Resumen Objetivo: El objetıvo de este estudio fue investigar el efecto de la isquemia inducida del cuerpo carotideo por la acídosis de líquido cefalorraquídeo en la médula espinal durante una hemorragia subaracnoidea (SAH). Metodo: Conejos híbridos (n = 23) fueron divididos en Control (n = 5), Sham (inyectados con 0.5 mil de solución isotónica) (n = 6), y SAH (n = 12) (inyectados en el 4º ventrículo con 0.5 ml de sangre autológa) y monitoreados por tres semanas. Se analizaron: El pH del líquido cerebro espinal, la densidad de las células ependimarias y el volúmen del canal cervical central. Resultados: La media del volumen del canal cervical central, la densidad de las células ependimarias degeneradas y los valores de pH fueron 1.056 + 0.053 mm3-6 + 2 per mm2-7.342 + 0.034, 1.321 + 0.12 mm3-35 + 9 per mm2-7.314 + 0.056 y 1.743 + 0.245 mm3-159 + 24 per mm2-7.257 + 0.049 en los grupos Control, Sham y SHA, respectivamente. La mayor densidad inducida de la neurona del cuerpo carotideo degenerado, disminuyó los valores de pH del líquido cefalorraquideo lo que podría dar como resultado un aumento en la descamación de las células ependimarias asi como la dilatación del canal central. Conclusión: Un aumento en la neurodegeneración del cuerpo carotideo puede reducir la degeneración de los ependimocitos y la dilatacióm del canal central siguiendo SAH.

Abstract Objective: We investigated the effect of carotid body ischemia-induced cerebrospinal fluid acidosis on spinal cord during subarachnoid hemorrhage (SAH). Methods: Twenty-three hybrid rabbits were divided into three groups: control (n = 5), Sham (injected with 0.5 ml isotonic) (n = 6), and the SAH (n = 12) (injected with 0.5 ml autologous blood into the 4th ventricle) and then monitored for 3 weeks. Cerebrospinal fluid pH and degenerated ependymal cell density and volume of cervical central canal were analyzed. Results: The mean cervical central canal volumes, degenerated ependymal cells densities, and cerebrospinal pH values were 1.056 ± 0.053 mm3-6 ± 2 per mm2-7.342 ± 0.034, 1.321 ± 0.12 mm3-35 ± 9 per mm2-7.314 ± 0.056, and 1.743 ± 0.245 mm3-159 ± 24 per mm2-7.257 ± 0.049 in the Control, Sham, and SAH groups, respectively. The more degenerated carotid body neuron density induced decreased cerebrospinal fluid pH values (p < 0.0001) could result in the more ependymal cells desquamation (p < 0.0005) and central canal dilatation (p < 0.00001). Conclusion: Increased neurodegeneration of carotid bodies can reduce cause cerebrospinal fluid pH-induced ependymal cell degeneration and central canal dilatation following SAH.

Conventional intubation for pulmonary management in children with a difficult airway may be very challenging even in skilled hands. Rapid advancements in respiratory care have reduced the incidence of difficult tracheal intubation and the incidence of complications have decreased accordingly. However, serious unexpected complications still occur in some patients today. Herein, we describe a syndromic newborn infant with a difficult airway who experienced migration of the endotracheal tube into the esophagus after displacement of the tube connector. We would like to share our experience and contribute to the literature with the presentation of this undesired event. To the best of our knowledge, no such complication has been reported in the neonatal literature before.

La intubación convencional para la asistencia respiratoria en niños con vía aérea dificultosa puede ser un desafío incluso en manos expertas. Los rápidos avances en la atención respiratoria han reducido la incidencia de intubación traqueal dificultosa y por ende las complicaciones. Sin embargo, en algunos pacientes, todavía ocurren complicaciones graves inesperadas. Describimos el caso de un neonato con secuencia de Pierre Robin con vía aérea dificultosa, que presentó una migración del tubo endotraqueal hacia el esófago luego de haberse desprendido del conector del tubo. Deseamos compartir esta experiencia ya que, de acuerdo con nuestro conocimiento, esta complicación no ha sido comunicada anteriormente en neonatos.

The aims of this study were to investigate the serum levels of some cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin 1ß (IL-1ß), IL-2R, IL-6, and IL-8] and nitric oxide (NO) levels in patients with untreated brucellosis and to test the correlation of these parameters with each other. The study was conducted on 67 subjects, 37 patients with brucellosis and 30 healthy individuals with no history of Brucella infection. Brucellosis was identified by a positive blood culture and/or increased Brucella antibodies in serological tests in addition to compatible clinical symptoms. Cytokine profile analysis was performed by the immulite chemiluminescent enzyme immunometric assay whose inter- and intra-assay coefficients of variance were 2.6-3.6 and 4.4-8.5%, respectively. The levels of nitrites/nitrates, which are representative of NO levels, were measured by the Griess method. Patients with brucellosis had significantly elevated serum levels of nitrites/nitrates, IL-2R, IL-6 and IL-8 (mean ± SD, 102.8 ± 23.8 µmol/l, 806.1 ± 58.5 U/ml, 21.1 ± 2.3 pg/ml, and 8.8 ± 1.6 pg/ml, respectively) compared to healthy controls, whereas TNF-alpha and IL-1ß levels were unchanged. No statistically significant correlation was detected between any of the studied cytokine levels and nitrate/nitrite concentrations according to Pearson's linear correlation test. We conclude that only IL-6, IL-8 and IL-2R are elevated in brucellosis and the extent of elevation depends on the severity and clinical pattern of the disease. Moderate elevation in serum NO was comparable to that observed in previous studies. This explains the absence or very rare occurrence of septic shock in brucellosis.