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Publicly Available Published by De Gruyter July 6, 2017

The unusual use of epidural anesthesia for effective treatment of transfusion related circulatory overload in a parturient

Ramon E. Abola and Joy Schabel


We present the use of epidural anesthesia for the management of transfusion associated circulatory overload. After a vaginal delivery, a patient with preeclampsia and postpartum hemorrhage developed respiratory failure following rapid transfusion and fluid resuscitation. Her dyspnea and clinical status markedly improved after receiving an epidural bolus of 2-chlroprocaine. This unusual application of epidural anesthesia induces similar physiological changes to standard medical therapy for pulmonary edema and volume overload.


We present the use of epidural anesthesia for the management of acute onset pulmonary edema in a patient with transfusion associated circulatory overload. This unusual application of epidural anesthesia induces similar physiological changes to standard medical therapy for pulmonary edema and volume overload. In a patient with an epidural in place, this is an option available to clinicians for management of the pregnant patient with volume overload.

Presentation of the case

A 24-year-old G1P0 at 39 + 6/7 weeks was admitted for induction of labor for preeclampsia. Her pregnancy was otherwise uncomplicated and she had no previous past medical history. She weighed 89 kg and had a body mass index (BMI) of 29. The patient had elevated blood pressure (systolic and diastolic blood pressures ranges 155–177 and 86–115 mm Hg, respectively) and proteinuria. Her admission hemoglobin was 12.3 g/dL.

Dinoprostone and oxytocin were utilized for induction of labor. A magnesium infusion was started for seizure prophylaxis. An epidural was placed when the patient’s cervical dilation had reached 2 cm. An 800 mL bolus of lactated ringers was given intravenously prior to epidural placement. An epidural catheter was placed between the 3rd and 4th lumbar vertebrae. Epidural analgesia was initiated with a bolus 7 mL of bupivacaine 0.25% and continued with patient controlled epidural analgesia.

A healthy female neonate was born by vaginal delivery with APGARs of 8 and 9, at 1 min and 5 min, respectively. The time period between the first dinoprostone placement and vaginal delivery was 40 h. Her estimated blood loss was 900 mL. Postpartum hemorrhage was secondary to uterine atony, and the patient received oxytocin and misoprostol.

Four hours after delivery, the patient complained of feeling lightheaded and dizzy. She was pale and her blood pressure was 70/40 mm Hg. Bimanual exam revealed uterine atony, and approximately 1 L of blood was expressed. The patient was given misoprostol, oxytocin and prostaglandin F2a over the next 30 min. Her hemoglobin level was 8.3 g/dL. She was given 1 L of 6% hetastarch (Hextend), and her blood pressure improved. The patient continued to have heavy vaginal bleeding, and an ultrasound examination showed a collection of blood in the uterus. Repeat bimanual exam expressed an additional 1L of blood. Due to the concern of ongoing bleeding, the patient was transfused 4 units of packed red blood cells and 2 units of fresh frozen plasma over 1 h.

Fifteen minutes after receiving the blood products, the patient’s blood pressure suddenly increased to 200/150 mm Hg and her respiratory rate was in the 40 s. Lung auscultation revealed bilateral crackles throughout all lung fields and her SpO2 was 89% on 100% non-rebreather facemask. An arterial blood gas revealed a pH of 7.35, pCO2 38 mm Hg, pO2 76 mm Hg on 100% oxygen. The working diagnosis was pulmonary edema secondary to transfusion associated circulatory overload.

With the goal of providing preload and afterload reduction, an epidural bolus was given with 15 mL of 3% 2-chloroprocaine over the course of 2 min. Within 3 min, the patient showed improvement in her respiratory rate, BP and SpO2. By 8 min the patient’s BP had improved to 170/90 mm Hg, her SpO2 improved to 98% on a non-rebreather facemask, and her respiratory rate had decreased to 28 breaths per min. Though a sensory level was not checked at that time, the patient reported “feeling numb” and could no longer feel the bimanual compression of the uterus provided by the obstetrician.

After the epidural bolus and improvement in her clinical status, the patient received furosemide 20 mg IV, 15 mg of labetalol IV, and hydralazine 15 mg IV. A chest X-ray showed mild pulmonary vascular congestion with a normal heart size. Her hemoglobin level was 10 g/dL. Her BPs remained within normal levels and oxygen was slowly weaned. The patient was able to breathe without difficulty. She was transferred to our postpartum unit the following day and discharged home on postpartum day number 3.


Our case demonstrates the unique use of epidural anesthesia for the management of pulmonary edema and respiratory failure. The rapid onset of the sympathetic block caused a decrease in both preload and afterload. These cardiovascular changes led to a prompt improvement in oxygenation and prevented the need for intubation and positive pressure ventilation. The administered epidural anesthesia functioned in a similar manner to arterial and venous vasodilators that are the mainstays of treatment for decompensated heart failure [1]. We chose this treatment modality because it was immediately available to us on the labor and delivery ward with an in situ epidural. Large volume resuscitation, especially in the vasoconstrictive state of preeclampsia, and decreased oncotic pressure associated with pregnancy, preeclampsia and magnesium are all likely contributors to the development of pulmonary edema.

Neuraxial anesthesia has been reported to decrease cardiac filling, central venous pressure, intrathoracic blood volume, pulmonary artery and pulmonary capillary wedge pressure with redistribution of the blood volume to the lower extremity and mesenteric vascular system [2], [3]. The use of neuraxial anesthesia has been previously described to decrease dyspnea in patients with pulmonary edema. Sarnoff and Ebner reported that the use of spinal anesthesia caused a prompt and definite correction of hypertension, dyspnea and pulmonary edema [4], [5]. Velickovic reported the use of continuous spinal anesthesia for cesarean delivery in a parturient with severe recurrent peripartum cardiomyopathy. The patient’s respiratory symptoms markedly improved with onset of the spinal block [6].

The use of epidural anesthesia in this manner may not be appropriate in patients who already are hypotensive or have comorbidities where hypotension will not be well tolerated. However, a recent review of neuraxial anesthesia in preeclamptic patients concludes that hypotension with neuraxial anesthesia occurs less in preeclamptic patients compared to normal women [7]. Additionally, after induction of epidural analgesia, especially if a high level of blockade is achieved, some patients may not tolerate the loss of their accessory muscles of respiration and require intubation.

The prompt improvement in respiratory and cardiovascular status in response to the epidural bolus suggests that epidural anesthesia may have a role in the management of acute decompensated heart failure in other critical patients. Further investigation is needed to determine the potential use of epidural anesthesia as a supplement or replacement for conventional pharmaco-therapy in the treatment of pulmonary edema.

Author’s Statement

  1. Conflict of interest: Authors state no conflict of interest.

Material and Methods

  1. Informed consent: Informed consent has been obtained from all individuals included in this study.

  2. Ethical approval: The research related to human subject use has complied with all the relevant national regulations, and institutional policies, and is in accordance with the tenets of the Helsinki Declaration, and has been approved by the authors’ institutional review board or equivalent committee.


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Received: 2017-04-28
Accepted: 2017-05-31
Published Online: 2017-07-06

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