SEVERE PREECLAMPSIA/CONTINUOUS SPINAL ANESTHESIA
From Anesthesiology Update 2007, sponsored by the David Geffen School of Medicine at the University of
California, Los Angeles, November 17, 2007
| SEVERE PREECLAMPSIA: ANESTHETIC IMPLICATIONS OF THE DISEASE AND THERAPIES Judi A. Turner,
MD, PhD, Clinical Instructor, Center for Health Sciences, Department of Anesthesiology, David Geffen School of Medicine
at the University of California, Los Angeles
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| Preeclampsia: occurs in 6% to ≤12% of pregnancies after 20 wk gestation; third leading cause of maternal mortality in
United States; diagnostic criteria include hypertension (sustained >140/90 mm Hg) and proteinuria >300 mg per day;
edema common but no longer diagnostic criterion; may be superimposed on chronic hypertension (look for changes in
level of blood pressure [BP] control); may progress to severe preeclampsia or eclampsia; signs should remit by 6 to 12
wk postpartum
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| Severe preeclampsia: sustained BP ≥160/110 mm Hg (measured twice); increased proteinuria (corresponds to increased
renal involvement and decreased glomerular filtration rate [GFR]); oliguria with urine output <400 mL over 24 hr; evidence
of other end-organ damage (eg, central nervous system [CNS] disturbance, pulmonary edema, epigastric pain,
thrombocytopenia, hemolysis, elevated liver enzymes, and low platelets [HELLP syndrome]) and evidence of fetal compromise
(eg, oligohydramnios); increased risk for placental abruption (especially with history of preeclampsia superimposed
on chronic hypertension)
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| Eclampsia: CNS involvement resulting in seizure; etiology probably multifactorial (vasoconstriction, ischemia, vasogenic
edema); no reliable tests for predicting development of eclampsia; risk for seizure ≈1%; antepartum and intrapartum periods
times of highest risk, but ≤40% of seizures occur in postpartum period; magnesium sulfate gold standard for reducing
risk for seizure in severe preeclampsia
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| Risk factors for preeclampsia: history of preeclampsia; nulliparity; history of hypertension (25% of those with chronic
hypertension develop preeclampsia); renal disease; diabetes; underlying vascular disease; black ethnicity; age >40 yr;
obesity; multi-fetus pregnancy; increased trophoblastic mass; paternity by man who fathered previous preeclamptic pregnancy
in another woman; factor V Leiden mutation
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| Etiology of preeclampsia: immunity modelself vs nonself, with loss of immunity control; disease state; danger
modelabnormal cell death in pregnancy; expression of specific danger signals and potential activation of antifetal immunity;
geneticsfactor V Leiden mutation; angiotensin receptor abnormalities; endothelial factorsabnormal invasion
of trophoblastic tissue; decreased prostaglandin production; increased thromboxane production; lead to uteroplacental insufficiency
or decreased circulation, ischemia, oxidative stress, and development of free radicals; platelet factors
platelet dysfunction; surface-mediated platelet activation causes decreased sensitivity to prostacyclin and increased
thromboxane production at activated platelet sites; in mild preeclampsia, lead to upregulation of renin-angiotensin-aldosterone
system in uteroplacental area; increases uteroplacental blood flow (BF); also cause maternal hypertension; in severe
cases, cause problems with renin-angiotensin system (maternal hypertension without additional uteroplacental BF)
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| Pathophysiology of preeclampsia: CNSvisual changes; hyperexcitability; eclampsia; cardiovascularincreased
sensitivity to endogenous and exogenous controls; hyperdynamic state may change to low output, high resistance state;
intravascular volume depletion common; respiratoryincreased pharyngolaryngeal edema (airway examination important);
lower colloid oncotic pressure; increased vascular permeability; increased risk for pulmonary edema;
hematologichypercoagulability; platelet activation; activation of fibrinolytic system; renaldecreased GFR; proteinuria;
oliguria correlates with severe disease; hepaticincreased serum transaminase and edema/bleeding; risk for
hepatic hemorrhage associated with high mortality; endocrineimbalance of thromboxane and prostaglandin;
uteroplacentaldecreased BF; intrauterine growth restriction; oligohydramnios
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| Obstetric management of preeclampsia: mild preeclampsiatypically done as outpatient; may include antihypertensive
agent; monitor closely; may include bed rest (depends on severity and patient history); frequent fetal monitoring as
part of expectant management; severe preeclampsiaexpectant management only if patient stable on antihypertensive
medications with stable laboratory values and reassuring fetal tests (recommended that only tertiary care hospital with
close maternal and fetal monitoring be used); antihypertensive medications include hydralazine, labetalol, and nifedipine;
goals include diastolic BP 90 to 105 mm Hg or mean arterial pressure (MAP) 100 to 125 mm Hg; nitroglycerin or nitroprusside
reserved for hypertensive emergency or encephalopathy; seizure prophylaxis with magnesium sulfate (loading
dose, 4-6 g; infusion, 1-4 g/hr; goal, serum concentration 5 to 8 mg/dL); continue for ≥24 hr postpartum; additional
definitive treatment always delivery of fetus and placenta, preferably vaginally; induced if at ≥37 wk gestational age, fetal
lungs mature, cervix favorable, or maternal or fetal deterioration occurs despite conservative management; prophylaxis
with aspirin not proven successful and not recommended; American College of Obstetricians and Gynecologists
(ACOG) guidelines confirm regional anesthesia (RA) appropriate in most patients without coagulopathy
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| Anesthetic implications of magnesium sulfate: side effects include headache, nausea, vomiting, flushing, and weakness;
direct vasodilation may improve uteroplacental BF; may decrease uterine tone, increasing risk for postpartum
bleeding; augmentation of neuromuscular blockade; inhibition of calcium-mediated presynaptic release of neurotransmitters;
analgesic properties; toxicity (loss of deep tendon reflex at 9-12 mg/dL; precursor to respiratory depression and cardiovascular
collapse that could happen at higher doses; treat with calcium chloride or calcium gluconate); neonatal
effects may include hypotonia and respiratory depression; increases risk for pulmonary edema (probably due to fluid
overload with continuous infusion); usually reserved for severe preeclampsia
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| Indications for urgent delivery in preeclampsia: severe refractory hypertension for >24 hr; worsening thrombocytopenia;
worsening hepatic or renal disease; eclampsia or premonitory signs of eclampsia (eg, neurologic changes); evidence
of fetal growth restriction
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| Anesthetic preoperative evaluation: history should determine severity of disease and degree of medical optimization;
careful physical examination, especially of airway and lungs, due to increased pharyngeal and pulmonary edema; assessment
of volume status (eg, changes in urine output); assessment of coagulation status
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| Pulmonary edema in preeclampsia: serious complication associated with 3% of cases of severe preeclampsia; consider
echocardiography if concerned about cardiac etiology; age and parity increase risk; often occurs in association with excess
fluid administration; high maternal (≈10%) and perinatal (≤50%) mortality
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| Anesthetic management of preeclamptic parturient: RA decreases risk for aspiration and failed intubation; general
anesthesia (GA) preferred in cases of suspected placental abruption, coagulopathy, severe pulmonary edema, eclampsia,
severe fetal distress, and patient refusal; RA may decrease swings in BP in response to painful stimuli in preeclampsia;
epidural considered standard in nonemergency cases; Foley catheter important part of monitoring; volume expansion typically
recommended (maximum bolus, 10 mL); in case of bleeding, avoid methylergonovine (Methergine), due to risk for
severe hypertension; carboprost (Hemabate) may be considered
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| Anesthesia and maternal mortality: anesthesia remains significant cause; in recent years, maternal mortality has declined
from 4 cases per million patients to 1 case per million patients; mortality risk with GA, 17 cases per million patients
(50% related to failed airway management); failed intubation 10 times more likely in obstetric patients
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| CONTINUOUS SPINAL ANESTHESIA (CSA)James Moore, MD, Associate Clinical Professor of Anesthesiology,
David Geffen School of Medicine at the University of California, Los Angeles
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| Cauda equina syndrome: in early 1990s, after many uses of spinal microcatheter, cauda equina syndrome reported; studies
initially indicated possible sacral pooling of hyperbaric local anesthetic; Food and Drug Administration withdrew use
of catheters <24-gauge (for spinal anesthesia) from US market; microcatheter still in use in Europe; investigations
showed that with high doses of hyperbaric local anesthetic (especially high-concentration lidocaine), possible for tip of
catheter to be positioned so that pooling occurred, allowing high concentration, neurotoxicity, and direct contact with
nerve tissue
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| Advantages and disadvantages of single-shot spinal anesthesia: advantagesreliable; rapid onset; simple to perform;
good motor block (compared to other neuraxial techniques); disadvantagesvariable duration; prolonged discharge;
hemodynamic effects
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| Determinants of extent and duration of spinal anesthesia: lumbosacral cerebrospinal fluid (CSF) volume; correlation
between CSF volume and block height, as defined by pin prick and transcutaneous electrical stimulation; important influences
include CSF density and velocity of CSF within subarachnoid space; some data indicate CSF density in men higher
than in women, especially pregnant women; with higher CSF density, higher spinal block may result from hypobaric solution
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| Spinal anesthesia vs epidural anesthesia: spinallocal anesthetic effect acts primarily within spinal cord; local anesthetic
initially placed at level lower than spinal cord; block sets up in most sacral portion of spinal cord; generally single-
shot technique; height determined by position, baricity, and dose; epiduralblock characteristics different because epidural
local anesthetics act within epidural space, primarily at level of nerve root; often results in segmental block; placed
at any level, as opposed to only lumbar areas; larger doses of local anesthetics cause concern for toxicity; anatomic barriers
include lumbar lordosis and size of sacral nerve roots; may make certain block characteristics, especially in low lumbosacral
area, less attractive, compared to dense spinal block
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| Spinal catheter vs combined spinal-epidural anesthesia: continuous spinallonger duration of effect, with benefits
similar to those of single-shot spinal, including good sacral root block, excellent motor block, use of low dose with low
concerns for toxicity, and good reliability; continuous epidural combined with single-shot spinalredosing primarily
has effect in lumbothoracic area; eventually lose spinal block; possibly less motor block with lumbothoracic top-up dosing;
lower incidence of postdural puncture headache than with spinal catheter; epidural catheterequipment widely
available in United States; epidural equipment routinely used to place spinal catheter; commonly used for postoperative
analgesia; reasons to use CSApotentially indefinite duration of spinal block, careful titration of initial dosing, better
motor block (compared to epidural), and minimal risk for postdural puncture headache in elderly
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| Dosing of CSA: Ben-David study (minidose bupivacaine-fentanyl spinal anesthesia for surgical repair of hip fracture in
elderly) found that anesthesia-related hypotension less pronounced in patients receiving bupivacaine (4 mg) plus fentanyl
than in patients receiving bupivacaine 10 mg; study of hyperbaric bupivacaine 7.5 mg, with or without epinephrine 0.2
mg, found many more subjects had complete motor block of lower extremities when epinephrine added; overall duration
of motor block also prolonged; epinephrine not advocated for outpatient use
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| Comparisons between CSA and other popular neuraxial techniques: analysis of elderly patients having lower-limb
surgery with bupivacaine 0.5%; with continuous spinal technique, patients received 5 mg, then 5 mg again if block below
T11; with lumbar epidural anesthesia, patients received 10 mL, then 5 mL if necessary; single-shot spinal group received
15-mg dose; change in MAP that occurred with single-shot spinal anesthesia and lumbar epidural anesthesia significant,
compared to no change with CSA; other studies also show less dosing of ephedrine and phenylephrine to support BP with
incrementally dosed CSA
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| Indications for CSA: severe aortic stenosis, lengthy surgery, need for good motor block, and sacral root block; CSA may
also be used when intending to perform epidural catheter placement but you get a wet tap; acceptable to proceed with
spinal catheter insertion; use 17-gauge epidural needle and epidural catheter, loss-of-resistance technique, and then insert
a little farther (identified by dural click upon entering subarachnoid space); speaker uses paramedian approach,
with tangential angle to spinal cord; paresthesias common, although usually benign, during spinal catheter insertion;
other equipment (eg, coaxially placed spinal needle through epidural needle, with catheter over needle) may soon be
available; speaker uses plain bupivacaine 0.5%, dosed appropriately for situation; for maximum motor block, consider
adding epinephrine (may make onset of block more rapid; could potentially increase risk for drop in BP); wait 15 to 20
min before redosing (90-120 min after initial dose); use transcutaneous electrical stimulation or nerve stimulator pads to
objectively assess block level; place at 2 dermatome levels above required location; once patient initially situated, verify
that able to give 60 mA of 50 Hz tetany for 5 sec (good correlation to surgical stimulation)
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| Obstetric anesthesia and labor analgesia: study of CSA for use in labor with aortic stenosis; patients initially given
intrathecal sufentanil, then administered combination ropivacaine and sufentanil; combination dosed for 21 hr after induction;
with occasional redosing, BP and heart rate stable throughout; report of CSA used during cesarean delivery
and surgical anesthesiasevere recurrent peripartum cardiomyopathy; also severe mitral regurgitation and pulmonary
hypertension; spinal catheter placed with incremental dosing of bupivacaine 0.5%, ≤10 mg, and T8 block conferred; initially
after spinal block, symptoms of heart failure markedly improved; nitroglycerin titrated to decreased BP (≈25%
decrease from baseline 5 min before delivery in anticipation of autotransfusion); when wet tap occurs and decision made
to insert spinal catheter, you may actually be substantially reducing the risk of postdural puncture headache; placing
epidural at another level leads to high incidence of postdural puncture headache; removing spinal catheter 1 day after delivery
substantially reduces incidence; weigh against potential risk of keeping catheter in place (eg, CSF leakage, aseptic
meningitis); regimen for labor analgesiaincludes loading dose of bupivacaine and fentanyl 10 µg; complications include
postdural puncture headache and difficulty threading catheter; assess risk of alternatives when choosing anesthetic
technique; insertion of 2 to 4 cm recommended, using lowest effective concentration (avoid lidocaine 5%); limit total
dose; change patient position if necessary
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Suggested Reading
American Society of Anesthesiologists Task Force on Obstetric Anesthesia: Practice guidelines for obstetric anesthesia:
an updated report by the American Society of Anesthesiologists Task Force on Obstetric Anesthesia. Anesthesiology
106:843, 2007; Ben-David B et al: Intrathecal fentanyl with small-dose dilute bupivacaine: better anesthesia without
prolonging recovery. Anesth Analg 85:560, 1997; Ben-David B et al: Minidose bupivacaine-fentanyl spinal anesthesia
for surgical repair of hip fracture in the aged. Anesthesiology 92:6, 2000; Cyna AM et al: Clinical update: obstetric anaesthesia.
Lancet 370:640, 2007; Haddad B et al: Maternal and perinatal outcomes during expectant management of 239
severe preeclamptic women between 24 and 33 weeks' gestation. Am J Obstet Gynecol 190:1590, 2004; Hawkins JL:
Maternal mortality: anesthetic implications. Int Anesthesiol Clin 40:1, 2002; Klimscha W et al: Continuous spinal anesthesia
with a microcatheter and low-dose bupivacaine decreases the hemodynamic effects of centroneuraxis blocks in elderly
patients. Anesth Analg 77:275, 1993; Minville V et al: Spinal anesthesia using single injection small-dose
bupivacaine versus continuous catheter injection techniques for surgical repair of hip fracture in elderly patients. Anesth
Analg 102:1559, 2006; Moore JM et al: The effect of epinephrine on small-dose hyperbaric bupivacaine spinal anesthesia:
clinical implications for ambulatory surgery. Anesth Analg 86:973, 1998; Santos AC et al: Spinal anesthesia for cesarean
delivery in severely preeclamptic women: don't throw out the baby with the bathwater! Anesth Analg 101:859,
2005; Santos AC, Birnbach DJ: Spinal anesthesia in the parturient with severe preeclampsia: time for reconsideration.
Anesth Analg 97:621, 2003; Sibai BM: Magnesium sulfate prophylaxis in preeclampsia: Lessons learned from recent trials.
Am J Obstet Gynecol 190:1520, 2004; Van de Velde M et al: Continuous spinal analgesia for labor pain in a parturient
with aortic stenosis. Int J Obstet Anesth 12:51, 2003; Visalyaputra S et al: Spinal versus epidural anesthesia for
cesarean delivery in severe preeclampsia: a prospective randomized, multicenter study. Anesth Analg 101:862, 2005.
Educational Objectives
| The goal of this program is to improve the anesthetic management of severe preeclampsia and compare continuous spinal
anesthesia with other popular neuraxial techniques. After hearing and assimilating this program, the clinician will be better
able to:
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 | 1. Review the incidence and diagnostic criteria for severe preeclampsia.
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 | 2. Summarize the obstetric management of severe preeclampsia.
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 | 3. Examine how severe preeclampsia and obstetric management of the disease affects anesthetic management.
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 | 4. Compare advantages and disadvantages of continuous spinal anesthesia (CSA) with those of other neuraxial techniques.
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 | 5. Identify the indications for CSA, focusing on obstetric anesthesia and labor analgesia.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and planning committee
members to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of
interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and
not a proprietary business or commercial interest. For this program, the faculty and planning committee reported nothing to
disclose.
Acknowledgements
Drs. Turner and Moore spoke in Los Angeles at Anesthesiology Update 2007, held November 17, 2007, and sponsored by
the David Geffen School of Medicine at the University of California, Los Angeles. The Audio-Digest Foundation thanks
the speakers and the sponsor for their cooperation in the production of this program.
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