Transcript Anesthetic Management of Preeclampsia and Eclampsia

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
advanced region: 46% of deaths
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:
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
Indications for expedited delivery:
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
Brain parenchymal vasodilation demonstrated in
preeclamptics by Doppler ultrasonography
increases release of prostacyclin
Potential adverse effects:
toxicity from overdose (respiratory, cardiac)
 bleeding
 hypotension with hemorrhage
 uterine contractility
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
may have increased CO or increased SVR
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
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.