Epidural - SAB - GA
Systemic Effects

(from lecture by Jeff Hollingsworth, M.D. 1/16/03)

Hypertensive disease is second only to thromboembolic disorders as a cause of maternal mortality in the U.S.
Accounts for 15-19% of maternal deaths in the United States and the U.K.
Preeclampsia is responsible for a significant percentage of these deaths yearly
Preeclampsia affects 5-8% of all pregnancies and 14-20% of primigravidas
85% of cases of preeclampsia affect women during their first pregnancy
According to ACOG, there are two distinct forms of hypertension during pregnancy: pregnancy-induced hypertension (PIH) and chronic hypertension. These may co-exist

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Preeclampsia: patients with PIH who have renal involvement causing proteinuria. 2 forms: mild and severe. Diagnostic criteria:
SBP 140 mm Hg or higher OR DBP 90mm Hg or higher occurring after 20 weeks of gestation in a woman whose blood pressure was previously normal
Proteinuria, with excretion of 0.3 g  or more in a 24 hour period
Severe preeclampsia (one or more of following):
SBP >= 160 mm Hg OR DBP >= 110 mm Hg on two occasions 6 or more hours apart in a pregnant woman on bed rest
Proteinuria with excretion > 5g in 24 hour urine
Oliguria, with less than 500ml over 24 hours
Pulmonary edema or cyanosis
Impairment of liver function
Visual or cerebral disturbances
Pain in epigastric area or right upper quadrant
Intrauterine growth restriction (IUGR)
when a woman with preeclampsia has new-onset grand mal seizures
HELLP syndrome:
severe preeclampsia and liver involvement (hemolysis, elevated liver enzymes, and low platelets)

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Several theories; all agree the presence of placental tissue is necessary
Most widely held theory centers on the failure of secondary trophoblastic invasion into the uterine wall
This is likely immunologic in origin, but the exact mechanism remains unclear (remember half the genes are from daddy)
In normal patients, by 20 weeks fetal trophoblastic cells have invaded and replaced the endothelium, internal elastic lamina, and musculoelastic media of the uterine spiral arteries (eliminating adrenergic receptors)
This creates a high flow/low pressure system in the placental bed
In preeclamptics, the absence of this process leave spiral arteries intact and responsive to vasopressors causing a lower flow high pressure placental circulation
It is postulated that this causes placental hypoperfusion which results in the release of cytokines and free radicals
These cytokines and free radicals cause widespread endothelial dysfunction including interendothelial cell leak, and an imbalance between vasoconstricting substances and vasodilating substances (thromboxane and prostacyclin)
Most commonly affects the placental decidual vessels and the renal microvasculature
Endothelial injury may cause arteriolar vasopasm in hepatic, cardiac, and cerebral circulations
The overall picture centers on vasospasm accompanied by intravascular volume depletion as well as endothelial dysfunction and vessel leak

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Systemic Effects

Increased and labile blood pressure
Decreased colloid oncotic pressure
Intravascular volume depletion
Systemic vasoconstriction
Congestive heart failure

Thrombocytopenia occurs in 15-30% of women with preeclampsia, platelet count < 100K in 10%
Hypercoagulable, increased risk for thromboembolic disease
Coagulopathy, activation of fibrinolysis
Disseminated intravascular coagulation

GFR averages 25% less than normal parturient
Proteinurea secondary to increased vascular permeability
Oliguria defined as < 400ml over 24 hrs
Rarely creatinine changes
Acute tubular necrosis

High risk of upper airway narrowing from pharyngolaryngeal edema
Pulmonary edema (noncardiogenic>cardiogenic)

Transaminases frequently elevated even in mild preeclamptics
Epigastric/Subcostal pain (distension of liver capsule by edema or subcapsular bleeding)
Coagulopathy (high INR)
Decreased drug metabolism

Visual disturbances (scotomata)
Intracranial hemorrhage
Seizures: ? hypertensive encephalopathy, vasospasm, microemboli, cerebral edema, thromboses, punctate hemorrhages

Decreased uteroplacental perfusion
IUGR/ olighydramnios
Placental abruption
Preterm labor and delivery

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Obstetric Management
The only true cure for preeclampsia is delivery of the placenta
Mild preeclampsia often managed on outpatient basis with weekly nonstress tests and/or biophysical profiles
Frequent laboratory testing (urine protein, platelets, LFT's) and BP measurement
Sometimes hospital admission and bed rest is warranted
When pregnancy is remote from term (28-32 weeks) some recommend delayed delivery with bed rest, antihypertensives, and intensive fetal monitoring
Must closely follow BP, UOP, Biophysical profiles, LFT's, platelets, Fluid balance
Magnesium is first line treatment for seizure prophylaxis
Magnesium is routinely continued postpartum because 25% of the cases of Eclampsia occur during this time

Induction of Labor - Indications:
37 weeks gestation
Fetal lung maturity
Favorable cervix
Increasing BP despite conservative measures
Any evidence of maternal or fetal deterioration warrants prompt delivery regardless of gestational age

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Anesthetic Considerations

Preoperative Assessment
A Airway - careful evaluation, often have pharyngolaryngeal edema (hoarseness or stridor)
B Breathing - O2 sat, listen for rales (occasionally pulmonary edema present)
C Circulation - blood pressure (often labile) risk of both severe hyper- and hypotension, look for exam signs of increased SVR and intravascular depletion (supine hypotensive syndrome)
C Cardiac - any signs of cardiac disease, CHF
D De head: Neuro - MS, premonitory sx's of seizure (HA, visual Sx's, other neuro findings)
E,F Electrolytes, Fluids: Renal - look at recent trends in UOP (oliguria?), BUN/creatinine
G GI - last meal, severity of GERD symptoms, abdominal pain? (Liver)
H Heme - platelets can be low (look at trend!), check coags if signs of liver involvement (HELLP), petechia/bruising
Magnesium - if on board must consider potentiation of nondepolarizing NM blockers, also can blunt vasopressor response (affects calcium facilitated neurotransmitter/catecholamine release)

Labor and Vaginal Delivery
Epidural analgesia has numerous advantages in the preeclamptic (mild and severe) and is the preferred method of analgesia/anesthesia
Offers superior pain control than IV analgesia without increase in C-section rate in this population
Attenuates hypertensive response to pain
Facilitates BP control
May improve intervillous blood flow
Increased risk of C-section in this population --> can use epidural for urgent/emergent C-section

Cesarean Delivery
Higher rate of c-section in preeclamptic population
For elective and non-urgent c-section in mild preeclamptics, epidural or SAB are safe, acceptable options
Often times urgent or emergent secondary to maternal or fetal decompensation
Epidural is preferred technique if no contraindications and time is available
In severe preeclampsia, there is some concern over the profound hypotension that can occur with SAB, preference being epidural if possible

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Epidural - technique
Prehydrate with crystalloid/colloid to help attenuate hypotension, which can be magnified in the face of preeclampsia
Epidural solution typically a low concentration of bupivicaine (.04-.125%)
Slow titration of local anesthetic
Ephedrine and left lateral tilt for hypotension refractory to fluid challenge
Elective cesarean delivery - epidural anesthetic options include:
0.5% Bupivicaine
0.5% Ropivicaine
2% Lidocaine with or w/o epinephrine
urgent or emergent c-section
Epidural - if already present, use it!
3% 2-chlorprocaine, OR
2% lidocaine with epinephrine
Some practitioners prefer not to use epinephrine in local secondary to concern for severe hypertensive response
Titrate in as gently as time will allow

Epidural - contraindications
Patient refusal - be sure patient has all of the correct information "my cousins step-aunt from Akron was paralyzed"
Local or systemic infection (sepsis)
Uncorrected hypovolemia/hemorrage
Approach varies from practitioner to practitioner
Very common in preeclampsia/PIH, one of the major criteria for HELLP
No definite minimum value has been defined
Most pick 75K-100K as a cutoff
Following trends of platelet counts ( e.g.. 130 --> 90 --> 70) is felt to be a better predictor of risk than a particular number

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Subarachnoid Block:
is used in both mild and severe preeclamptics, elective and  urgent cases
Some controversy regarding use in severe preeclamptics
Biggest concern over intravascular depletion and profound hypotensive response from SAB
Hood et al claim in recent retrospective review:
no difference in degree of hypotension in SAB vs. Epidural in severe preeclamptics
Argue that SAB is fast, reliable, safer alternative to GA
In patients with degree of coagulopathy, smaller needle(25-27g) reduces risk of epidural hematoma
As in epidural, preload with crystalloid 10cc/kg to 1L. Be ready with ephedrine
Usually a 10.5 to 13.0mg dose of 0.75% "heavy bupivicaine", sitting or lateral position

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General Anesthesia:
avoid it if you can
Major risks:
Difficulty with airway
Risk of aspiration
Hypertensive response to laryngoscopy

Difficulty Airway:
Pharyngolaryngeal edema is common in preeclamptics as they have lower plasma oncotic pressure, and generalized edema
May not be recognized until laryngoscopy
Have assortment of ETT(5-0, 5-5, 6-0)
Short handles
Fiberoptic cart, difficult airway cart in room

Risk of aspiration:
Sodium Citrate orally
Cricoid/RSI - thiopental and succinylcholine
Magnesium on board can potentiate non-depolarizing neuromuscular blockers
Orogastric tube

Hypertensive response to laryngoscopy:
concern for ICH, increased myocardial O2 demands, pulmonary edema, decreased UBF
May use hydralazine, labetalol, SNP, NTG, fentanyl
Be careful with IVF, as third spacing is common

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Problems to consider
IV access in an edematous, dry patient
Bleeding/  fluid management
Coagulopathy, need for FFP, platelets
Backup plan (this will likely involve airway)

Hydralazine 5mg IV incrementally
Labetalol 5-10 mg IV
May need SNP gtt or NTG gtt in severe cases
Some OB's like to use Methyldopa

Fluids, but beware of noncardiogenic pulmonary edema
Ephedrine, expect a dramatic response to pressors
Left uterine tilt
Phenylephrine, may not contribute to uterine vasoconstriction as much as once thought

IV/ monitoring:
Try to have an extra IV in place in patients that are high risk of going to c-section
Arterial line in patients with obesity, severe HTN (requiring SNP/ NTG gtt), ongoing hemorrhage/abruption
CVP/PAC may be useful in those with pulmonary edema

Blood products:
In severe preeclamptics and/or HELLP patients, be sure to type and cross for RBC's, FFP, platelets
Also in suspected abruption, possible DIC

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American College of Obstetricians and Gynecologists. Hypertension in Pregnancy. ACOG Technical Bulletin No. 219, Washington, D.C., January 1996.
Berg CJ, Atrash HK, Koonin LM, Tucker M. Pregnancy-related mortality in the United States, 1987-1990. Obstet Gynecol 1996; 88:161-7.
Chesnut DH. Obstetric Anesthesia. Mosby, 1999. pp. 875-920.
American College of Obstetricians and Gynecologists. Diagnosis and Management of Preeclampsia and Eclampsia. ACOG practice Bulletin No. 33. Obstet Gynecol Jan. 2002.
Am J Obstet Gynecol 1989; 161:1200-4
Lancet 341:1447-1451, 1993
Hood DD and Curry R. Spinal versus Epidural Anesthesia for Cesarean Section in Severely Preeclamptic Patients. Anesthesiology 1999; 90: 1276-1282.

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