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Preeclampsia and Eclampsia: Anesthetic Management

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Preeclampsia and Eclampsia: Anesthetic Management Anita M. Backus, MD Assistant Clinical Professor Director of Obstetric Anesthesia UCLA Medical Center – PowerPoint PPT presentation

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Title: Preeclampsia and Eclampsia: Anesthetic Management


1
Preeclampsia and Eclampsia Anesthetic Management
  • Anita M. Backus, MD
  • Assistant Clinical Professor
  • Director of Obstetric Anesthesia
  • UCLA Medical Center
  • Los Angeles, California

www.anaesthesia.co.in anaesthesia.co.in_at_gmail.c
om
2
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

3
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

4
Preeclampsia Definition
  • Hypertension
  • gt 140/90
  • relative ? no longer considered diagnostic
  • Proteinuria
  • gt 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

5
Criteria for Severe Preeclampsia
  • SBP gt 160 mm Hg
  • DBP gt 110 mm Hg
  • Proteinuria gt 5 g/24 or 3-4 on dipstick
  • Oliguria lt 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

6
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 gt 40 years
  • African-American race
  • Diabetes mellitus

7
Etiology and Prevention
  • Etiology is unknown.
  • Many theories
  • genetic
  • immunologic
  • dietary deficiency (calcium, magnesium, zinc)
  • supplementation has not proven effective
  • placental source (ischemia)

8
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)

9
Preeclampsia Prophylaxis Aspirin
  • Aspirin has been extensively studied as a
    targeted therapy to ? thromboxane production
  • CLASP study, 1994, multicenter, randomized
  • CLASP Collaborative Group, Lancet
    1994343619-29
  • 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

10
Preeclampsia Prophylaxis Aspirin
  • NIH study of high-risk patients, randomized,
    60 mg aspirin daily vs. placebo
  • Caritis, et al., N Engl J Med 1998338701-5
  • 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

11
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
    1999180499-506
  • present in normal pregnancy
  • excessive in preeclampsia
  • Proposed source of inflammatory stimulus placenta

12
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)

13
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

14
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

15
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.

16
Pathophysiology
  • Coagulation
  • Generally hypercoagulable with evidence of
    platelet activation and increased fibrinolysis
  • Thrombocytopenia is common, but fewer than 10
    have platelet count lt 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

17
Obstetric Management
  • Classically stabilize and deliver
  • Medical management while awaiting delivery
  • use of steroids X 48 hours if fetus lt 34 wks
  • antihypertensives to maintain DBP lt 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

18
Antihypertensive Therapy
  • Most commonly, for acute control hydralazine,
    labetolol
  • Nifedipine may be used, but unexpected
    hypotension may occur when given with MgSO4
  • 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

19
Seizure Prophylaxis Treatment
  • Magnesium sulfate vs. phenytoin for seizure
    prophylaxis in preeclampsia
  • Lucas, et al., N Engl J Med 1995333201-5.
  • 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
    19953451455
  • Mg pts were 52 or 67 less likely to have a
    recurrent seizure than diazepam or phenytoin pts

20
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

21
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

22
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

23
Treatment of Eclampsia
  • Seizures are usually short-lived.
  • If necessary, small doses of barbiturate or
    benzodiazepine (STP, 50 mg, or midazolam, 1-2 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.

24
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

25
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 19866531-6
  • 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 19917720-6
  • ? vascular resistance relief of vasospasm

26
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 198259158-61.
  • 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 199889A1033

27
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

28
Regional vs. General Anesthesia for C/S in Severe
Preeclampsia
  • General vs. spinal (CSE) vs. epidural
  • Wallace, et al., Obstet Gynecol 199586193-9
  • 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 pre-load
    5 mg boluses of ephedrine for SBP ? 100

29
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
    non-reassuring FHR pattern
  • In an urgent situation there might not be time to
    adequately control hypertension pre-op prior to
    inducing general anesthesia

30
Epidural vs. Spinal Anesthesia for C/S in Severe
Preeclampsia
  • Hood, et al., Anesthesiology 1999901276-82
  • 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

31
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

32
Regional vs. General Anesthesia in Preeclampsia
  • General anesthesia is a well-known hazard in
    obstetric anesthesia
  • 16X more likely to result in anesthetic-related
    maternal mortality
  • Mostly due to airway/respiratory complications,
    which would only be exaggerated in preeclampsia
  • Hawkins, Anesthesiology 199786273

33
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
    gt100K, many would proceed at 80-100K, lt80K some
    would proceed (esp. spinal)

34
Platelets Regional Anesthesia in Preeclampsia
  • When placing a regional block in a patient with a
    platelet count lt 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
    1990161-30
  • Low-dose aspirin is not a contraindication to
    regional anesthesia in preeclampsia
  • CLASP study 1422 women on aspirin received
    epidurals without any bleeding complications

35
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

36
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.

37
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

38
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.

39
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.

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om
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