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Preeclampsia and Eclampsia:

Anesthetic Management

Harfah, Ns
Assistant Clitical Specialist Nursing
Director of Anesthesia and Reanimation
Univ of Indonesian

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, thromboxanes 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,
mg aspirin daily vs. placebo

60

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 Postpartum
Normal pregnancy: 22 mm Hg
17 mm Hg
Preeclampsia: 18 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, LFTs, 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 MgSO 4
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:
4-7 meq/L
Patellar reflexes lost:
8-10 meq/L
Respiratory depression:
10-15 meq/L
Respiratory paralysis:
12-15 meq/L
Cardiac arrest: 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, 12 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 anestheticrelated 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.