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Difficult Airway Management Caused by Local Anesthetic Allergy During Emergent Cesarean Delivery: A Case Report

Maxey-Jones, Courtney L. MD*; Palmerton, Alec MD; Farmer, Jocelyn R. MD, PhD; Bateman, Brian T. MD, MSc

doi: 10.1213/XAA.0000000000000533
Case Reports: Case Report

Difficult airway management in the gravid patient is a well-described phenomenon. We present a case of emergent cesarean delivery complicated by a “cannot intubate, cannot ventilate” scenario that was later determined to be secondary to an allergic, IgE-mediated reaction to epidurally administered local anesthetic.

From the *Department of Anesthesiology, University of Cincinnati, Cincinnati, Ohio; Departments of Anesthesia, Critical Care, and Pain Medicine, and Allergy and Immunology, Massachusetts General Hospital, Boston, Massachusetts.

Accepted for publication February 2, 2017.

Funding: None.

The authors declare no conflicts of interest.

Address correspondence to Courtney L. Maxey-Jones, MD, Department of Anesthesiology, University of Cincinnati, Medical Sciences Bldg, Room 3502, 231 Albert Sabin Way, PO Box 670531, Cincinnati, OH 45267. Address e-mail to

Airway management in parturients can be challenging. We present a case of a parturient for emergent cesarean delivery who initially had a reassuring airway examination but developed an IgE-mediated immediate hypersensitivity reaction to epidurally administered local anesthetic leading to severe angioedema and difficult airway management. The patient provided written consent for publication of a case report.

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A 30-year-old G2P0010 black woman presented in spontaneous labor after an uneventful antenatal period. She had no significant medical or surgical history and no known allergies. She was 155 cm tall; weighed 73.2 kg; and had vital signs, a physical examination, and laboratory values within normal limits. Her airway examination was a reassuring Mallampati II with normal mouth opening, neck range of motion, and thyromental distance. A lumbar epidural was placed uneventfully, a test dose of 3 mL of lidocaine 1.5% with epinephrine 1:200,000 was negative, and patient- controlled epidural analgesia using bupivacaine 0.0625% with fentanyl 2 μg/mL achieved excellent pain relief.

After approximately 10 hours of labor, an increasing frequency of deep variable decelerations precluded effective augmentation of labor and necessitated an urgent nonemergent cesarean delivery for arrest of dilation. A dose of 15 mL lidocaine 2% with 1:200,000 epinephrine and 0.1 mEq/mL bicarbonate was administered epidurally in 5 mL increments en route to the operating room. After positioning on the operating table, cardiotocography revealed severe fetal bradycardia at 70 beats per minute despite normal maternal vital signs and left uterine displacement. Epidural anesthesia was not adequate for emergency cesarean delivery, so 15 mL of 3% chloroprocaine was administered epidurally, while the patient breathed 100% oxygen by sealed facemask, and the surgical team prepped and draped her abdomen. Repeated testing before skin incision revealed inadequate epidural anesthesia, and repeated airway examination was unchanged, so a rapid sequence induction of general anesthesia was performed using propofol, succinylcholine, and cricoid pressure. Video laryngoscopy using a conventional C-MAC #3 by a first-year resident revealed a Grade 1 view but with significant arytenoid edema that precluded passage of a 7.0 mm styletted endotracheal tube. A second attempt, by an attending anesthesiologist, revealed a Grade 4 view of edematous soft tissue. During this second intubation attempt, the oxygen saturation declined rapidly, reaching a nadir of 60% to 65%. Mask ventilation was unsuccessful despite chin lift, jaw thrust, 2-handed mask, oral airway placement, and high-inspiratory pressures. The team called for help. A size 4.5 Air-Q laryngeal mask airway supported minimal ventilation, which increased the oxygen saturation to 85% to 88%. The obstetricians proceeded with incision and delivery. The neonate had Apgar scores of 7 and 9 and was transported to the regular care nursery. After delivery, a fiberoptic bronchoscope inserted through the laryngeal mask airway revealed edema of all laryngeal structures. The scope was pushed through the edematous vocal cords, and a 6.5 mm endotracheal tube was forcefully advanced over the scope with the confirmation of successful intubation verified via the presence of end-tidal carbon dioxide and bilateral breath sounds. Hand ventilation with 100% oxygen quickly restored the saturation to >95%. The patient remained hemodynamically stable throughout this event with no rash or urticaria; after intubation, peak airway pressures were within normal limits. Intravenous dexamethasone was administered. Over the next hour, lower lip and tongue edema became evident. The surgery was completed, and the patient was transported intubated to the surgical intensive care unit. She received several additional IV doses of dexamethasone and was extubated approximately 6 hours later after improvement in her oral edema and a leak test indicating a significant leak. A tryptase level sent approximately 3.5 hours after the event (there was an unintended delay between when this test was ordered and sent) was within normal limits (2.8 ng/mL). An allergy consult evaluated the patient for hereditary angioedema, and all tests were within normal limits (C3, C4, CH50, C1 inhibitor level, and function). The patient was discharged 3 days after delivery with instructions to avoid all medications used in the operating room until she could return for formal allergy testing.

Six weeks later, the patient returned for allergy testing, where she had negative epicutaneous and intradermal skin testing to penicillin G, benzylpenicilloyl polylysine (Pre-Pen, AllerQuest, LLC, Plainville, CT), cefazolin, midazolam, propofol, succinylcholine, preservative-free lidocaine, and chloroprocaine. However, 15 minutes after a simultaneous subcutaneous challenge with 0.1 mL of 1% chloroprocaine and 0.1 mL of 1% preservative-free lidocaine, she developed nasal congestion, a hoarse voice, relative hypotension (90s/60s), and angioedema of the lips and oropharynx consistent with an IgE-mediated anaphylactic reaction. Intramuscular epinephrine and oral prednisone, diphenhydramine, and fexofenadine were administered with resolution of symptoms. Six weeks later, the patient returned for skin testing and a subcutaneous challenge with bupivacaine, which was negative. Therefore, the patient was cleared to receive bupivacaine and was given a medical alert bracelet for continued avoidance of lidocaine and chloroprocaine.

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A difficult airway has been described as a “clinical situation in which a conventionally trained anesthesiologist experiences difficulty with facemask ventilation of the upper airway, difficulty with tracheal intubation, or both.”1 For obstetric patients, the incidence of inability to intubate has been widely reported to be 1 in 300 to 400.2,3 According to both the American Society of Anesthesiologists Task Force on Management of the Difficult Airway and other obstetric-specific difficult airway algorithms, the next appropriate step in managing patients in cases of inability to mask ventilate and inability to intubate includes placement of a supraglottic airway, as was performed in this case.1,2

The etiology of difficult airway management in this patient was initially unclear. The differential included trauma from recurrent attempts, hereditary angioedema, and an allergic reaction. Review of her initial airway examination was unremarkable, and there were no specific characteristics found that would predict difficult intubation or mask ventilation. It was unlikely that the severity of laryngopharyngeal, oropharyngeal, tongue, and lip swelling and edema was secondary to traumatic intubation attempts because the edema was readily apparent after only 1 intubation attempt. Hereditary angioedema is an exceedingly rare disease, and this patient had no personal or familial history of angioedema. In addition, results of laboratory analysis for hereditary angioedema were normal. In terms of a potential allergic reaction in this case, angioedema can be an isolated presentation of drug allergy as well as a component feature of systemic anaphylaxis. Urticaria and angioedema are the most frequent presenting features of anaphylaxis, seen in 80% to 90% of patients.4 Although urticaria was not present in this case, it can be particularly difficult to appreciate on those with a dark skin tone. Serum tryptase peaks 1 to 2 hours after an anaphylactic event with a half-life of 2 hours such that it would be expected to be elevated in our patient.5 However, a normal tryptase level has been reported in up to 50% of patients with perianesthesia hypersensitivity reactions.6 In the current case, a systemic hypersensitivity reaction was replicated on subcutaneous challenge with simultaneous chloroprocaine and lidocaine in the outpatient setting, confirming an immediate hypersensitivity IgE-mediated reaction to local anesthetic as the etiology of this patient’s difficult airway. Given that the patient tolerated the epidural test dose, lidocaine is less likely to be the cause of the reaction, but this could be definitively established with repeat testing.

Local anesthetics are commonly found in a patient’s allergy list. Careful review of symptoms attributed to local anesthetics often reveal reactions that are not consistent with anaphylaxis. Vasovagal episodes associated with injection/infiltration, systemic effects of the epinephrine contained in local anesthetic solutions, or anaphylaxis to latex gloves used during injection are often the source of adverse reaction. True local anesthetic-induced immediate drug hypersensitivity (IgE-mediated) is present in <1% of adverse reactions to local anesthetics.7 In suspected allergic reaction to local anesthetics, testing for immediate and later hypersensitivity reactions to local anesthetics as well as latex and preservatives should be performed.8

Local anesthetics can be divided into 2 subgroups based on their chemical structure. The benzoic acid esters, including chloroprocaine, are metabolized by pseudocholinesterase to form para-aminobenzoic acid. The amides such as lidocaine and bupivacaine are metabolized in the liver. Adverse reactions associated with esters are likely related to sensitivity to the para-aminobenzoic acid metabolite. Theoretically, crossreactivity between the groups should be negligible; however, among the amide anesthetics, IgE-mediated crossreactivity has been demonstrated.9,10

This case highlights the potential for anaphylaxis whenever local anesthetics are used, despite the low incidence of true allergy to local anesthetics. In addition, this case demonstrates the importance of considering culprit medications that have been administered via nonintravenous routes. Finally, this case highlights the fact that angioedema can be the primary manifestation of an allergic, IgE-mediated reaction and can occur without other overt signs of anaphylaxis.

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Name: Courtney L. Maxey-Jones, MD.

Contribution: This author helped care for the patient, and write, edit and prepare the manuscript.

Name: Alec Palmerton, MD.

Contribution: This author helped care for the patient, and write and edit the manuscript.

Name: Jocelyn R. Farmer, MD, PhD.

Contribution: This author helped care for the patient, and write and edit the manuscript.

Name: Brian T. Bateman, MD, MSc.

Contribution: This author helped care for the patient, and write and edit the manuscript.

This manuscript was handled by: Jill M. Mhyre, MD.

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