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 Los Angeles, California. www.anaesthesia.co.in anaesthesia.co.in@gmail.com. Preeclampsia: Epidemiology. Incidence widely quoted at 5-7%

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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

Los Angeles, California

www.anaesthesia.co.inanaesthesia.co.in@gmail.com


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


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


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


SBP > 160 mm Hg

DBP > 110 mm Hg

Proteinuria > 5 g/24° or 3-4+ on dipstick

Oliguria < 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

Criteria for Severe Preeclampsia


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 > 40 years

  • African-American race

  • Diabetes mellitus


Etiology and Prevention

  • Etiology is unknown.

  • Many theories:

    • genetic

    • immunologic

    • dietary deficiency (calcium, magnesium, zinc)

      • supplementation has not proven effective

    • placental source (ischemia)


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, thromboxane’s effects dominate

    •  thromboxane (from platelets, placenta)

    •  prostacyclin (from endothelium, placenta)


Preeclampsia Prophylaxis: Aspirin

  • Aspirin has been extensively studied as a targeted therapy to  thromboxane production

  • CLASP study, 1994, multicenter, randomized

    CLASP Collaborative Group, Lancet 1994;343:619-29

    • 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


Preeclampsia Prophylaxis: Aspirin

  • NIH study of high-risk patients, randomized, 60 mg aspirin daily vs. placebo

    Caritis, et al., N Engl J Med 1998;338:701-5

    • 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


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

    • present in normal pregnancy

    • excessive in preeclampsia

    • Proposed source of inflammatory stimulus: placenta


  • 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:

      AntepartumPostpartum

      Normal pregnancy:22 mm Hg17 mm Hg

      Preeclampsia:18 mm Hg14 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

      • Renal function recovers quickly postpartum


    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:

      • use of steroids X 48 hours if fetus < 34 wks

      • antihypertensives to maintain DBP < 105-110

      • magnesium sulfate for seizure prophylaxis

      • monitor fluid balance, I/O, daily weights, symptoms, reflexes, HCT, plts, LFT’s, proteinuria

    • Indications for expedited 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 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


    Seizure Prophylaxis & Treatment

    • Magnesium sulfate vs. phenytoin for seizure prophylaxis in preeclampsia

      Lucas, et al., N Engl J Med 1995;333:201-5.

      • 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 1995;345:1455

      • Mg pts were 52% or 67% less likely to have a recurrent seizure than diazepam or phenytoin pts


    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

      • increases release of prostacyclin

    • Potential adverse effects:

      • toxicity from overdose (respiratory, cardiac)

      •  bleeding

      •  hypotension with hemorrhage

      •  uterine contractility


    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


  • 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.


    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


    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 1986;65:31-6

    • 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 1991;77:20-6

      •  vascular resistance & relief of vasospasm


    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 1982;59:158-61.

    • 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 1998;89:A1033


    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


    Regional vs. General Anesthesia for C/S in Severe Preeclampsia

    • General vs. spinal (CSE) vs. epidural

      Wallace, et al., Obstet Gynecol 1995;86:193-9

      • 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


    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


    Epidural vs. Spinal Anesthesia for C/S in Severe Preeclampsia

    • Hood, et al., Anesthesiology 1999;90:1276-82

    • 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


    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


    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 1997;86:273


    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 >100K, many would proceed at 80-100K, <80K some would proceed (esp. spinal)


    Platelets & Regional Anesthesia in Preeclampsia

    • When placing a regional block in a patient with a platelet count < 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 1990;16:;1-30

    • Low-dose aspirin is not a contraindication to regional anesthesia in preeclampsia

      • CLASP study: 1422 women on aspirin received epidurals without any bleeding complications


    Hazards of General Anesthesiain 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


    Hazards of General Anesthesiain 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.


    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


    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.

    www.anaesthesia.co.inanaesthesia.co.in@gmail.com


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