium.
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www.siumed.edu/~dking2/erg/images/placenta.jpg
Say “OUCH!”
Pre-E
mediators
Poor placentation
Pre-eclampsia: ischemic chorionic villi release pre-E mediators into maternal blood.
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Hemodynamic review:
MAP = SVR x CO.
We ignore CVP since it is small compared to MAP.
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Hemodynamic issues in pre-eclampsia
• We could work on CO or SVR, since
MAP = CO x SVR.
We usually work on both CO and SVR, but different drugs affect the two components to different degrees.
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SAB / epidural cause sympathectomy
www.cvphysiology.com/Blood%20Pressure/BP019.htm
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Post-partum BP control
• Hydralazine – arteriolar vasodilator. Decreases SVR. Tendency is to cause tachycardia. 5 mg IV q15 minutes
• Labetalol – alpha and beta blocker. Dilates arterioles (dec SVR) and slows heart rate and reduces contractility (dec CO). 10-20 mg IV q 10 minutes.
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Why treat BP in pre-eclampsia?
• Decrease stroke, CHF, renal damage?
• This has never been proven by RCT.
• But we do it anyway!
• Goal is modest decrease in BP. DBP 90-100 mm Hg.
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Other BP meds in pre-eclampsia
• Nitroglycerin– venodilator, can be given sublingually or IV.
• Sodium nitroprusside– IV. Needs arterial line.Primarily arteriolar dilator.
• Nifedipine– Ca++ channel blockers. Arteriolar dilator. Can be used for BP control and also as a tocolytic. Caution should be used when used with Mg++.
• Esmolol– sort acting beta blocker. Adjunct to decrease HR in BP control.
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Pre-eclampsia complication:pulmonary edema
• Fluid overload / pulmonary edema– – respiratory distress– Low SpO2 (“low sats”)– Rales on auscultation
• Can progress to ARDS
• May need intubation
• Call anesthesia for evaluation
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Pre-eclampsia complications: pulmonary edema
• Fluid overload / pulmonary edema–
– Albumin (oncotic pressure) decreases in normal pregnancy.
– Lower in pre-eclampsia due to protein loss into interstitial space
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Respiratory function in pre-eclampsia
• Edema of the airway
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Pre-eclampsia complications: blindness and seizures
• Blindness / blurred vision– Edema in occipital cortex (retina is normal)– Disorientation / fear– Visual impairment usually resolves completely
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Pre-eclampsia complications: blindness and seizures
• Seizure: neurological event but also a respiratory event!
• Remember: suction, oxygen, ambu bag, IV access, call anesthesiologist to help.
• Ante-partum, fetal oxygenation is at risk.
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MgSO4 seizure prophylaxis
• Mg++ in severe pre-E reduces seizures by about 60% (from 1.9% 0.8%)
• Mg++ use in mild pre-eclampsia is controversial but it is used at UCSD.
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Magnesium toxicity
• 1.7-2.4 mg / dL– Normal
• 5-9 mg / dL– therapeutic range for seizure prevention
• Loss of patellar reflexes (but watch out for epidural)– 12 mg / dL
• Respiratory arrest – 15-20 mg / dL
• Asystole– 25 mg / dL
• Mg++ levels OK, but try clinical assessment!
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Magnesium toxicity• Multiple blood draws– think central or arterial line or
blue valve from IV catheter. Avoid repeated sticks?• Treatment:
• Stop Mg++
• Give Ca++ (1 gm Ca gluconate or 300 mg CaCl2
• Assist ventilation (Ambu bag). Intubation if necessary.
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Magnesium toxicity
• Uterine atony (Mg++ is a uterine relaxant)
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Hematologic aspects of pre-E:
• Exacerbated normal hypercoagulability of normal pregnancy.
If DIC occurs, fibrinolysis will occur as well (+ Fibrin dimer test)
Platelet activation and adhesion / consumption.
We commonly follow trend of platelets.
Regional OK if > 50-100K.
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Prolongation of PT / PTT or decreased fibrinogen in pre-E
• Uncommon (thrombocytopenia is common).
• Low fibrinogen implies DIC.
• Liver damage decreased synthesis of fibrinogen and clotting factors?
• Bottom line: if fibrinogen or PT/PTT are abnormal, patient has a more serious problem than “just” thrombocytopenia.
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Pre-eclampsia complications
• Disseminated intravascular coagulation (“DIC”)– Consumption of platelets and clotting factors
d/t damaged endothelium– Diffuse ooze from incision, IV sites– Major emergency– IV access, pRBCs, FFP, cryoprecipitate– Will need ICU, ?intubation, arterial line
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Hemolysis from fibrin stands
www.nejm.org/.../2005/20050804/images/s19.jpg
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Liver in pre-eclampsia
• Elevated liver enzymes (AST, ALT)
• Edema– swelling– epigastric / RUQ pain
• Hemorrhage into liver (hematoma)
• Rupture of hematoma through liver capsule (“liver rupture”).
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Factitious thrombocytopenia
• Platelet clumping due to EDTA anticoagulant or cold
www.nejm.org/.../2005/20050804/images/s19.jpg
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Renal function in pre-eclampsia
• Normal pregnancy involves increased GFR and decreased creatinine, e.g. 0.80.6 mg/dL.
• Renal dysfunction in pre-eclampsia may be associated with a “normal” creatinine, eg. 1.0.
• Increased uric acid in pre-eclampsia
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Renal failure after pre-E
• Oliguria almost always gets better after delivery.
• Renal failure due to pre-E is rare (unless there is pre-existing renal disease).
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Oliguria
• Urine output less than 30 mL / hr for more than 3 hours, despite crystalloid boluse(s) of 300-500 mL.
• Is the Foley in the bladder? Is it kinked?
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Summary
• Pre-eclampsia is associated with endothelial dysfunction.
• Normal balance between vasodilation and vasoconstriction tips toward constriction.
• Capillaries become leaky– edema (and proteinuria) everywhere.
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Summary
• Old-fashioned term “toxemia of pregnancy” is very accurate!
• Placenta is ischemic because implantation has not gone well.
• Pre-eclampsia: a disorder of implantation.
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Summary
• Pre-eclampsia may involve an early hyperdynamic phase (increased CO), followed by a vasoconstrictive phase (high SVR).
• Later on, pre-eclampsia involves intense arteriolar constrictive, with high BPs and reflected pressure waves leading to heart strain and possible CHF.
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Summary
• The endothelial damage of pre-eclampsia can activate the coagulation system.
• Thrombocytopenia occasionally occurs but hypofibrinogemia and prolonged PT/PTT are rare and very worrisome.
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Overall management
• Seizure prophylaxis
• Hemodynamic state—invasive monitoring
• Fluid restriction (but boluses for oliguria).
• Review of platelets, PT, PTT, fibrinogen
• Evaluation of airway (swelling) and pulmonary status (edema)
• Pulmonary edema most common after delivery (mobilization of edema fluid).
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Neonatal issues in pre-eclampsia
• IUGR
• Prematurity
• Hypoxia
• Mother will be afraid for the baby!
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Maternal CNS issues in pre-eclampsia
• Confusion or somnolence due to cerebral edema
• Somnolence due to MgSO4 therapy
• Post-ictal state (has patient had a seizure?)
• Is patient afraid?
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Summary care for patient with severe pre-eclampsia
• Emotional support– anxiety for self, neonate, CNS changes due to disease and therapy.
• Pain from surgery– helped by neuraxial anesthesia and neuraxial opioids.
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Summary of care for patient with severe pre-eclampsia
• Follow BP– may increase as spinal wears off. This is normal.
• Goal of BP control is high normal– don’t overshoot.
• Treat pain, not just give antihypertensives.
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Summary of care for patient with severe pre-eclampsia
• Judicious fluid restriction (unless post-partum hemorrhage).
• Continue magnesium sulfate.
• Monitor urine output.
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Summary of care for patient with severe pre-eclampsia
• Monitor for post-partum hemorrhage
• Prolonged labor, MgSO4 can predispose to uterine atony.
• Monitor for DIC. Oozing at IV and other venipuncture sites.
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How can anesthesiologist help the patient in the PACU?
• IV access: central line or arterial line for repeated blood draws and BP monitoring?
• IV med assistance: what to give? How fast will it work?
• Monitor for pulmonary / cardiac dysfunction– rales, low Sp02.
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How can anesthesiologist help the patient in the PACU?
• Manage seizing patient– airway, vomiting.
• Have suction, ambu bag, crash cart nearby.
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The End