Pneumomediastinum and pneumothorax during emergency tracheotomy under spontaneous ventilation: Macklin meets Müeller? / Neumomediastino y neumotórax en la traqueotomía urgente en ventilación espontánea. Cuando Macklin encontró a Müeller

Potentially serious complications associated to emergency tracheotomy continue being a matter of concern. We review the pathogenesis of gas leakage in this setting and discuss about the possible mechanisms involved in its cause. We present two cases of pneumomediastinum, subcutaneous emphysema and pneumothorax in the context of emergency tracheotomy under spontaneous ventilation, finally resolved by chest drainage. The combination of overly negative pleural pressures due to extreme inspiratory efforts in the context of an almost completely obstructed airway together with over-pressurized alveoli because of gaseous entrapment secondary to serious expiratory obstruction appears to be the most plausible primary cause of air leaks in our patients. Understanding the underlying mechanisms evolved in its production will help clinicians to suspect and diagnose this phenomenon (AU)

Las complicaciones graves asociadas a la traqueotomía urgente continúan siendo un desafío clínico. En este trabajo revisamos y discutimos la fisiopatología de la fuga aérea en el contexto de la traqueotomía urgente. Presentamos dos casos de neumomediastino, enfisema subcutáneo y neumotórax en el curso de sendas traqueotomías urgentes realizadas sobre pacientes en ventilación espontánea que se resolvieron tras inserción de drenaje pleural. Nuestra conclusión es que la combinación de presiones pleurales inspiratorias muy negativas por el esfuerzo inspiratorio contra una vía aérea obstruida junto con la presencia de alveolos hiper-presurizados por el atrapamiento gaseoso espiratorio constituyen la base etiopatogénica del proceso. La comprensión de los mecanismos que subyacen en la generación del neumotórax y neumomediastino en este contexto facilitará que los clínicos sospechen y diagnostiquen el cuadro (AU)

Topical application of betahistine improves eustachian tube function in an animal model.

CONCLUSION: Betahistine dihydrochloride, a drug used widely in the systemic treatment of balance disorders such as Ménière's disease, was found to improve eustachian tube function when applied topically in the nasopharynx of rats. OBJECTIVES: The study tested the effect of betahistine, a histamine receptor agonist, on eustachian tube function and tested the involvement of H1 and H3 histamine receptors. METHODS: Eustachian tube function was measured in anaesthetized rats while middle ear pressure was increased and then monitored during induced swallowing. Betahistine and other drugs were applied topically in the nasopharynx, bulla and epipharynx, and administered intraperitoneally. RESULTS: Systemic application of betahistine hardly changed eustachian tube function, but topical application significantly improved it. The action of topical betahistine was unaffected by the HI receptor antagonist mepyramine and was mimicked by the H3 agonist, ciproxifan.

Ventilator-induced lung injury upregulates and activates gelatinases and EMMPRIN: attenuation by the synthetic matrix metalloproteinase inhibitor, Prinomastat (AG3340).

Mechanical ventilation has become an indispensable therapeutic modality for patients with respiratory failure. However, a serious potential complication of MV is the newly recognized ventilator-induced acute lung injury. There is strong evidence suggesting that matrix metalloproteinases (MMPs) play an important role in the development of acute lung injury. Another factor to be considered is extracellular matrix metalloproteinase inducer (EMMPRIN). EMMPRIN is responsible for inducing fibroblasts to produce/secrete MMPs. In this report we sought to determine: (1) the role played by MMPs and EMMPRIN in the development of ventilator-induced lung injury (VILI) in an in vivo rat model of high volume ventilation; and (2) whether the synthetic MMP inhibitor Prinomastat (AG3340) could prevent this type of lung injury. We have demonstrated that high volume ventilation caused acute lung injury. This was accompanied by an upregulation of gelatinase A, gelatinase B, MT1-MMP, and EMMPRIN mRNA demonstrated by in situ hybridization. Pretreatment with the MMP inhibitor Prinomastat attenuated the lung injury caused by high volume ventilation. Our results suggest that MMPs play an important role in the development of VILI in rat lungs and that the MMP-inhibitor Prinomastat is effective in attenuating this type of lung injury.