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Preeclampsia and Eclampsia: Anesthetic Management

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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  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.inanaesthesia.co.in@gmail.com

  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 • > 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

  5. 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

  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 > 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, thromboxane’s 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 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

  10. 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

  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 1999;180:499-506 • 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 < 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 < 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

  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 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

  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 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

  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 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

  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 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

  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 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

  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 1997;86:273

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

  34. 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

  35. 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

  36. 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.

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

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