RESUMEN
BACKGROUND: Spinal cord injury (SCI) produces acute hemodynamic alterations through disruption of sympathetic output of the autonomic nervous system and places individuals with SCI at high risk of secondary ischemic insult to the spinal cord as well as to other organs. The purpose of this study was to examine hemodynamics and serum vasopressin concentration in the acute period following complete cervical SCI in piglets. METHODS: We developed a new model of traumatic complete cervical SCI in piglets and measured acute hemodynamic variables and serum arginine vasopressin (AVP) concentrations at baseline and for 4 h after SCI under fentanyl anesthesia. RESULTS: Complete cervical SCI caused an immediate tachycardia which lasted for approximately 1 h, immediate hypotension which was sustained for the 4-h duration of the study, decreases in both systemic and pulmonary vascular resistance, and a compensatory increase in cardiac output, which resulted initially from an increase in heart rate (HR) but was later sustained after resolution of tachycardia by an increase in cardiac stroke volume. Serum AVP concentration increased significantly after SCI and did not change in the control group. Neurogenic shock did not occur due to the robust increase in cardiac output and cardiac stroke volume. CONCLUSIONS: Complete cervical SCI produces hemodynamic alterations consistent with the withdrawal of sympathetic tone. Although mean arterial pressure (MAP) decreased significantly after SCI, the increase in serum vasopressin may have played a role in maintaining blood pressure and preventing circulatory collapse, a complication which is encountered frequently in patients with cervical and upper thoracic SCI.
Asunto(s)
Arginina Vasopresina/sangre , Hemodinámica , Traumatismos de la Médula Espinal/fisiopatología , Animales , Animales Recién Nacidos , Presión Sanguínea , Gasto Cardíaco , Vértebras Cervicales , Frecuencia Cardíaca , Imagen por Resonancia Magnética , Circulación Pulmonar , Médula Espinal/patología , Traumatismos de la Médula Espinal/sangre , Traumatismos de la Médula Espinal/diagnóstico , Volumen Sistólico , Porcinos , Factores de Tiempo , Resistencia VascularRESUMEN
A 5-year-old female presented with anasarca secondary to protein-losing enteropathy after fenestrated extracardiac Fontan. There was no response to digoxin, furosemide, spironolactone and captopril. She had coarctation of the aorta and left pulmonary artery stenosis resistant to multiple surgical and balloon interventions. Stent expansion of these lesions resulted in the patient's recovery from protein-losing enteropathy.