Presentation is loading. Please wait.

Presentation is loading. Please wait.

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

Similar presentations

Presentation on theme: "Preeclampsia and Eclampsia Ravindra Prasad, M.D. UNC-Chapel Hill Morning Conference Nov. 7 and 8, 1996."— Presentation transcript:

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: 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 O 2 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 disease present 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 % N 2 O in O 2 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

51 Vaginal delivery - SAB 2 disadvantages –risk of PDPH - use small gauge, pencil point needles –cannot extend block if need to do c-section

52 Cesarean Section often indicated b/c of deterioration of intrauterine environment or mother’s condition If there is time (may need 30 minutes to slowly raise level), and no contraindications, epidural anesthesia is technique of choice

53 C-section - Epidural anesthesia may add fentanyl 50-75 µg to speed onset, prolong duration, improve quality of block, and dec visceral discomfort from uterine exteriorization and interiorization, and peritoneal retraction advantages of epidural –as above for CLE –maternal bonding –epidural morphine for 24 hrs excellent analgesia, or post-op infusion –avoid GA/RSI/aspiration risk/sudden inc. in BP (which is assoc. with pulmonary edema, cerebral edema, and intracranial hemorrhage)

54 C-section - SAB sudden establishment of T4 level often assoc. with sudden, profound sympathectomy prophylactic ephedrine may be risky still preferable to GA for some (controversial) hyperbaric lidocaine 70-80 mg, bupivacaine 12-15 mg, tetracaine 9-11 mg with epinephrine 100-200 µg may add fentanyl of morphine to improve quality, dec. visceral discomfort, and provide post-op pain relief

55 C-section - General Anesthesia 1 considerations –upper airway edema –drug interactions (e.g. magnesium) –marked hypertensive responses to intubation, surgical stimulation, extubation

56 C-section - General Anesthesia 2 airway –usual pre-op evaluation –look for dysphonia, dysphoria, dyspnea, respiratory distress –small diameter ETT –be prepared for difficult intubation –consider awake intubation –do not traumatize nasal passages (suction, airway,...) can cause difficult-to-control epistaxis (and don’t use nasal phenylephrine)

57 C-section - General Anesthesia 3 magnesium –more sensitive to muscle relaxants –succinylcholine 1.5 mg/kg, up to 120 mg –no other relaxants unless surgeons require it and nerve stimulator indicates need –may give 5-10 mg succinylcholine boluses (not infusion - pseudocholinesterase levels significantly decreased in preeclamptics) –if use NDMR, give v small doses, e.g. vecuronium 1-2 mg –can usually avoid additional muscle relaxants if give 2/3 MAC volatile agent + 60-70% N2O after delivery

58 C-section - General Anesthesia 4 stimulation –can cause marked inc. in BP, HR, and circulating catecholamines –multips age > 25 at greatest risk –pre-treatment with lidocaine d/n work –can pre-treat with opioids, though this may cause neonatal depression –decrease DBP to about 95 mmHg –labetolol - give incrementally, up to 0.5-1 mg/kg prior to induction –NTG - may improve placental gas exchange –SNP - in preeclamptics, an altered response to SNP-induced vasodilation can cause sudden hypotension at very low doses (0.3 µg/kg/min) –Trimethaphan –CCBs –see table for advantages/disadvantages

59 C-section - General Anesthesia 5 Anesthetic –up to 2/3 MAC volatile agent (0.5% halothane, 0.75% isoflurane) in oxygen alone until delivery - higher concentrations may be assoc. with inc. uterine bleeding (atony), neonatal depression –prevent hypoxia (maternal left-shift of hemoglobin curve) –keep ETCO2 >25 mmHg before delivery (alkalosis ==> further left-shift)


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

Similar presentations

Ads by Google