Preeclampsia and Eclampsia: Anesthetic Management Anita M. Backus, MD Assistant Clinical Professor Director of Obstetric Anesthesia UCLA Medical Center Los Angeles, California Preeclampsia: Epidemiology Incidence widely quoted at 5-7% varies greatly depending on the population Remains a major cause of maternal mortality U.S. (1987-90) PIH: 17.6% of mat. deaths, 3rd leading cause • Preeclampsia (9.4%); eclampsia (7.4%) Mexico (1990-95) PIH: 26% of deaths (2204), 2nd leading cause In the most developed and medically Hypertension during Pregnancy: Classification Pregnancy-induced hypertension Hypertension without proteinuria/edema Preeclampsia mild severe Eclampsia Coincidental HTN: preexisting or persistent Pregnancy-aggravated HTN superimposed preeclampsia superimposed eclampsia Transient HTN: occurs in 3rd trimester, mild Preeclampsia: Definition Hypertension > 140/90 relative no longer considered diagnostic Proteinuria > 300 mg/24 hours or 1+ on urine dipstick not mandatory for diagnosis; may occur late Edema (non-dependent) so common & difficult to quantify it is rarely evoked to make or refute the diagnosis Criteria for Severe Preeclampsia SBP > 160 mm Hg DBP > 110 mm Hg Proteinuria > 5 g/24° or 3-4+ on dipstick Oliguria < 500 cc/24° serum creatinine Pulmonary edema or cyanosis CNS symptoms (HA, vision changes) Abdominal (RUQ) pain Any feature of HELLP hemolysis liver enzymes thrombocytopenia IUGR or oligohydramnios Preeclampsia: Risk Factors Nulliparity (or, more correctly, primipaternity) Chronic renal disease Angiotensinogen gene T235 Chronic hypertension Antiphospholipid antibody syndrome Multiple gestation Family or personal history of preeclampsia Age > 40 years African-American race Diabetes mellitus Etiology and Prevention Etiology is unknown. Many theories: genetic immunologic dietary deficiency (calcium, magnesium, zinc) supplementation has not proven effective placental source (ischemia) Etiology and Prevention A major underlying defect is a relative deficiency of prostacyclin vs. thromboxane Normally (non-preeclamptic) there is an 8-10 fold in prostacyclin with a smaller in thromboxane prostacyclin salutatory effects dominate vasodilation, platelet aggregation, uterine tone In preeclampsia, thromboxane’s effects dominate thromboxane (from platelets, placenta) prostacyclin (from endothelium, placenta) Preeclampsia Prophylaxis: Aspirin Aspirin has been extensively studied as a targeted therapy to thromboxane production CLASP study, 1994, multicenter, randomized CLASP Collaborative Group, Lancet 1994;343:619-29 9364 women, risk factors for PIH or IUGR or who had PIH or IUGR 60 mg ASA daily vs. placebo Small reduction (12%) in occurrence of PIH Small reduction in preterm deliveries: 20 vs 22% No difference in neonatal outcome Preeclampsia Prophylaxis: Aspirin NIH study of high-risk patients, randomized, 60 mg aspirin daily vs. placebo Caritis, et al., N Engl J Med 1998;338:701-5 pre-gestational DM (471 patients) chronic hypertension (774 patients) multifetal gestations (688 patients) prior history of preeclampsia (606 patients) No reduction in development of preeclampsia in any subgroup or groups in aggregate No difference in perinatal death, preterm delivery, IUGR, maternal or fetal hemorrhagic complications Preeclampsia: Mechanism At this time the most widely accepted proposed mechanism for preeclampsia is: global endothelial cell dysfunction Redman: endothelial cell dysfunction is just one manifestation of a broader intravascular inflammatory response Redman, et al., Am J Obstet Gynecol 1999;180:499-506 present in normal pregnancy excessive in preeclampsia Proposed source of inflammatory stimulus: placenta Pathophysiology: Cardiovascular In severe preeclampsia, typically hyperdynamic with normal-high CO, normal-mod. high SVR, and normal PCWP and CVP. Despite normal filling pressures, intravascular fluid volume is reduced (30-40% in severe PIH) Variations in presentation depending on prior treatment and severity and duration of disease Total body water is increased (generalized edema) Pathophysiology: Cardiovascular Preeclamptic patients are prone to develop pulmonary edema due to reduced colloid oncotic pressure (COP), which falls further postpartum: Colloid oncotic pressure: Antepartum Normal pregnancy: 22 mm Hg Preeclampsia: 18 mm Hg Postpartum 17 mm Hg 14 mm Hg Pathophysiology Respiratory: Airway is edematous; use smaller ET tube (6.5) risk of pulmonary edema; 70% postpartum Renal: Renal blood flow & GFR are decreased Renal failure due to plasma volume or renal artery vasospasm Proteinuria due to glomerulopathy glomerular capillary endothelial swelling w/subendothelial protein deposits Renal function recovers quickly postpartum Pathophysiology: Hepatic RUQ pain is a serious complaint warrants imaging, especially when accompanied by liver enzymes caused by liver swelling, periportal hemorrhage, subcapsular hematoma, hepatic rupture (30% mortality) HELLP syndrome occurs in ~ 20% of severe preeclamptics. Pathophysiology Coagulation: Generally hypercoagulable with evidence of platelet activation and increased fibrinolysis Thrombocytopenia is common, but fewer than 10% have platelet count < 100,000 DIC may occur, esp. with placental abruption Neurologic: Symptoms: headache, visual changes, seizures Hyperreflexia is usually present Eclamptic seizures may occur even w/out BP Possible causes: hypertensive encephalopathy, cerebral edema, thrombosis, hemorrhage, vasospasm Obstetric Management Classically “stabilize and deliver” Medical management while awaiting delivery: Indications for expedited delivery: use of steroids X 48 hours if fetus < 34 wks antihypertensives to maintain DBP < 105-110 magnesium sulfate for seizure prophylaxis monitor fluid balance, I/O, daily weights, symptoms, reflexes, HCT, plts, LFT’s, proteinuria fetal distress BP despite aggressive Rx worsening end-organ function development or worsening of HELLP syndrome development of eclampsia Antihypertensive Therapy Most commonly, for acute control: hydralazine, labetolol Nifedipine may be used, but unexpected hypotension may occur when given with MgSO4 For refractory hypertension: nitroglycerin or nitroprusside may be used Nitroprusside dose and duration should be limited to avoid fetal cyanide toxicity Usually require invasive arterial pressure mon Angiotensin-converting enzyme (ACE) inhibitors contraindicated due to severe adverse fetal effects Seizure Prophylaxis & Treatment Magnesium sulfate vs. phenytoin for seizure prophylaxis in preeclampsia Lucas, et al., N Engl J Med 1995;333:201-5. 2138 patients (75% had mild PIH) Maternal & fetal outcomes similar except 10 seizures in the phenytoin group (0 in MgSO4) Mg vs. diazepam & Mg vs. phenytoin for preventing recurrent seizures in eclamptics Eclampsia Trial Collaborative Group, Lancet 1995;345:1455 Mg pts were 52% or 67% less likely to have a recurrent seizure than diazepam or phenytoin pts Seizure Prophylaxis Evidence is strong that magnesium sulfate is indicated for seizure treatment in eclamptics seizure prophylaxis in severe preeclamptics Role of magnesium prophylaxis in mild preeclamptics is less clear awaits large, prospective, randomized, placebo-controlled trial Magnesium Sulfate Magnesium sulfate has many effects; its mechanism in seizure control is not clear. NMDA (N-methyl-D-aspartate) antagonist vasodilator increases release of prostacyclin Potential adverse effects: toxicity from overdose (respiratory, cardiac) bleeding hypotension with hemorrhage uterine contractility Brain parenchymal vasodilation demonstrated in preeclamptics by Doppler ultrasonography Magnesium Sulfate Renally excreted Preeclamptics prone to renal failure Magnesium levels must be monitored frequently either clinically (patellar reflexes) or by checking serum levels q 6-8 hours Therapeutic level: Patellar reflexes lost: Respiratory depression: Respiratory paralysis: Cardiac arrest: 4-7 meq/L 8-10 meq/L 10-15 meq/L 12-15 meq/L 25-30 meq/L Treatment of magnesium toxicity: stop MgSO4, IV calcium, manage airway Treatment of Eclampsia Seizures are usually short-lived. If necessary, small doses of barbiturate or benzodiazepine (STP, 50 mg, or midazolam, 1-2 mg) and supplemental oxygen by mask. If seizure persists or patient is not breathing, rapid sequence induction with cricoid pressure and intubation should be performed. Patient may be extubated once she is completely awake, recovered from neuromuscular blockade, and magnesium sulfate has been administered. Anesthetic Goals of Labor Analgesia in Preeclampsia To establish & maintain hemodynamic stability (control hypertension & avoid hypotension) To provide excellent labor analgesia To prevent complications of preeclampsia intracerebral hemorrhage renal failure pulmonary edema eclampsia To be able to rapidly provide anesthesia for C/S Benefits of Regional Analgesia for Labor in Preeclampsia Superior pain relief over parenteral narcotics Beneficial hemodynamic effects: 20% reduction in blood pressure with a small reduction in SVR & maintenance of CI Newsome, Anes Anal 1986;65:31-6 Doppler velocimetry shows epidural analgesia reduces the S-D flow ratio in the uterine artery by 25% to levels seen in non-preeclamptics Ramos-Santos, et al., Obstet Gynecol 1991;77:20-6 vascular resistance & relief of vasospasm Benefits of Regional Analgesia for Labor in Preeclampsia Epidural analgesia intervillous blood flow 77% in severe preeclamptics without maternal BP or FHR abnormalities Jouppila, et al., Obstet Gynecol 1982;59:158-61. Large series (385) preeclamptic patients; labor epidural analgesia vs. PCIA meperidine No difference in FHR abnormalities or C/S forceps in epi group but 0.125% bupi infusion naloxone use, umb artery pH, 1 min Apgar in PCIA group Lucas, et al., Anesthesiology 1998;89:A1033 Regional Anesthesia & Preeclampsia One of the most important advantages of labor epidural analgesia is that it provides a route for rapid initiation of anesthesia for emergency C/S. In the past there were concerns re: use of regional anesthesia for C/S in preeclamptics possibility of severe BP 2° sympathectomy in patient with volume contraction risk of pulmonary edema due to excessive fluid administration with regional block risk with use of pressor agents to treat BP Regional vs. General Anesthesia for C/S in Severe Preeclampsia General vs. spinal (CSE) vs. epidural Wallace, et al., Obstet Gynecol 1995;86:193-9 Prospective, randomized study All these types of anesthesia were used safely BP on laryngoscopy avoided by controlling hypertension pre-op with hydralazine; IV NTG & lidocaine immediately pre-intubation BP with regional avoided by 1000 cc LR preload & 5 mg boluses of ephedrine for SBP 100 Regional vs. General Anesthesia for C/S in Severe Preeclampsia BP 20% lower in regional vs general groups at skin incision only; no difference in min pressures Regional pts received 800 cc more IV fluid 2200 cc vs. 1500 cc No associated pulmonary edema Infant outcomes were similar Caveat: cases were not urgent; none for nonreassuring FHR pattern In an urgent situation there might not be time to adequately control hypertension pre-op prior to inducing general anesthesia Epidural vs. Spinal Anesthesia for C/S in Severe Preeclampsia Hood, et al., Anesthesiology 1999;90:1276-82 Retrospective study Lowest intraoperative blood pressures not different Total ephedrine use was small & not different Spinal group received 400 cc more IV fluid No pulmonary edema attributable to intraop fluid Maternal & infant outcomes were similar Regional vs. General Anesthesia in Preeclampsia Epidural anesthesia would probably be preferred by many anesthesiologists in a severely preeclamptic pt in a non-urgent setting For urgent cases it is reassuring to know that spinal is also safe This allows us to avoid general anesthesia with the potential for encountering a swollen, difficult airway and/or labile hypertension Regional vs. General Anesthesia in Preeclampsia General anesthesia is a well-known hazard in obstetric anesthesia: 16X more likely to result in anesthetic-related maternal mortality Mostly due to airway/respiratory complications, which would only be exaggerated in preeclampsia Hawkins, Anesthesiology 1997;86:273 Platelets & Regional Anesthesia in Preeclampsia Prior to placing regional block in a preeclamptic it is recommended to check the platelet count. No concrete evidence at to the lowest safe platelet count for regional anesthesia in preeclampsia Any clinical evidence of DIC would contraindicate regional In the absence of such signs, most anesthesiologists would proceed at plt count >100K, many would proceed at 80-100K, <80K some would proceed (esp. spinal) Platelets & Regional Anesthesia in Preeclampsia When placing a regional block in a patient with a platelet count < 100K, the most important thing is to monitor resolution of block closely Bleeding time has been discredited as an indicator of epidural bleeding risk and is not indicated. Channing-Rogers, Semin Thromb Hemost 1990;16:;1-30 Low-dose aspirin is not a contraindication to regional anesthesia in preeclampsia CLASP study: 1422 women on aspirin received epidurals without any bleeding complications Hazards of General Anesthesia in Preeclampsia Airway edema is common Mandatory to reexamine the airway soon before induction Edema may appear or worsen at any time during the course of disease tongue & facial, as well as laryngeal Laryngoscopy and intubation may severe BP Labetolol & NTG are commonly used acutely Fentanyl (2.5 mcg/kg), alfentanil (10 mcg/kg), lidocaine may be given to blunt response Hazards of General Anesthesia in Preeclampsia Magnesium sulfate potentiates depolarizing & non-depolarizing muscle relaxants Pre-curarization is not indicated. Initial dose of succinylcholine is not reduced. Neuromuscular blockade should be monitored & reversal confirmed. Invasive Central Hemodynamic Monitoring in Preeclampsia Usually reserved for patients with complications oliguria unresponsive to modest fluid challenge (500 cc LR X 2) pulmonary edema refractory hypertension Poor correlation between CVP and PCWP in PIH However, at most centers anesthesiologists would begin with CVP & follow trend not arbitrarily hydrate to a certain number If poor response, change to PA catheter may have increased CO or increased SVR Conclusions Preeclampsia is a serious multi-organ system disorder of pregnancy that continues to defy our complete understanding. It is characterized by global endothelial cell dysfunction. The cause remains unknown. There is no effective prophylaxis. Conclusions Delivery is the only effective cure. Magnesium sulfate is now proven as the best medication to prevent and treat eclampsia. Epidural analgesia for labor pain management & regional anesthesia for C/S have many beneficial effects & are preferred.
Pages to are hidden for
"Preeclampsia and Eclampsia Anesthetic Management"Please download to view full document