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Preeclampsia and Eclampsia

Preeclampsia and Eclampsia. Ravindra Prasad, M.D. UNC-Chapel Hill Morning Conference Nov. 7 and 8, 1996. HTN during pregnancy:. Preeclampsia HTN, generalized edema, proteinuria after 20th week gestation (mostly after 24th) (hyperreflexia) Eclampsia

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Preeclampsia and Eclampsia

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  1. Preeclampsia and Eclampsia Ravindra Prasad, M.D. UNC-Chapel Hill Morning Conference Nov. 7 and 8, 1996

  2. HTN during pregnancy: • Preeclampsia • HTN, generalized edema, proteinuria • after 20th week gestation (mostly after 24th) • (hyperreflexia) • Eclampsia • Preeclampsia + grand mal seizure unrelated to other neurologic disease • Chronic HTN • HTN before 20th wk, or > 6 wks. postpartum • Chronic HTN with superimposed (Pre)eclampsia • Gestational HTN • Isolated HTN (no edema, proteinuria) late in pregnancy (last wks) • Resolves within 2 wks postpartum • PIH • all of above associated with pregnancy

  3. Preeclampsia/eclampsia • BP • inc. in SBP  30 mmHg, or SBP > 140 • inc. in DBP  15 mmHg, or DBP > 90 • inc. in MAP  20 mmHg, or MAP > 105 • (measured in lateral position, at least 6 hrs apart) • Proteinuria • > 300 mg protein/liter in 24 hr urine collection • >1 gm protein/liter (1+ or 2+ dipstick) in two samples >6 hrs apart • Edema • generalized, not just dependent • Gestational age • > 20 wks • earlier than 20wks if molar pregnancy

  4. Preeclampsia/eclampsia, severe • SBP > 160 • DBP > 110 • MAP > 120 • Proteinuria: > 5 gm/24 hrs (3+ or 4+ dipstick) • oliguria: <500 ml urine/24 hrs • HA or CNS changes • epigastric (liver) pain • pulmonary edema or cyanosis • HELLP Syndrome (hemolysis, elevated liver enzymes, low platelets)

  5. Incidence • Preeclampsia: 2.6-7 % of all pregnancies • Eclampsia: 0.02-0.07 % of all pregnancies • onset before (44, 17%), during (37, 52%), or after (19, 34%) delivery • if after, 43% within 4 hrs., 86% within 24 hrs • Risk factors • <20 yo vs. >20 yo: 5x incidence • Unmarried > married • Medicaid > private insurance

  6. Morbidity/mortality: Maternal • leading cause of maternal death (20-40%) in US, England, and Scandinavia • intracranial hemorrhage (#1 cause of mortality) • CHF with pulmonary edema • aspiration of gastric contents • postpartum hemorrhage • DIC • ARF • ruptured liver • septic shock

  7. Morbidity/mortality: Fetal • intrauterine mortality • *placental infarction • retarded placental growth • abruptio placentae • acute infection of amniotic fluid • morbidity • severe maternal HTN assoc. with inc. incidence of mental retardation, global and motor dysfunction•mortality > 93% if severe preeclampsia develops before 24 wks gestation

  8. Perinatal morbidity/mortality • related to preterm birth • respiratory distress • intracranial hemorrhage • SGA • meconium aspiration

  9. Morbidity/mortality: Eclampsia • maternal mortality 0.4-11.9% (higher with greater age and parity and number of seizures) • perinatal mortality 20-30%

  10. Etiology • Unknown • The normal balance is lost between vasodilators / anticoagulants (PGE2, prostacyclin, NO, tissue plasminogen activator) and vasoconstrictors / procoagulants (thromboxane, angiotensin, tissue plasminogen inhibitor) • Imbalance may be related to endothelial cell injury, or to placental trophoblastic production of thromboxane

  11. Etiology

  12. Pathophysiology: Airway • excess sodium and water retention • decreased colloid oncotic pressure from proteinuria • inc. upper airway/laryngeal edema • magnesium, sedatives, narcotics can ==> hypoxia, hypercarbia

  13. Pathophysiology: Coagulation • thrombocytopenia (platelets < 150,000 in 11-50%) • (?due to consumption at sites of endothelial damage or immune mechanism) • altered platelet function (prostaglandin imbalance) • increased platelet turnover (more immature platelets) • slight inc. in PTT (statistically, but not clinically significant - 29.8±6.6 vs 26.4±1.8)

  14. Pathophysiology: Cardiovascular 1 • inc BP • widespread vasoconstriction • Plasma volumes markedly decreased, RBC mass unchanged • inc. blood viscosity • normal-hyperdynamic LV function • inc. in BP related to inc. CO more than to inc. SVR

  15. Pathophysiology: Cardiovascular 2 • inc. response to vasoactive drugs • CVP tends to be low (except, if pulmonary edema, almost always  6) • PCWP tends to be normal, but IVF supplementation can cause pulmonary edema in some patients • inc. levels of renin, angiotensin, catecholamines, and atrial natriuretic factor

  16. Pathophysiology: Pulmonary edema • 2.9-5% of patients • more likely older multiparae with preexisting cHTN • may be related to • Colloid oncotic pressure may be decreased • capillary endothelial damage • usually assoc. with sepsis, DIC, abruptio, preexisting cHTN, and/or excessive IVF • usually in first few postpartum days

  17. Pathophysiology: Renal • dec renal blood flow (renal artery vasospasm vs. volume overload with cardiac dysfunction) • loss of protein (proteinuria) • ARF (8%) with oliguria may occur (even with normo- or hypervolemia), esp. if abruptio placentae with DIC, HELLP, or cHTN also present • inc. uric acid levels • renal changes may reverse with resolution of disease (not known), though preeclampsia + cHTN often ==> permanent renal damage

  18. Pathophysiology: Hematologic • left shift of hemoglobin dissociation curve (= dec O2 unloading to fetus) (mechanism: ? inc. catabolism of RBCs ==> inc. carboxyhemoglobin) • hemolysis (intense vasospasm ==> endothelial disruption ==> platelet adherence, fibrin deposition)

  19. Pathophysiology: CNS • cerebral edema and/or change in CBF may cause sx (HA, visual changes, irritability) • cerebral hemorrhage may occur, though BPs rarely are beyond limits of cerebral autoregulation • 45% of eclamptics will have some CT abnormality • 90% of eclamptics will have abnormal EEG

  20. Pathophysiology: HELLP Syndrome • usually before 36 wks gestation • symptoms: • malaise 90% • epigastric pain 90% • N/V 50% • some with flu-like symptoms • rapidly progressive, to DIC, liver failure, renal failure: requires immediate delivery • platelet count nadir 24-48 hrs postpartum

  21. Pathophysiology: Hepatic • usually little involvement • if severe preeclampsia or HELLP, can have more involvement: • periportal hemorrhages • ischemic lesions • generalized swelling • subcapsular hematoma • hepatic swelling ==> epigastric pain • hyperreflexia • inc. CNS irritability

  22. Pathophysiology: Uteroplacental • uterine and placental blood flow dec 50-70%, due to: • vasospasm from decreased uterine prod of vasodilators • inc. viscosity • catecholamines can cause exaggerated vasospastic response • hyperactive uterus • inc. sensitivity to oxytocin • rapid labor, painful contractions common • PTL frequent • placenta often small, with infarcts, fibrin deposition, calcification, and abruption • inc. incidence of abruptio placentae (10%)

  23. Pathophysiology: other • Total plasma albumin decreased • inc. fibrin split products • dec levels plasma cholinesterase

  24. Therapy • Delivery of fetus • Pregnancy allowed to continue until it becomes a danger to fetus (unable to support fetal growth) or mother • Vaginal delivery not contraindicated if fetus tolerates • C-section indicated if • markedly premature, but viable fetus • significant compromise of intrauterine environment: • falling BPP • fetal distress • mother rapidly deteriorating

  25. Therapy, continued pregnancy • Goals • minimize vasospasm • inc. circulation (esp. to uterus, placenta, and kidneys) • inc. intravascular volume • correct acid-base and electrolyte abnormalities • dec CNS hyperactivity • Bed rest, lateral decubitus position may dec BP • Normal diet (no sodium or fluid restriction) • adequate hydration and intravascular volume expansion may lower BP

  26. Magnesium: Beneficial effects 1 • (therapeutic = 4-6 mEq/L, toxicity if >10 mEq/L) • Anticonvulsant (CNS depressant) • Vasodilation (mild: decreases smooth muscle contraction, depresses catecholamine release) • inc. uterine blood flow • inc. renal blood flow • dec BP (not reliable) • inc. prostacyclin release by endothelial cells

  27. Magnesium: Beneficial effects 2 • dec plasma renin activity • dec ACEs • dec vascular response to pressors • dec platelet aggregation • bronchodilation • tocolysis • improves uterine blood flow • decreases uterine hyperactivity

  28. Magnesium: Detriments 1 • tocolysis • prolonged labor • inc. postpartum hemorrhage • dec FHR variability

  29. Magnesium: Detriments 2 • myoneural blocking effects • generalized muscle weakness • inc. sensitivity to muscle relaxants, esp. NDMRs (decreases the amount of ACh released, the depolarizing effect of ACh, and the muscle membrane excitability) • neonatal effects • lower Apgar scores • dec muscle tone, respiratory depression, apnea (only with maternal overdose)

  30. Magnesium overdose • weakness • respiratory insufficiency • cardiac failure • usually after decrease in DTRs • symptoms may be partially overcome by iv calcium (in mom, this will antagonize the anticonvulsant effects of Mg also)

  31. Antihypertensives • Indicated if SBP>160 or DBP>110 despite Mg therapy

  32. Antihypertensives: Hydralazine • decreases precapillary arteriolar resistance ==> dec BP • however, assoc. inc. CO and inc. HR may counterbalance BP effect • increases renal blood flow • maximum effect 20-30 min. after iv dose • duration 2-3 hrs • may dec uterine blood flow • assoc. with fetal distress • may be assoc. with neonatal thrombocytopenia

  33. Antihypertensives: Labetolol • nonselective beta blockade • selective post-synaptic alpha-1 blockade • beta:alpha = 3:1 (oral) or 7:1 (iv) • may also cause beta-2 related vasodilation • more rapid onset than hydralazine • lacks hydralazine’s side effects (inc. HR, nausea, HA, excessive dec BP, dec uterine blood flow)

  34. Antihypertensives: Calcium channel blockers • vascular smooth muscle relaxants ==> dec SVR • potent uterine relaxants (may inc. risk of postpartum hemorrhage if given close to delivery time) • inc. renal blood flow, UOP • nifedipine preferred (lacks associated tachycardia) • caution if also using magnesium - hypotension, respiratory difficulty, and additive cardiac toxicity (Mg may also be working as a CCB)

  35. Antihypertensives • Methyldopa • esp. if cHTN • alpha-1 blockers • Clonidine • Prazosin • Propanolol • clinically, appears safe for mom and fetus • Esmolol • Beta-1 selective • ewe studies: fetal beta blockade, hypoxemia - additional studies needed • Trimethaphan, SNP, NTG • usually for acute control of BP on induction and emergence, GA

  36. Convulsions: treatment 1 • Must control seizure, then deliver baby • mortality increased by # of seizures • STP 50-100 mg, Diazepam 2.5-5 mg, midazolam 1-2 mg, magnesium 2-4 gm • Then, to prevent additional seizure, magnesium 2-4 gm/hr, or other anticonvulsant • If seizure continue, may indicate additional CNS pathology • venous thrombosis • intracerebral hemorrhage • cerebral edema

  37. Convulsions: treatment 2 • Give O2 • If cannot control quickly, RSI - protect airway and prevent aspiration • postictal depression may require ventilation (prevent hypoxia, hypercarbia) • Give bicarbonate if metabolic acidosis develops • If CHF or pulmonary edema, diurese • If cerebral edema, consider mannitol (if adequate UOP only) and/or dexamethasone 10-16 mg

  38. Monitoring 1 • Frequent BP - NIBP usually OK • Foley - monitor UOP, protein excretion • FHR and uterine contraction monitoring • preeclampsia: dec uterine and placental blood flow, uterine hyperactivity (long, frequent contractions) - fetus may not tolerate; may need to section • SpO2 (early sign of pulmonary edema)

  39. Monitoring 2 • ABP if pulmonary edema, ventilated, or require freq. ABGs, or if on vasodilator gtts • CVP if severe disease, esp. if marked HTN or oliguria, or major conduction analgesia • PAC if LV failure or other cardiac diseasepresent or refractory oliguria

  40. Monitoring: Indications for PAC • Unresponsive or refractory HTN: inc. SVR vs. inc. CO? • Pulmonary edema: LV failure vs. inc. SVR vs. volume overload vs. dec colloid oncotic pressure (can try to dec. PCWP to less than oncotic pressure, in effort to minimize pulmonary fluid shifts)? • Persistent arterial desaturation: cardiac vs. noncardiac? • Oliguria unresponsive to modest fluid loading: low preload vs. severe inc. in SVR with low CO vs. selective renal artery vasoconstriction?

  41. General considerations 1 • avoid rapid infusion of dextrose-containing fluids (maternal hyperglycemia is assoc. with fetal hypoglycemia, hyperbilirubinemia) • use balanced salt solutions (giving free water may lead to water intoxication) • volume-loading for epidural • NS/LR - rapid dosing of 2L BSS may lower colloid oncotic pressure for 24 hrs • 5% albumin - in severe preeclamptics, 500-1000cc increases CO, dec SVR with minimal lowering of MAP

  42. General considerations 2 • monitor CVP/UOP/signs of pulmonary edema if giving large volumes quickly • maintain left lateral position • give O2 during delivery

  43. Vaginal delivery • narcotics - give early, small dose to minimize neonatal depression • 30-40 % N2O in O2 for first stage of labor - augment with pudendal block or local for forceps delivery • may add 0.3-0.5% isoflurane for additional analgesia • or may add ketamine (up to 0.75 mg/kg) incrementally for additional analgesia • not ideal obstetric conditions

  44. Vaginal delivery - CLE 1 • contraindications • significant coagulation abnormalities (decreasing platelet count, esp if < 100,000 may be a relative contraindication) • ±septicemia • marked untreated hypovolemia

  45. Vaginal delivery - CLE 2 • benefits • ideal conditions for vaginal delivery, including forceps/vacuum • can be used for c-section • decreases O2 requirements during labor • prevents pain-related hyperventilation during labor (which can dec uterine blood flow and cause maternal metabolic acidosis) • significantly decreases circulating catecholamines • improves intervillous blood flow

  46. Vaginal delivery - CLE 3 • potential problems • sudden hypotension may dec intervillous blood flow • local anesthetics may dec beat-to-beat variability (slightly) and thus impede diagnosis of fetal hypoxia and distress (occurs with lidocaine, not bupivacaine • local anesthetic may predispose to convulsions • can avoid problems • avoid aortocaval compression • ensure adequate hydration - may monitor CVP • small doses ephedrine • dec intervillous blood flow only occurs if dec BP (if managed correctly, actually increase uterine artery and intervillous blood flow) • other analgesics cause great(er) loss of beat-to-beat variability

  47. Vaginal delivery - CLE 4 • Preparation • control BP; DBP<110 • confirm coagulation times OK • monitors (as above) • prehydrate, CVP up to 6 cm water (500 cc usually enough for CLE; 1-2L for c/s, and may want to substitute some colloid) • Place early (avoid narcotic-related fetal depression)

  48. Vaginal delivery - CLE 5: details • T10-L1 for Stage I: pain from uterine contraction, cervical dilation (T11-12) • if BP OK, extend block slowly to cover T8-S5 for rest of labor and delivery • Stage II: pain from distention of lower vagina, vulva, and perineum, S2-4 • analgesia for forceps delivery, episiotomy • perineal analgesia • prevents uncontrollable bearing down by the mother, which is assoc. with sudden changes in CV and CNS systems • minimizes likelihood of precipitous delivery of preterm or SGA neonate, which is assoc. with neonatal intracerebral hemorrhage

  49. Vaginal delivery - CLE 6: details • may add fentanyl/epinephrine to inc. quality/duration of block • For c-section, extend block to T4 (going from T8 ==> T4 causes less hypotension than if start with lower level)

  50. Vaginal delivery - SAB 1 • if delivery imminent, saddle block to T10 level • BP usually maintained if • block no higher than T10 • maintain LUD • prehydrate • hyperbaric lidocaine 35-50 mg, bupivacaine 5-7.5 mg, or tetracaine 4-6 mg • add fentanyl 15-25 µg for better quality/duration

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