Succinylcholine Cannot Relieve an Airway Obstruction Caused by Pharyngeal and Laryngeal Edema

Abstract

In Response: We thank Khorasani et al. for their comments on our case report of traumatic asphyxia. Before answering their questions, we would like to comment on the title of their letter "Succinylcholine cannot relieve an airway obstruction caused by pharyngeal and laryngeal edema." We did not state or imply in our article that succinylcholine relieves edema-induced airway obstruction, and we do not wish to impart this message to our readers. Khorasani et al. disagree with the induction of general anesthesia after failure of awake direct laryngoscopy and ventilation via mask. They attribute our inability to ventilate purely to airway obstruction and discount the possible contribution of severe agitation. Indeed, we believe that agitation, by causing straining and Valsalva, can and did play a role in converting a partial to a complete airway obstruction. Significant reduction of chest wall compliance from agitation may also have been responsible for difficulty of ventilation. They ask why we failed to intubate the trachea after administering IV anesthetic and muscle relaxant if we could ventilate and visualize the larynx. We stated that ventilation became easier, but we did not indicate that the larynx could be visualized; we stated, "orotracheal intubation…remained impossible because of severe pharyngeal and laryngeal edema." We suspect that traumatic asphyxia resulted in distorted anatomy, preventing adequate visualization of the larynx. As indicated in the Discussion, the rationale for using anesthetic and muscle relaxant after failed awake laryngoscopy was to facilitate ventilation and laryngoscopic intubation while cricothyroidotomy was initiated. It should be emphasized that we took this action after preparations for performing a cricothyroidotomy, including identification of the cricothyroid membrane, were completed. The degree of controversy regarding airway management strategy in patients with trauma-related airway compromise is not surprising given the complexity of circumstances surrounding the clinical picture. Recently, the use of anesthetics and muscle relaxants, as opposed to awake intubation, was recommended for penetrating airway injuries after a retrospective review revealed one death when the operator persisted with an awake nasal intubation in a patient with an expanding cervical hematoma [1]. A similar view was supported after reviewing another series of patients with penetrating trauma to the cervical airway [2]. In this series, seven patients required tracheostomy after attempted awake intubation was unsuccessful. The alternative to our management would be to perform the cricothyroidotomy awake or to deliver an inhalational agent via mask in an effort to preserve spontaneous breathing. The former, although possible, may be associated with injury to cervical structures if the patient is agitated and flailing. In addition, stress associated with this technique may lead to severe hemodynamic changes and, possibly, in undesirable coronary or cerebrovascular events. The latter is very likely to result in laryngeal spasm and aspiration of gastric contents. We believe that in some situations, when securing of the airway is required in the trauma patient, the induction of general anesthesia with muscle paralysis after complete preparation for surgical airway may be preferable to awake intubation. Severe patient agitation, lack of cooperation, total upper airway obstruction, cervical vascular injury, and seizures or status epilepticus, are possible indications for this approach. Cautious and experienced clinical judgement best dictates optimal management. However, one must a priori consider alternatives and not futilely persist when the technique first attempted is unsuccessful. We agree with Khorasani et al. that the reported arterial blood gas result is incorrect. The value 15.8 mEq/L, in our article as HCO3-, was actually the base deficit; the value for HCO3- was 10.5 mEq/L. The last issue that Khorasani et al. mention is our failure to explain the rationale for massive transfusion. We are somewhat surprised that they do not feel that decreasing hemoglobin level and hypotension are adequate indications for massive transfusion of blood products. It is common knowledge that hemorrhage is a complication of approximately 25% of pelvic fractures, and requires massive transfusion [3]. Our patient had severe hemorrhage and persistent hypotension from a bleeding right hypogastric artery. Although his pulmonary artery pressures and cardiac output were normal, pulmonary artery catheter placement and monitoring occurred after a significant volume had been transfused. Levon M. Capan, MD Kenneth Sutin, MD Department of Anesthesiology; New York University School of Medicine; New York, NY 10016 Pedro F. Ibarra, MD Clinica Reina Sofia; Bogota, Colombia Staffan Wahlander, MD Department of Anesthesiology; New York University School of Medicine; New York, NY 10016