With damage-control laparotomies, the traumatic ECF rate is increasing and is a different entity than nontraumatic ECF. Although the two populations have similar mortality rates, the trauma cohort demonstrates higher spontaneous closure rates and a curiously higher rate of development in men. Fistula output was not predictive of spontaneous closure.

A. Barker has no conflicts of interest, financial or otherwise. B. Wagener has an ongoing collaboration with Sadis Matalon (co-author of the primary review) and has published a paper with him within the last 3 yr. Furthermore, B. Wagener is a co-investigator on both the outpatient and inpatient tranexamic acid studies mentioned in the letter. Editor S. Matalon was not involved in the peer review process of this manuscript.

Carbon monoxide (CO) is the most common cause of poisoning and poisoning-related death in the United States. It is a tasteless and odorless poisonous gas produced from incomplete combustion of hydrocarbons, such as those produced by cars and heating systems. CO rapidly binds to hemoglobin to form carboxyhemoglobin, leading to tissue hypoxia, multiple-organ failure, and cardiovascular collapse. CO also binds to myocardial myoglobin, preventing oxidative phosphorylation in cardiac mitochondria and resulting in cardiac ischemia or stunning and cardiogenic pulmonary edema. Treatment of CO poisoning is mainly supportive, and supplemental oxygen remains the cornerstone of therapy, whereas hyperbaric oxygen therapy is considered for patients with evidence of neurological and myocardial injury. Extracorporeal membrane oxygenation (ECMO) has been utilized effectively in patients with respiratory failure and hemodynamic instability, but its use has rarely been reported in patients with CO poisoning. We report the successful use of venoarterial ECMO in a patient with severe CO poisoning and multiple-organ failure.