Introduction
• 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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Definitions
• Preeclampsia: patients with PIH who have renal involvement causing proteinuria. 2 forms: mild and severe. Diagnostic criteria:
Preeclampsia:
– 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
– Thrombocytopenia
– Intrauterine growth restriction (IUGR)
• Eclampsia:
– 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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Pathophysiology
• 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

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

Hematologic
– 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

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

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

Hepatic
– 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

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

Uteroplacental
– 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
• Labor
– 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)
• Coagulopathy
• Uncorrected hypovolemia/hemorrage
• Thrombocytopenia
– 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
– Hypertension
– Hypotension
– IV access in an edematous, dry patient
– Bleeding/  fluid management
– Coagulopathy, need for FFP, platelets
– Backup plan (this will likely involve airway)

Hypertension:
– 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

Hypotension:
– 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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Bibliography
• 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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