P021: MANAGEMENT OF A DIFFICULT AIRWAY DUE TO SEVERE OROPHARYNGEAL ANGIOEDEMA
Mariah Gosling, MD; Elizabeth Mahanna Gabrielli, MD
University of Miami/Jackson Health System
Angioedema is the swelling of the subcutaneous and submucosal layers of the skin that occurs with extravasation of plasma into interstitial spaces due to increased vascular permeability [1]. It most commonly affects the face, lips, neck, extremities, oral cavity, larynx and gut [2]. The two main classifications of angioedema are acquired (drug-induced, allergic, complement-mediated) and hereditary due to C1-inhibitor deficiency. The pathophysiology of angioedema is most commonly histamine-mediated, secondary to mast-cells and basophil activation or bradykinin-mediated in the setting of hereditary angioedema. Angiotensin-converting enzyme inhibitor-associated angioedema causes decreased degradation of bradykinin leading to edema. It clinically presents as angioedema without urticaria or itching [3] and is common in African Americans. Importantly, it can develop anytime but is common in the first week of exposure.
Oropharyngeal angioedema is a potentially life threatening condition that often necessitates urgent airway evaluation and intervention as asphyxiation is the leading cause of death in these patients. Angioedema can rapidly progress within hours leading to airway obstruction in up to 15% of patients [4]. The intubation of a patient with severe angioedema can be extremely difficult due to swelling, distortion of airway anatomy and pooling of secretions. It has been estimated that in these patients requiring a definitive airway, cricothyrotomy or tracheostomy is needed in up to 50% of cases [4].
An 80 year old male with HTN and hx of TIA, presented to the emergency department with assumed lisinopril induced angioedema. Upon evaluation, the patient’s SpO2 was 100% and he was receiving an albuterol nebulizer treatment. At this point the patient had received decadron, diphenhydramine, epinephrine 0.3mg (given by rescue) and tranexamic acid. Fresh frozen plasma was ordered but had not been administered. The patient was sitting straight up in bed, leaning forward with copious amounts of drooling. His tongue was exceedingly swollen and protruding out of his mouth with swollen lips. He was unable to clear his secretions and his mouth opening was so limited it would not accommodate an ovassapian oral airway. High flow nasal cannula was started while we prepared intubation equipment. Since surgery was not in house, a cricothyroidotomy kit was obtained at bedside.
Viscous 2% lidocaine was squirted into the back of the throat and the patient was instructed to gurgle this solution. A phenylephrine (200 mcg) saturated 4x4 gauze was placed in the nostrils. A 30F nasal airway was utilized to dilate a nostril while a 6.5 nasal ETT was loaded onto a flexible bronchoscope. For sedation, 1mg of versed and 30 mg ketamine was administered, 10 mg at a time. The flexible bronchoscope demonstrated a challenging airway with copious secretions, swollen airway anatomy and a small vocal cord opening. The patient remained hemodynamically stable with unchanged oxygenation. The patient was successfully intubated and remained intubated for 9 days.