A 32-year-old woman, gravida 1 para 0, at 39 weeks gestation is admitted to labor and delivery for regular contractions. On admission, blood pressure is 120/80 mm Hg and pulse is 88/min. Fetal heart rate tracing shows a baseline of 130/min, moderate variability, multiple accelerations, and no decelerations. The cervix is 7 cm dilated and 100% effaced, and fetal vertex is at 0 station. Soon after admission, spontaneous rupture of membranes with a large amount of clear amniotic fluid is noted, and the patient requests epidural analgesia for pain management. She receives epidural anesthesia consisting of bupivacaine and fentanyl and, immediately after induction, begins to feel light-headed. Blood pressure is 84/50 mm Hg, pulse is 120/min, and respirations are 15/min. Fetal heart rate tracing shows a baseline of 150/min and recurrent late decelerations. The lungs are clear to auscultation bilaterally. Cervical examination is unchanged from admission. Bilateral upper and lower extremities have intact deep tendon reflexes. The lower extremities have decreased strength, and the upper extremities have normal strength. Which of the following is the most likely cause of this patient's acute decompensation?
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This patient with acute light-headedness, hypotension, and late fetal decelerations is experiencing epidural-associated hypotension, a common side effect of epidural analgesia. This type of analgesia is commonly used during delivery because it provides continuous pain relief throughout labor by infusing dilute concentrations of local anesthetic (eg, bupivacaine) and opioid (eg, fentanyl) through a catheter placed below the L4 vertebra in the epidural space, blocking the following fibers:
T10-S4 motor and sensory fibers provide pain control during the first stage (uterine contractions via T10-L1) and second stage (perineal stretching via S2-S4) of labor. Lower extremity weakness is expected because L2-L5 nerve roots innervate the legs.
L5 sympathetic fibers decrease lower extremity vascular tone. This causes vasodilation and venous pooling, which decreases right heart venous return, diminishes cardiac output, and often causes symptomatic hypotension (eg, light-headedness). Compensatory tachycardia develops in response to the decreased cardiac output.
Patients with prolonged or profound maternal hypotension can have decreased uteroplacental perfusion, resulting in late fetal decelerations. Treatment includes maternal position change (left uterine displacement) to improve venous return, intravenous fluid bolus, and/or vasopressor administration (eg, phenylephrine, ephedrine).
(Choice A) Amniotic fluid embolism is often characterized by the triad of hypotension, hypoxia, and coagulopathy. Clinical findings include increased bleeding (vaginal and intravenous line sites) and diffuse crackles throughout the lungs (pulmonary edema secondary to heart failure), which are not seen in this patient.
(Choice C) High spinal or total spinal anesthesia can occur if the epidural catheter accidentally punctures the dura and anesthetic enters the subarachnoid (ie, intrathecal) space. Patients often have an exaggerated ascending paralysis with upper extremity weakness (eg, C5-C7 blockade) and respiratory paralysis due to blockade of the diaphragm (eg, C3-C5), neither of which is seen in this patient.
(Choice D) Local anesthetic system toxicity can rarely occur with epidural analgesia (eg, bupivacaine). When the anesthetic is absorbed into the maternal circulation, it initially blocks inhibitory neural pathways to cause CNS overactivity (eg, perioral numbness, tinnitus), potentially followed by seizure. In addition, patients often develop increased cardiovascular sympathetic activity (eg, hypertension, tachycardia), followed by cardiovascular collapse.
(Choice E) Opioid toxicity is rare with neuraxial administration; however, patients with systemic opioid toxicity typically have mild hypotension and/or bradycardia and a depressed respiratory rate (<12/min).
Educational objective:
Hypotension, a common adverse effect of epidural analgesia, is caused by blood redistribution to the lower extremities because of venous pooling from sympathetic blockade.