Tuberculosis (TB) is an uncommon cause of severe respiratory failure, even in highly endemic regions. Mortality in cases requiring mechanical ventilation (MV) varies between 60 and 90%. The use of extracorporeal membrane oxygenation (ECMO) is not frequently needed in TB. We report the case of a 24 year old woman diagnosed with bilateral pneumonia that required MV and intensive care, patient was managed with prone ventilation for 48 h, but persisted in refractory hypoxemia. Etiological study was only positive for mycobacterium tuberculosis. As a rescue therapy arterio-venous extracorporeal CO2 removal was started and lased for 4 days, but fails to support the patient due to greater impairment of oxygenation. Veno-venous ECMO was then initiated, thus normalizes gas exchanged and allows lungs to rest. ECMO was maintained for 36 days, with two episodes of serious complication treated successfully. Given the absence of clinical improvement and the lack of nosocomial infection, at 42-day of ICU stay methylprednisolone 250 mg daily for 4 days was started, since secondary organizing pneumonia associated with TB was suspected. Thereafter progressive improvement in pulmonary mechanics and reduction of pulmonary opacities was observed, allowing the final withdrawal of ECMO. Percutaneous tracheostomy was performed and the patient remained connected until her transfer to her base hospital at day 59 of admission to our unit. The tracheostomy was removed prior to hospital discharge, and the patient is today at home. Prolonged ECMO support is a useful and potentially successful tool in catastrophic respiratory failure caused by TB.
This study was intended to investigate changes in cardiac biomarkers and pulmonary hemodynamic effects of invasive treatment in patients with intermediate-risk (hemodynamic stability with evidence of right ventricle dysfunction and/or myocardial injury) pulmonary embolism. Also, to also evaluate if natriuretic peptide type-B (NT-proBNP) plasma levels are associated with right ventricle function and pulmonary arterial pressures. Interventional study: Fourteen normotensive adult patients with acute and radiologically massive pulmonary embolism plus positive biomarkers and evidences of right ventricle dysfunction underwent invasive pulmonary angiography for invasive treatment consisting on mechanical thrombus fragmentation and catheter-directed intrathrombus thrombolysis. Angiography was repeated after 12-24 h to reevaluate perfusion status. Plasma biomarkers were monitored before and 8-h after intervention. Biomarkers were initially elevated in all patients. Eleven patients (78.6%) exhibited significant angiographic reperfusion. NT-proBNP and mean pulmonary arterial pressure decreased significantly in all of them [3693 (1803, 8862) to 1951 (1309, 7918) pg/ml; P = 0.008) and 40.0 (24.0, 46.0) to 22.0 (14.0, 27.0) mmHg; P = 0.003, respectively]. No significant variation was observed in troponin-T levels. In patients with high-risk pulmonary embolism, NT-proBNP plasma levels experience rapid and significant reduction after successful invasive treatment. In pulmonary embolism, serial measurements of NT-proBNP could be useful as a tracking tool to assess the success or failure of the thrombolytic treatment.
Controversies in massive pulmonary embolismpuc.cl P or largo tiempo la literatura médica se ha referido de distinta manera al tromboem bolismo pulmonar (TEP) que amenaza la vida. Diagnósticos como TEP mayor 1 , TEP anatómicamente masivo, TEP radiológicamente masivo y TEP angiográficamente masivo 2 , TEP grave y TEP masivo 3 son utilizados frecuente y a veces indistintamente al referirse a este tipo de pacientes. Esta variabilidad en las definiciones puede llegar a ser un obstáculo en la comprensión de la patología, contribuyendo a crear confusión en el clínico y dificultando la interpretación de las publicaciones sobre el tema.Durante algún tiempo, la condición de gravedad del TEP se asoció a la magnitud del compromiso anatómico. De esta manera, el TEP anatómica o radiológicamente masivo (obstruc ción mayor de 50% de los vasos pulmonares o de dos o más arterias lobares) 2,4 se asumió como un cuadro de similar gravedad al TEP con compro miso hemodinámico.La gravedad de los pacientes con TEP depende de la clínica y no exclusivamente de la extensión de compromiso radiológico o anatómico. El prin cipal criterio para calificar un TEP como masivo es la hipotensión arterial sistemica 5 , es decir, un paciente con TEP masivo radiológico o angiográ fico no necesariamente cursa con compromiso hemodinámico. El impacto clínico y los resultados dependen no solamente del tamaño del émbolo o de la carga embólica, sino también del estado cardiopulmonar basal del paciente.En los casos fatales, la mayoría de las muer tes se producen dentro de la primera hora de la presentación clínica y los TEP anatómicamente masivos son responsables de solamente la mitad de estos casos 6 .El TEP tiene una mortalidad y morbilidad asociada que se mantiene elevada a pesar de avan ces en terapia y diagnóstico. La mortalidad varía ampliamente dependiendo de la gravedad clínica de la embolia y está en rangos de menos de 1% hasta más de 50% en los casos más graves 7 11 . El TEP masivo está asociado a un peor pronóstico y a tasas de mortalidad de hasta 65% en la fase aguda 12 . La mayoría de las muertes secundarias al TEP se deben a falla cardiaca refractaria y no a insuficiencia respiratoria.La presencia de disfunción o falla ventricular derecha secundaria a una sobrecarga aguda de presión, es el elemento fisiopatológico más im portante para definir la gravedad de los pacientes y el pronóstico clínico a corto plazo 13 .El grado de disfunción ventricular derecha
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