Residency · Residency · Anesthesiology
Preeclampsia and Eclampsia: Anesthetic Considerations
Introduction
Preeclampsia is a multisystem disorder of pregnancy characterized by new-onset hypertension (systolic blood pressure of 140 mmHg or greater, or diastolic blood pressure of 90 mmHg or greater) and proteinuria or end-organ dysfunction after 20 weeks of gestation. Eclampsia refers to the occurrence of generalized tonic-clonic seizures in a preeclamptic patient that are not attributable to other causes. These conditions remain leading causes of maternal and perinatal morbidity and mortality worldwide.
Pathophysiology
The disease begins with abnormal placentation, in which defective spiral artery remodeling leads to placental ischemia. This triggers the release of antiangiogenic factors, including sFlt-1 and soluble endoglin, which cause widespread endothelial dysfunction. The downstream consequences include systemic vasospasm, increased vascular permeability, and activation of the coagulation cascade.
End-organ effects span multiple systems. In the brain, vasogenic edema can produce posterior reversible encephalopathy syndrome (PRES) and seizures. Hepatic involvement manifests as periportal necrosis, subcapsular hematoma, and HELLP syndrome. Renal injury involves glomerular endotheliosis, decreased GFR, and proteinuria. Hematologic derangements include thrombocytopenia, microangiopathic hemolytic anemia, and disseminated intravascular coagulation.
Classification and Severity
Preeclampsia Without Severe Features
Preeclampsia without severe features is defined by blood pressure readings of 140 to 159 over 90 to 109 mmHg on two occasions at least 4 hours apart, accompanied by proteinuria of 300 mg or more per 24 hours or a protein-to-creatinine ratio of 0.3 or greater.
Preeclampsia With Severe Features
Severe features include systolic blood pressure of 160 mmHg or greater or diastolic blood pressure of 110 mmHg or greater, a platelet count below 100,000 per microliter, elevated liver transaminases to twice the normal value, serum creatinine above 1.1 mg/dL or doubling of the baseline, pulmonary edema, and new-onset headache or visual disturbances.
| Feature | Without Severe Features | With Severe Features |
|---|---|---|
| Blood pressure | 140–159 / 90–109 mmHg | ≥160 / ≥110 mmHg |
| Platelet count | Normal | <100,000/mcL |
| Liver enzymes | Normal | ≥2x upper normal |
| Creatinine | Normal | >1.1 mg/dL or doubled |
| Pulmonary edema | Absent | Present |
| CNS symptoms | Absent | Headache, visual changes |
| Magnesium Level (mEq/L) | Clinical Effect |
|---|---|
| 4–7 | Therapeutic range (seizure prophylaxis) |
| 7–10 | Loss of deep tendon reflexes |
| >12 | Respiratory arrest |
| >25 | Cardiac arrest |
HELLP Syndrome
HELLP syndrome is defined by hemolysis, elevated liver enzymes, and low platelets. Notably, it may occur without classic hypertension or proteinuria in up to 15% of cases.
Anesthetic Assessment and Planning
The preoperative assessment should include a complete blood count with platelet count, liver function tests, creatinine, and coagulation studies. The airway must be assessed early because preeclamptic patients frequently have significant upper airway edema. Volume status requires careful evaluation, as these patients are intravascularly depleted despite total body fluid overload. Neurologic status should be documented, including the presence of headache, visual changes, or hyperreflexia. The magnesium sulfate infusion rate should be reviewed, and the patient should be checked for signs of toxicity such as loss of deep tendon reflexes and respiratory depression.
Magnesium Sulfate Considerations
The standard loading dose of magnesium sulfate is 4 to 6 g IV over 15 to 20 minutes, followed by a maintenance infusion of 1 to 2 g per hour. The therapeutic serum level is 4 to 7 mEq/L. Magnesium potentiates both depolarizing and nondepolarizing neuromuscular blockers. At toxic levels, loss of reflexes occurs above 7 mEq/L, respiratory arrest above 12 mEq/L, and cardiac arrest above 25 mEq/L. The antidote for magnesium toxicity is calcium gluconate 1 g IV.
Neuraxial Anesthesia for Labor and Cesarean Delivery
Neuraxial anesthesia is preferred when not contraindicated. The platelet threshold for neuraxial placement is debated, but most practitioners accept a count of 70,000 per microliter or greater if the trend is stable and coagulation is otherwise normal. Early epidural placement is recommended because airway management may be extremely difficult in these patients. Careful, incremental dosing is essential to avoid precipitous hypotension in a volume-depleted patient. Epinephrine-containing test doses should be avoided in severely hypertensive patients when possible. Spinal anesthesia is acceptable for cesarean delivery, but titrated dosing via a combined spinal-epidural technique may be advantageous.
General Anesthesia Considerations
General anesthesia is reserved for emergent situations, failed neuraxial anesthesia, or severe coagulopathy. Laryngoscopy and intubation provoke a severe hypertensive response that should be treated with remifentanil 1 mcg/kg, esmolol 1 to 2 mg/kg, or lidocaine 1.5 mg/kg IV. The anesthesiologist should anticipate a difficult airway due to pharyngolaryngeal edema and use a smaller endotracheal tube (6.0 to 6.5 mm). Ketamine should be avoided because it raises blood pressure, and ergot alkaloids should be avoided because of the risk of vasospasm. An arterial line for beat-to-beat blood pressure monitoring is indicated in severe cases.
Blood Pressure Management
Labetalol is given as 10 to 20 mg IV boluses titrated to effect, to a maximum of 300 mg. Hydralazine is administered at 5 to 10 mg IV every 20 minutes. Nicardipine is delivered as an infusion at 5 to 15 mg per hour for refractory hypertension. Clevidipine is an ultra-short-acting calcium channel blocker given by infusion. The target is reduction of severe hypertension to below 160/110 mmHg within 30 to 60 minutes. ACE inhibitors and nitroprusside must be avoided in the antepartum period.
Postpartum Considerations
The risk of eclamptic seizures persists for up to 48 to 72 hours postpartum. Magnesium sulfate should be continued for at least 24 hours after delivery. Preeclampsia increases the risk of postpartum hemorrhage, which must be monitored closely. Nonsteroidal anti-inflammatory drugs may be used cautiously but should be avoided in severe renal impairment. Close monitoring in a high-acuity setting is essential throughout the postpartum period.
Clinical Pearls
Place the epidural early in laboring preeclamptic patients because the airway may worsen rapidly, and emergent general anesthesia carries high risk. A falling platelet count is more concerning than a single low value; the count should be trended before and after neuraxial placement. Magnesium sulfate potentiates neuromuscular blockade, so initial doses of nondepolarizing agents should be reduced and a nerve stimulator used. The definitive treatment of preeclampsia is delivery of the placenta; anesthetic management is supportive and temporizing. Preeclamptic patients are intravascularly depleted, and judicious fluid resuscitation (typically 1 to 2 mL/kg/hr of crystalloid) is appropriate, but overaggressive hydration risks pulmonary edema.
References
- American College of Obstetricians and Gynecologists. Gestational Hypertension and Preeclampsia: ACOG Practice Bulletin No. 222. Obstet Gynecol. 2020;135(6):e237-e260.
- Dennis AT. Management of pre-eclampsia: issues for anaesthetists. Anaesthesia. 2012;67(9):1009-1020.
- Henke VG, Bateman BT, Leffert LR. Focused review: spinal anesthesia in severe preeclampsia. Anesth Analg. 2013;117(3):686-693.
- Magee LA, et al. The CHIPS Randomized Controlled Trial (Control of Hypertension in Pregnancy Study). N Engl J Med. 2015;372:407-417.