Professional Documents
Culture Documents
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
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
60
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
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
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:
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
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
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 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.
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
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.