Preeclampsia in the Parturient Implications in Anesthesia

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Preeclampsia in the ParturientImplications in
Anesthesia

• Robyn C. Ward, CRNA, MS
• LCDR, NC, USN
• Naval Medical Center San Diego

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

• Discuss preeclampsia risk factors,
  pathophysiology, obstetric/anesthetic management
• Discuss eclampsia
• Discuss HELLP syndrome

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Introduction

• Preeclampsia is a major cause of maternal and
  perinatal morbidity and mortality
• Direct fetal effects
• Indirect effects due to preterm deliveries
• Affects 5 of all pregnancies
• 35-300 deaths per 1000 births (twice that of
  normotensive pregnancies)

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Classification 4 Categories

• Gestational hypertension
• Chronic hypertension
• Chronic hypertension w/ superimposed preeclampsia
• Preeclampsia mild, moderate, or severe

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Gestational Hypertension

• Transient HTN of BP gt 140/90 without proteinuria
  or end-organ damage
• May occur late in pregnancy, during labor, or
  within 24 hrs postpartum
• BP returns to normal within 10 days postpartum

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Chronic Hypertension

• Begins prior to pregnancy
• BP gt 140/90
• Occurs prior to 20th week gestation
• Not associated with proteinuria or end-organ
  damage
• Continues well after delivery

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Preeclampsia Mild to Severe

• Occurs after 20 weeks gestation
• Triad
• Hypertension
• Proteinuria
• Edema

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Preeclampsia - Mild

• Hypertension SBP gt 140 mm Hg, DBP gt 90 mm Hg
• Proteinuria gt 300 mg/24 hr
• Generalized edema

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Preeclampsia - Severe

• Hypertension SBP gt 160 mm Hg, DBP gt 110 mm Hg
• Proteinuria gt 5 g in 24 hr
• Generalized edema
• Evidence of end-organ damage
• Oliguria U/O lt 400 ml/24 hr and/or elevated
  serum creatinine
• Cerebral edema w/ visual disturbances (blurred
  vision) or headache

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Preeclampsia Severe (cont)

• Evidence of end-organ damage (cont.)
• Pulmonary edema
• Hepatocellular dysfunction
• Elevated liver enzymes
• Epigastric or RUQ pain
• HELLP syndrome
• Intrauterine growth restriction or
  oligohydramnios

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Risk Factors

• Maternal Pre-existing Conditions
• Maternal Specific Factors
• Partner-Related Factors
• Pregnancy-Associated Factors

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Maternal Pre-existing Conditions

• Chronic hypertension
• Renal disease
• Diabetes mellitus
• Obesity

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Maternal Specific Factors

• Advance maternal age gt 40
• Familial predisposition
• Nulliparity and young age
• History of preeclampsia

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Partner-Related Factors

• Paternal antigens
• Immune maladaptation
• Trophoblastic invasion at 12 weeks
• Second invasion at 14-16 weeks changes spiral
  arteries from high to low resistance vessels
  prostacyclin and nitric oxide are released from
  endethelium
• Second invasion fails in preeclampsia

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Pregnancy-Associated Factors

• Multiple gestation increased risk
• Congenital anomalies
• Antepartum urinary tract infection

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Pathophysiology

• Immunologic factors
• Genetic factors
• Endothelial factors
• Platelet factors
• Calcium

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Immunologic Factors

• Fifty percent genes from father
• Fetal trophoblast invades maternal deciduas after
  implantation
• Second trophoblastic invasion at 14-16 weeks
  normally disrupts maternal spiral arteries
  changing them to low resistance vessels
• This 2nd wave of invasion fails in preeclampsia

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Genetic Factors

• Possibly recessive genetic inheritance
• Variant angiotensinogen gene T 235 if
  homozygous, 20 fold increased risk for
  preeclampsia

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Endothelial Factors

• Vascular endothelial damage
• Occurs in placental deciduas, renal
  microvasculature and, potentially, hepatic,
  myocardial and cerebral circulations
• Failure of trophoblast invasion causes increases
  production of free radicals which exacerbate
  endothelial damage
• Overall result is deficiency of prostacyclin
  (vasodilator) in relation to thromboxane
  (vasoconstrictor)

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Platelet Factors

• Surface mediated platelet activation occurs in
  absence of prostacyclin
• Favors platelet adhesion to damaged surface
  lining of spiral arteries
• Further platelet aggregation promoted by platelet
  release of dense granules, including TXA2 and 5HT

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Platelet Factors (cont.)

• Mild preeclampsia, 5HT binds to endothelial 5HT-1
  receptors
• stimulates partial recovery of endothelial
  prostacyclin and nitric oxide release
• Prostacyclin stimulates renin angiotensin
  aldosterone system, which improves placental
  perfusion by inducing maternal HTN

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Platelet Factors (cont.)

• Severe preeclampsia, serotonin cannot interact
  with 5HT-1 receptors on endothelium
• Binds instead to 5HT-2 receptors on vascular
  smooth muscle cells and platelet membranes
• Results in worsening HTN and intravascular
  thrombosis

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Calcium

• Calcium increases slowly throughout normal
  pregnancy to maintain vascular tone
• In preeclampsia, this increase is much greater by
  3rd trimester due to increased cellular membrane
  permeability

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Clinical Manifestations

• Cardiovascular
• Respiratory
• Neurologic
• Renal
• Hematologic
• Hepatic
• Uteroplacental unit

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Cardiovascular

• HTN
• Intravascular volume depletion
• shift of intravascular fluid and protein to
  extravascular space due to decreased colloid
  oncotic pressure and increased capillary
  permeability (due to endothelial cell damage)

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Respiratory

• Upper AW narrowing from pharyngolaryngeal edema
• difficulty in intubation
• Pulmonary edema in 3 of cases
• Increased capillary permeability
• Decreased colloid oncotic pressure
• LV dysfunction
• Excessive fluid administration

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Neurologic

• Cerebral irritation due to CNS edema
• Headache 40 of patients
• Nausea, excitability, apprehension and visual
  disturbances (blurred vision)
• Hyperreflexia/Clonus seizures if progresses to
  eclampsia
• Intracranial hemorrhage is leading cause of
  maternal death from preeclampsia

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Renal

• Diminished renal perfusion and glomerular
  filtration
• Proteinuria
• Decreased uric acid clearance
• Oliguria lt 400 ml/24 hrs
• Elevated serum creatinine

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Hematologic

• Elevated Hct secondary to plasma volume
  contraction
• Thrombocytopenia in 30 of patients
• PLT lt 100K correlates with severe disease
• Activation of coagulation cascade can occur
• Increased incidence of placental abruption which
  can result in DIC

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Hepatic

• Impaired liver function can be caused by
• Periportal hepatic necrosis
• Subscapular hemorrhages
• Fibrin deposition in hepatic sinusoids
• Elevated liver enzymes (HELLP)

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Uteroplacental Unit

• Uteroplacental insufficiency due to increased
  vascular resistance, decreased plasma volume, and
  increased blood viscosity
• Compromises uterine blood flow by 50-70

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Treatment

• Obstetric management
• Adequate fetal surveillance
• Antihypertensive management
• Anticonvulsant therapy
• Anesthetic management of labor
• Safe analgesia for labor and anesthesia for
  delivery

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Obstetric Management

• Expectant management (lt 34 weeks)
• Bed rest and sedation
• Antihypertensive therapy
• Monitoring of weight, U/O and DTRs
• MgSO4 for seizure prophylaxis

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Obstetric Management

• Aggressive management
• Induction of labor/delivery within 48-72 hours
• Delivery is only curative treatment
• If possible, time allowed for 2 doses of steroids
  to mother to promote fetal lung maturity
• Indications for immediate delivery
• Uncontrolled HTN gt 160/110
• Oliguria/renal dysfunction
• Liver dysfunction
• Imminent eclampsia
• Pulmonary edema
• Fetal compromise

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Fetal Surveillance

• Fetal ultrasound
• Continuous electronic fetal monitoring
• Monitor for
• Loss of beat-to-beat variability of FHR and
  periodic late decelerations

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Antihypertensive Management

• Goal control HTN and maintain uteroplacental
  perfusion
• Acute therapy Long Term
• Hydralazine Alpha methyl dopa
• Labetalol (IV) Labetalol (po)
• Nifedipine
• Nitroglycerin
• Nitroprusside

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Anticonvulsant Therapy

• MgSO4 first line agent in U.S.
• Cerebral vasodilator
• Central anticonvulsant effect
• Peripheral vasodilator effect
• Other
• Phenytoin (Dilantin)
• Diazepam

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Magnesium

• Dose
• 4-6 g over 20 min w/ infusion of 1-2 g/hr
• Therapeutic range 4-8 mg/dl
• Side effects sedation, skeletal/muscle
  weakness, decreased uterine activity, decreased
  FHR variability, prolonged labor, uterine atony,
  prolongation of NM blockade, neonatal hypotonia

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Magnesium (cont.)

• Toxicity
• 4-8 mg/dl therapeutic
• 10-12 mg/dl loss of DTRs
• 12-15 mg/dl respiratory arrest
• 20-25 mg/dl cardiac arrest
• Treatment
• Calcium gluconate 10 ml of 10 solution IV over 2
  minutes
• Oxygen
• Mechanical ventilation if necessary

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Anesthetic Management of Labor

• Preanesthetic assessment
• Airway
• Aspiration prophylaxis
• Auscultation of lungs
• Fluid balance
• Hemodynamic status
• Left uterine displacement
• Renal function
• Coagulation status

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Analgesia for Labor

• Continuous lumbar epidural Advantages
• Decreased circulating catecholamines
• Decreased uterine vascular resistance
• Improved uteroplacental blood flow
• Avoids risk of general anesthesia

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Epidural Placement

• R/O coagulopathy, LUD, oxygen, continuous fetal
  monitoring
• Careful crystalloid preload (250-500 ml)
• Local anesthetic Bupivicaine (slow onset)
• Epinephrine consider avoiding
• Slow, incremental dosing
• Ephedrine (in smaller doses) for hypotension lt
  20 of baseline

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Anesthesia for Delivery

• Non-emergent C-section
• Epidural anesthesia thought to allow for
  incremental dosing, potentially avoiding
  precipitous hypotension
• Spinal anesthesia recent retrospective study
  (Hood Curry, 1999) found no difference in
  hemodynamic changes after spinal or epidural
  anesthesia
• Conclusion spinal is safe alternative to
  epidural w/ added advantage of quicker onset and
  better quality of sensory blockade especially in
  urgent situations

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Anesthesia for Delivery

• Emergent C-section
• Epidural previously placed, well functioning
• Spinal if no epidural placed and if FHR stable
• General anesthesia
• Coagulopathy
• Patient refusal of regional
• Fetal bradycardia prohibits placement in time

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Eclampsia

• Convulsions that occur during pregnancy in a
  woman whose condition also meets criteria for
  preeclampsia and who has no other previous
  neurologic disease or diagnosis of epilepsy
• Etiology uncertain cerebral edema, ischemia
• Tonic-clonic in nature
• Life threatening emergency

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Eclampsia (cont.)

• 50 have evidence of severe preeclampsia
• Classical presentation of preeclampsia may be
  absent or mildly abnormal in 30 of patients

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Management of Eclampsia

• Goals
• Stabilization of the mother/seizure control
• MgSO4 therapy 4-6 g over 20 min followed by
  infusion of 1-3 g/hr, OR
• Thiopental or diazepam followed by MgSO4 infusion
• Avoid anticonvulsant polypharmacy
• Airway management
• Avoiding aspiration

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Obstetric Management of Eclampsia

• Factors to consider patients condition,
  gestational age, cervical exam, and fetal well
  being
• Induction of labor if patient is seizure free,
  stable, favorable cervix, and reassuring fetal
  heart tracing
• Urgent c-section if patient continues to have
  breakthrough seizures

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Anesthetic Management of Eclampsia

• Aspiration precautions
• Careful airway assessment
• Guidelines for use of regional vs. general
  anesthesia similar to patients with severe
  preeclampsia

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ABCs of Seizure Control

• Airway
• Breathing
• Circulation
• Drugs
• Blood Pressure

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HELLP Syndrome

• Severe preeclampsia complicated by
• Hemolysis
• Elevated liver enzymes
• Low platelets
• First reported by Weinstein in 1982
• Occurs in 12 of pregnancies complicated by
  preeclampsia or eclampsia

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HELLP Syndrome

• Clinical presentation (extremely variable)
• RUQ or epigastric pain
• N/V
• Malaise
• Headache, visual disturbances
• Weight gain/edema

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Differential Diagnosis of HELLP

• Biliary colic, cholecystitis
• Hepatitis
• Gastroesophageal reflux
• Gastroenteritis
• Pancreatitis
• Ureteral calculi or pyelonephritis
• ITP or TTP

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Laboratory Findings in HELLP

• Hemolysis
• Abnormal peripheral smear
• Total bilirubin gt 1.2 mg/dl
• LDH gt 600 IU/L
• Liver Enzymes
• AST (SGOT) gt 70 IU/L
• Platelet count
• lt 100,000

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Management of HELLP Syndrome

• Stabilize mother control BP, prevent seizures
• Evaluate fetus
• Determine optimal timing and route for delivery
• Provide continued monitoring and management
  during postpartum period
• All women should receive MgSO4

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HELLP New Treatments

• Dexamethasone 10 mg IV q12hr when platelets lt
  100,000
• Platelets for active bleeding, or if lt 20,000
• Plasmapheresis limited success, but not
  routinely recommended

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HELLP Syndrome

• Expeditious delivery usually warranted
• Poor maternal and fetal outcome if delivery
  delayed
• Infants gt 28 weeks gestation are routinely
  delivered 48 hrs after first maternal dose of
  dexamethasone
• Diagnosis occasionally missed as some patients
  present without triad of preeclampsia

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HELLP Syndrome (cont.)

• Regional Anesthesia?
• Platelet counts gt 80-100K usually safe to receive
  regional without risk of hematoma
• If lt 70-80K, risks of hematoma vs risks of GA
  must be weighed
• In presence of easy predicted AW, regional
  generally avoided
• Presence of difficult AW, regional anesthesia may
  be considered after platelet transfusion prior to
  procedure

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References

• Chandrasekhar, Datta Anesthetic management of
  the preeclamptic parturient Current Reviews for
  Nurse Anesthetists 25(3) 25-40, 2002.
• Gambling D, Writer D Hypertensive disorders in
  pregnancy. In Chestnut DH Obstetric
  Anesthesia, Principles and Practice (3rd ed).
  Mosby, 2004.
• Hood D, Curry R Spinal versus epidural
  anesthesia for cesarean section in severely
  preeclamptic patients A retrospective survey.
  Anesthesiology 90 1276-1282, 1999.

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