P Prodhan1, D Casavant, M D Medlock, P Yager, J Kim, N Noviski. 1. Division of Pediatric Critical Care Medicine, Massachusetts General Hospital for Children, Boston, Massachusetts 02114, USA. pprodhan@partners.org
Abstract
UNLABELLED: Many cadaveric organs for transplantation come from patients dying of sudden intracranial catastrophes. Cardiopulmonary dysfunction after such neurogenic insults is a well-recognized entity. The pulmonary dysfunction usually presents as florid pulmonary edema within minutes to hours after the initial intracranial insult and may occur in isolation or co-exist with overt or subclinical myocardial dysfunction. This may result in severe hypoxia, which threatens survival and outcomes in salvageable cases and organ preservation in patients who would be potential organ donors. Thus, rapid initiation of strategies aimed at ameliorating hypoxia after an acute neurogenic insult is paramount. Strategies aimed at improving acute hypoxia include maximizing ventilator support, diuretics, and volume resuscitation. Cardiac dysfunction may require use of ionotropes. We report the case of a 16-year-old female who developed catastrophic acute posterior fossa intracranial bleeding with resulting intractable hypoxia due to neurogenic cardiopulmonary dysfunction that responded dramatically to inhaled nitric oxide (INO). The patient went on to successfully donate organs following a non-heart-beating donor protocol. This therapy, to our knowledge, has never been described previously for use in patients with hypoxia secondary to neurogenic cardiopulmonary dysfunction. CONCLUSIONS: We document for the first time a dramatic response of hypoxia to INO in neurogenic cardiopulmonary dysfunction. This therapy ameliorates hypoxia, which may have vital implications in minimizing secondary brain injury in salvageable cases and optimizing organ preservation in potential organ donors with catastrophic intracranial insults.
UNLABELLED: Many cadaveric organs for transplantation come from patients dying of sudden intracranial catastrophes. Cardiopulmonary dysfunction after such neurogenic insults is a well-recognized entity. The pulmonary dysfunction usually presents as florid pulmonary edema within minutes to hours after the initial intracranial insult and may occur in isolation or co-exist with overt or subclinical myocardial dysfunction. This may result in severe hypoxia, which threatens survival and outcomes in salvageable cases and organ preservation in patients who would be potential organ donors. Thus, rapid initiation of strategies aimed at ameliorating hypoxia after an acute neurogenic insult is paramount. Strategies aimed at improving acute hypoxia include maximizing ventilator support, diuretics, and volume resuscitation. Cardiac dysfunction may require use of ionotropes. We report the case of a 16-year-old female who developed catastrophic acute posterior fossa intracranial bleeding with resulting intractable hypoxia due to neurogenic cardiopulmonary dysfunction that responded dramatically to inhaled nitric oxide (INO). The patient went on to successfully donate organs following a non-heart-beating donor protocol. This therapy, to our knowledge, has never been described previously for use in patients with hypoxia secondary to neurogenic cardiopulmonary dysfunction. CONCLUSIONS: We document for the first time a dramatic response of hypoxia to INO in neurogenic cardiopulmonary dysfunction. This therapy ameliorates hypoxia, which may have vital implications in minimizing secondary brain injury in salvageable cases and optimizing organ preservation in potential organ donors with catastrophic intracranial insults.