Preeclampsia and Eclampsia Anesthetic Management

					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.


				
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